Search

This study investigates the impact of weather information sources on consequences associated with extreme heat events, employing a cross-sectional survey conducted on hospitalized individuals who have experienced heat stress in Central Vietnam. Multiple information channels, including official agencies and social media, were found to significantly reduce the Cost of Illness (COI) associated with heat-related ailments. Social media, in particular, emerged as a potent tool for climate adaptation. Improving the clarity and accessibility of weather information through official channels is crucial, especially for households with varying income levels. Demographic factors such as age and gender should be considered when fine-tuning communication strategies, with special attention given to individuals with underlying medical conditions, who are particularly susceptible to extreme heat effects. These findings underscore the need to maximize the reach of weather-related information and reduce economic burdens on affected populations. This provides valuable insights for policymakers aiming to bolster climate resilience in vulnerable regions like Vietnam, emphasizing the significance of diverse information sources and tailored communication in climate change adaptation., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2023 Published by Elsevier Inc. CC BY-NC-ND 4.0.)

Phosphor-converted white light-emitting diodes (WLEDs) have received significant attention; however, the leaked light from their blue InGaN chips has an undesirable effect on human health. Hence, it is necessary to develop red, green, and blue-emitting phosphors, which can be excited by an NUV chip instead of a blue chip. Herein, green-emitting ZnO:Cu 2+ phosphors have been successfully synthesized by a simple and facile thermal diffusion method. The obtained powder shows a broad emission band peaking at 525 nm and a strong absorption peak at 377 nm. The ZnO:5%Cu 2+ phosphor annealed at 800 °C in 2 hours revealed a lifetime of 0.57 ms, an activation energy of 0.212 eV, and the highest emission intensity with ( x , y ) CIE colour coordinates (0.3130, 0.5253). A WLED prototype has been fabricated by coating the ZnO:5%Cu 2+ phosphor on an NUV 375 nm LED chip, where this coated phosphor shows a high quantum efficiency (QE) of 56.6%. This is, so far, the highest reported QE value for ZnO-based phosphors. These results suggest that the ZnO:Cu 2+ phosphor could be an excellent candidate for NUV-pumped phosphor-converted WLED applications.

Eu 3+ -doped phosphors have been much attractive owing to their narrow-band red emission peak at 610-630 nm with high color purity; however, the weak and narrow absorption band in the NUV region limits their applications. Doping a higher amount of Eu 3+ ions into a non-concentration quenching host could be key to enhancing the efficiency of the absorption value and emission intensity. Hence, the design of Eu 3+ -heavily doped phosphors with a suitable host lattice is key for applications. In this study, red-emitting Eu 3+ -doped Gd(BO 2 ) 3 -Y 3 BO 6 -GdBO 3 (GdYGd:Eu 3+ ) phosphor with a high quantum efficiency of 58.4% and excellent color purity of 99.5% is reported for the first time. The phosphor is efficiently excited by NUV light at 394 nm and emits a strong red emission band in the 590-710 nm range, peaking at 612 nm. The optimal annealing temperature and Eu 3+ doping content to obtain the strongest PL intensity are 1100 °C and 20 mol%, respectively. The optimized GdYGd:Eu 3+ phosphor possesses a high activation energy of 0.319 eV and a lifetime of 1.14 ms. An illustration of phosphor-coated NUV LED with chromaticity coordinates ( x = 0.5636, y = 0.2961) was successfully synthesized, demonstrating the great potential of GdYGd:Eu 3+ phosphor for NUV-pumped WLED applications., Competing Interests: There are no conflicts to declare., (This journal is © The Royal Society of Chemistry.)

We study phase transition properties of the two-dimensional q-state clock model by an extensive Monte Carlo simulation. By analyzing the Binder ratio and its temperature derivative, we confirm that the two-dimensional q-state clock model exhibits two distinct Kosterlitz-Thouless phase transitions for q=5,6 but it has one second-order phase transition for q=4. The critical temperatures are estimated quite accurately from the crossing behavior of the Binder ratio (for q<5) and from negative divergent dips of the derivative of the Binder ratio (for q≥5) around these critical points. We also calculate the correlation length, the helicity modulus, and the derivative of the helicity modulus, and analyze their behaviors in different phases in detail.

SARS Coronavirus-2 is one of the most widespread viruses globally during the 21 st century, whose severity and ability to cause severe pneumonia and death vary. We performed a comprehensive systematic review of all studies that met our standardised criteria and then extracted data on the age, symptoms, and different treatments of Covid-19 patients and the prognosis of this disease during follow-up. Cases in this study were divided according to severity and death status and meta-analysed separately using raw mean and single proportion methods. We included 171 complete studies including 62,909 confirmed cases of Covid-19, of which 148 studies were meta-analysed. Symptoms clearly emerged in an escalating manner from mild-moderate symptoms, pneumonia, severe-critical to the group of non-survivors. Hypertension (Pooled proportion (PP): 0.48 [95% Confident interval (CI): 0.35-0.61]), diabetes (PP: 0.23 [95% CI: 0.16-0.33]) and smoking (PP: 0.12 [95% CI: 0.03-0.38]) were highest regarding pre-infection comorbidities in the non-survivor group. While acute respiratory distress syndrome (PP: 0.49 [95% CI: 0.29-0.78]), (PP: 0.63 [95% CI: 0.34-0.97]) remained one of the most common complications in the severe and death group respectively. Bilateral ground-glass opacification (PP: 0.68 [95% CI: 0.59-0.75]) was the most visible radiological image. The mortality rates estimated (PP: 0.11 [95% CI: 0.06-0.19]), (PP: 0.03 [95% CI: 0.01-0.05]), and (PP: 0.01 [95% CI: 0-0.3]) in severe-critical, pneumonia and mild-moderate groups respectively. This study can serve as a high evidence guideline for different clinical presentations of Covid-19, graded from mild to severe, and for special forms like pneumonia and death groups., (© 2021 John Wiley & Sons Ltd.)

Aim: Diuretics are a cornerstone in treatment of heart failure (HF). Torasemide is a loop diuretic with a potential advantage over other diuretics. We aim to meta-analyse and compare the effect of torasemide with furosemide in HF patients., Methods: A comprehensive literature search using 12 databases including PubMed, Scopus, and Web of Science was performed. All randomized controlled trials (RCTs) comparing furosemide and torasemide in HF patients were included and meta-analysed. We assessed the risk of bias using Cochrane Collaboration's tool. The protocol was registered in PROSPERO (CRD42016046112)., Results: Eighteen RCTs with 1598 patients were included. There was a significant difference between torasemide 20 mg and furosemide 40 mg in increasing the urine volume (standard difference of the mean (SDM) [95% confidence interval] = -0.78 [-1.52 to -0.053], P = .036). Torasemide 10 mg and 10 to 20 mg have a significant effect on potassium excretion in comparison with furosemide 25 to 40 mg (P = .018 and .023, respectively). In general, torasemide and furosemide have no significant difference in mortality, edema improvement, weight loss, heart rate, and reducing systolic/diastolic blood pressure. However, oral torasemide has a significant lower hospital stay P < .001 and superior effect in improving ejection fraction P = .029., Conclusion: Although not all results are statistically significant, torasemide has potential advantages on multiple aspects of HF management when compared with furosemide. More studies are needed to clarify these effects., (© 2019 John Wiley & Sons, Ltd.)

The relationship between the severity of dengue infection and allergy is still obscure. We conducted an electronic search across 12 databases for relevant articles reporting allergic symptoms, dengue infection, and dengue classification. These studies were categorized according to dengue severity and allergy symptoms, and a meta-analysis was performed by pooling the studies in each category. Among the included 57 articles, pruritus was the most common allergic sign followed by non-specified allergy and asthma (28.6%, 13%, and 6.5%, respectively). Despite the reported significant association of dengue with pruritus and total IgE level (P < 0.05), in comparison with non-dengue cases and healthy controls, there was no association between the different severe dengue group with pruritus, skin allergy, food allergy or asthma. However, removing the largest study revealed a significant association between asthma with dengue hemorrhagic fever (DHF) rather than dengue fever (DF). In comparison with DF, DHF was associated with IgE positivity. Furthermore, specific-IgE level was higher in secondary DF rather than primary DF. There was a possible association between allergy symptoms and dengue severity progression. Further studies are needed to clarify this association.

Background: The massive abundance of studies relating to tropical medicine and health has increased strikingly over the last few decades. In the field of tropical medicine and health, a well-conducted systematic review and meta-analysis (SR/MA) is considered a feasible solution for keeping clinicians abreast of current evidence-based medicine. Understanding of SR/MA steps is of paramount importance for its conduction. It is not easy to be done as there are obstacles that could face the researcher. To solve those hindrances, this methodology study aimed to provide a step-by-step approach mainly for beginners and junior researchers, in the field of tropical medicine and other health care fields, on how to properly conduct a SR/MA, in which all the steps here depicts our experience and expertise combined with the already well-known and accepted international guidance.We suggest that all steps of SR/MA should be done independently by 2-3 reviewers' discussion, to ensure data quality and accuracy., Conclusion: SR/MA steps include the development of research question, forming criteria, search strategy, searching databases, protocol registration, title, abstract, full-text screening, manual searching, extracting data, quality assessment, data checking, statistical analysis, double data checking, and manuscript writing., Competing Interests: Competing interestsThe authors declare that they have no competing interests.

Systematic reviews and/or meta-analyses generally provide the best evidence for medical research. Authors are recommended to use flow diagrams to present the review process, allowing for better understanding among readers. However, no studies as of yet have assessed the quality of flow diagrams in systematic review/meta-analyses. Our study aims to evaluate the quality of systematic review/meta-analyses over a period of ten years, by assessing the quality of the flow diagrams, and the correlation to the methodological quality. Two hundred articles of "systematic review" and/or "meta-analysis" from January 2004 to August 2015 were randomly retrieved in Pubmed to be assessed for the flow diagram and methodological qualities. The flow diagrams were evaluated using a 16-grade scale corresponding to the four stages of PRISMA flow diagram. It composes four parts: Identification, Screening, Eligibility and Inclusion. Of the 200 articles screened, 154 articles were included and were assessed with AMSTAR checklist. Among them, 78 articles (50.6%) had the flow diagram. Over ten years, the proportion of papers with flow diagram available had been increasing significantly with regression coefficient beta = 5.649 (p = 0.002). However, the improvement in quality of the flow diagram increased slightly but not significantly (regression coefficient beta = 0.177, p = 0.133). Our analysis showed high variation in the proportion of articles that reported flow diagram components. The lowest proportions were 1% for reporting methods of duplicates removal in screening phase, followed by 6% for manual search in identification phase, 22% for number of studies for each specific/subgroup analysis, 27% for number of articles retrieved from each database, and 31% for number of studies included in qualitative analysis. The flow diagram quality was correlated with the methodological quality with the Pearson's coefficient r = 0.32 (p = 0.0039). Therefore, this review suggests that the reporting quality of flow diagram is less satisfactory, hence not maximizing the potential benefit of the flow diagrams. A guideline with standardized flow diagram is recommended to improve the quality of systematic reviews, and to enable better reader comprehension of the review process., Competing Interests: The authors have declared that no competing interests exist.

Leukemia is the most commonly diagnosed childhood cancer, although its etiology is still largely unknown. Growing evidence supports a role for infection in the etiology of acute lymphocytic leukemia (ALL), and the involvement of the immune system suggests that vaccination may also play a role. However, the findings presented in the published literature are inconsistent. Therefore, we conducted a PRISMA systematic review and meta-analysis. 14 studies were identified and meta-analyzed. Vaccinations studied comprised Bacillus Calmette-Guérin (BCG) vaccine, Triple vaccine, Hepatitis B vaccine (HBV), Polio, Measles, Rubella, Mumps, trivalent MMR vaccine and Haemophilus influenza type B (HiB) vaccine. We observed a protective association between any vaccination in the first year of life and risk of childhood leukemia (summary odds ratio (OR) 0.58 [95% confidence interval (CI) 0.36-0.91]). When individual vaccines were analysed, some evidence of an association was seen only for BCG (summary OR 0.73 [95% CI 0.50-1.08]). In conclusion, early vaccination appears to be associated with a reduced risk of childhood leukemia. This finding may be underpinned by the association observed for BCG. Given the relatively imprecise nature of the results of this meta-analysis, our findings should be interpreted cautiously and replicated in future studies.

We report a case of carotid endarterectomy and clipping of an ipsilateral internal carotid artery aneurysm in a patient with complete contralateral carotid stenosis. The patient developed an ischaemic electroencephalographic (EEG) tracing on temporary carotid clamping and bypass shunt was contraindicated. We used thiopentone titrated to EEG burst suppression for pharmacological cerebral protection during the subsequent prolonged carotid clamp necessary for carotid endarterectomy. We review the use of thiopentone for this purpose, in particular the evidence for efficacy, mechanism of action and optimal dosage and timing of administration.

Small-volume resuscitation using hypertonic saline (7.5%) is effective for various types of shock. Recently, hypertonic saline has been proposed for fluid management in patients with impaired cardiovascular function. Whether hypertonic saline is safe in the compromised heart during coronary occlusion is not known. We examined the effects of hypertonic saline at 4 mL.kg-1 on myocardial function and blood flow during acute coronary occlusion. In anesthetized dogs, the left ventricle (LV) was instrumented with pressure and ultrasonic dimension transducers. Myocardial contractility was assessed using percent of systolic shortenings measured in both normal or ischemic regions. Blood flow distribution was measured using radioactive microspheres. Percent of systolic shortening and blood flow in the normal myocardium, unaltered by coronary occlusion, increased significantly after hypertonic saline from 11.0 +/- 1.1% to 13.7 +/- 1.4% and from 120 +/- 13 mL.min-1.100 g-1 to 169 +/- 13 mL.min-1.100 g-1, respectively. In the ischemic myocardium, occlusion of the left anterior descending coronary artery markedly decreased percent of systolic shortening from 13.0 +/- 1.2% to 9.3 +/- .9% and blood flow from 98 +/- 13 mL.min-1.100 g-1 to 19 +/- 10 mL.min-1.100 g-1. At peak effect of hypertonic saline contractility and blood flow in the ischemic myocardium decreased to 7.4 +/- .8% and 12 +/- 5 mL.min-1.100 g-1, respectively. Five of the nine dogs developed premature ventricular beats during hypertonic saline infusion. However, no significant changes were observed when normal saline was given at equivalent volumes to hypertonic saline in six dogs. Hypertonic saline was associated with significant increases in heart rate (from 116 +/- 3 beats.min-1 to 129 +/- 5 beats.min-1) and cardiac output (from 2.54 +/- .17 L.min-1 to 3.32 +/- .26 L.min-1). Except for an improved perfusion in the skin, hepatic arterial, and coronary beds, blood flow to the muscle, spleen, jejunum, kidney, and brain was not significantly altered by hypertonic saline. Our data demonstrates variant effects of hypertonic saline on either normal or ischemic myocardium. Whereas contractile function and blood flow in the normal myocardium were improved after hypertonic saline infusion, further decreases in blood flow and contractile function in region distal to coronary occlusion could lead to worsening of ischemic injury. These data suggest that hypertonic saline may be deleterious in hearts with impaired contractile function caused by ischemia.

Resuscitation using small volumes (3-5 mL/kg) of 7.5% hypertonic saline (HTS) is effective for hemorrhagic shock. Whether HTS is beneficial for the initial resuscitation of burn injury is not clear. We compared the hemodynamic effects of HTS versus lactated Ringer's solution (LR) and examined organ tissue perfusion during burn resuscitation (R). Full thickness scald burn (35% of total body surface area) was induced in pentobarbital-anesthetized rats. Regional blood flows were measured using radioactive microspheres before and 30 min after burn, and after R with either HTS (4 mL/kg) or LR (at a dose required for equivalent restoration of arterial blood pressure). Data from the HTS-or LR-resuscitated groups were compared to those from a nonresuscitated group (n = 10 in each group). Mean arterial pressure decreased 30% after burn (from 120 +/- 4 to 84 +/- 5 mm Hg, mean +/- SEM) and returned toward baseline (112 +/- 7 mm Hg) at 10 min after R with HTS (4 mL/kg) or LR (22.6 +/- 0.7 mL/kg), but subsequently decreased to 100 +/- 7 mm Hg with HTS and 105 +/- 5 mm Hg with LR at 30 min. In contrast to LR, resuscitation using HTS was associated with tachycardia. Blood flows to the skin and muscle of the normal or burn regions did not change after fluid resuscitation as compared to a nonresuscitated group. Fluid resuscitation transiently increased intestinal perfusion. Similar improvements in blood flow to the spleen were observed with HTS and LR at 10 min after R (from 128 +/- 10 to 156 +/- 15 and from 113 +/- 10 to 145 +/- 26 mL.min-1 x 100 g-1, respectively). However, at 30 min after R, splenic perfusion in the LR group was not different from that in the nonresuscitated group. Blood flows to the brain and kidney increased 39% and 42%, respectively, with HTS. HTS was also associated with pronounced improvements in blood flows to the heart (from 346 +/- 20 to 631 +/- 37 mL.min-1 x 100 g-1), liver (from 36 +/- 2 to 62 +/- 4 mL.min-1 x 100 g-1), and testis (from 29 +/- 2 to 43 +/- 2 mL.min-1 x 100g-1). Resuscitation using HTS was associated with rapid improvement in organ tissue perfusion in anesthetized rats subjected to burn injury. In comparison to LR, greater increases in blood flows to the heart, kidney, liver, and testis were observed with HTS. The results suggest that significant improvement in blood flow distribution can be achieved using HTS at less than one fifth the volume of LR for the initial treatment of burn shock.

Objective: To develop a method of measuring end-systolic elastance from information obtained outside the ventricle and thereby simplify its transduction., Design: Prospective, within-animal comparative analysis., Setting: University-based laboratory study., Participants: Six mixed-breed dogs., Interventions: Instrumentation included minor axis sonomicrometry, ascending aortic flow probe, aortic and ventricular pressure transducers, and constricting cuffs on the vena cavae and aorta., Measurements and Main Results: Elastance was determined from the equation PES = EES (VED - VES), where VED - VES is stroke volume and PES is end-systolic arterial pressure. EES was derived from both preload and afterload manipulation. Cardiac performance indices were calculated automatically by computer under conditions of varying load and inotropy. This extraventricular method of elastance calculation was compared by linear regression and analysis of variance to preload recruitable stroke work, traditional EES determination (using ventricular dimension instead of volume), and LVdP/dt at 50 mmHg. EES measured from the aortic sites correlated well with the other contractility indicators (p < 0.003 in all cases) and demonstrated more sensitivity and stability under loading manipulation than traditional EES. A strong relationship between the change in stroke volume and end-systolic ventricular diameter during acute aortic constriction (r = 0.924, p < 0.0001) was observed, and the mean r value for the individual outflow elastance measurements was 0.97 +/- 0.02., Conclusions: In this study, measurement of EES from the ventricular outflow tract during progressive aortic constriction produced results more consistent and descriptive than EES by traditional techniques and has the potential for obtaining elastance measurements from possibly less invasive techniques.

The spinal cord is an important site where inhaled anesthetics suppress movement in response to noxious stimuli. Inhaled anesthetics also act in peripheral tissues, although it is unclear whether these actions influence anesthetic requirements. In six isoflurane-anesthetized mongrel dogs, we placed Y cannulas in the lower aorta and vena cava, allowing us to divert blood to, and infuse blood from, a bubble oxygenator/roller pump system or to maintain normal blood flow. This technique permits a greatly diminished isoflurane concentration at the site of the noxious stimulus (tail), while maintaining isoflurane in the remainder of the body. After baseline minimum alveolar anesthetic concentration (MAC1) was determined, venous blood from the lower body was diverted to the bubble oxygenator and reinfused into the lower body via the aortic cannula; MAC2 was determined with isoflurane in the lower body at approximately 0.2%, and MAC3 was determined with isoflurane in the lower body matched to the end-tidal isoflurane. Bypass was terminated, the native circulation established, and MAC4 determined. MAC1, 2, 3, and 4 were (mean +/- SD) 1.3 +/- 0.3%, 1.2 +/- 0.1%, 1.2 +/- 0.2%, and 1.1 +/- 0.2%, respectively (P > 0.05). We conclude that the peripheral effects of isoflurane do not influence the response to a noxious stimulus.

We examined the hypothesis that the coronary vasomotor responses to etomidate (ETO), propofol (PRO), and sodium thiopental (STP) are mediated through contrasting effects on the resting nitric oxide (NO)-dependent vasodilator tone that opposes adrenergic vasoconstrictor activity in the intact dog. Circumflex flow (CxF) responses to randomized intracoronary microinjections (0.3 mL) of normal saline (NS), alkalinized saline (AS), intralipid (IL), adenosine (ADE, 17 micrograms), acetylcholine (ACh, 1.25 micrograms), ETO (6, 12, 60 micrograms), PRO (30, 60, 300 micrograms), and STP (75, 150, 750 micrograms) were quantified in eight isoflurane-anesthetized dogs with fixed ventricular rates (100 bpm). Injections were repeated during intravenous (IV) infusion (50 mg/kg + 1 mg.kg-1.min-1) of NG-nitro-L-arginine methyl ester (L-NAME). ADE and ACh transiently increased CxF to 305% +/- 20% (P < 0.001) and 310% +/- 29% (P < 0.001) of resting values, respectively. ETO had no effect, whereas PRO (300 micrograms) provoked small transient increases in CxF to 135% +/- 4% (P < 0.05) of control. Responses to STP (750 micrograms) were characterized by momentary decreases to 74% +/- 4% (P < 0.001), followed immediately by increases to 183% +/- 11% (P < 0.001) of resting values; NS AS, and IL had no effect. The momentary decreases with STP (750 micrograms) were significantly augmented during NO inhibition with CxF declining to 49% +/- 7% (P < 0.001) of resting values, whereas the secondary increase was unchanged. With L-NAME, CxF responses to ACh were attenuated to 32% +/- 3% (P < 0.001) of control, whereas responses to ADE, ETO, and PRO were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

During acute myocardial ischaemia, the function of the unaffected muscle is the primary determinant of residual cardiac performance. We compared six methods of measuring regional function in the remaining non-ischaemic segment after acute ligation of the left anterior descending (LAD) coronary artery in 16 dogs. Preparation included left ventricular micromanometers, regional sonomicrometer transducers to measure segment length and wall thickness, caval occluders and left atrial catheters for injection of radioactive microspheres to measure regional blood flow. Pulmonary artery, central venous and systemic arterial pressures were measured and regional coronary venous blood was collected for direct myocardial oxygen consumption (VO2) calculations. Under basal high-dose fentanyl-neuromuscular blocker anaesthesia, the LAD was occluded after addition of halothane or isoflurane at 0.5 or 1.5 MAC concentrations. Regional myocardial function of the non-ischaemic segment was assessed by the following computer-derived indices: percent systolic wall thickening (% WT), velocity of shortening (vs), percent systolic shortening (%SS), regional stroke work (RSW), regional preload recruitable stroke work (RPRSW) and regional end-systolic elastance (Ees). No index demonstrated enhanced function in the non-ischaemic segment after LAD ligation and all monitors, except Ees, were sensitive to depression of function represented by a decrease in values after administration of halothane and isoflurane (P < 0.05). Ees values increased with the addition of isoflurane and remained constant with halothane. Circulating concentrations of catecholamines were unchanged after ischaemia, while inhalation agents caused a decrease in the concentrations of adrenaline and dopamine (P < 0.05), but not noradrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)

Background: As part of studies aimed at better defining the effects of anesthetics at different anatomic sites, we have developed a model of preferentially delivering inhaled anesthetics to the in situ goat brain, using a bubble oxygenator and roller pump. We tested the hypotheses that (1) this model excludes the cerebral circulation from the body; (2) the concentration of halothane in the oxygenator exhaust correlates with the concentration of halothane in the oxygenator arterial blood., Methods: After ligation of the occipital arteries in six halothane-anesthetized goats, we used a bubble oxygenator to perfuse the brain preferentially (exclusive of the body) via a carotid artery, draining cranial venous blood back into the oxygenator via the isolated jugular veins. (In goats, the vertebral arteries do not directly contribute to the cerebral circulation, and internal jugular veins and extracranial internal carotid arteries are absent). The extent of isolation was determined with radioactive microspheres injected into the left atrium during the following periods: (1) baseline; (2) during bypass when the blood pressure in the head equalled that in the body; (3) during bypass when the blood pressure in the body exceeded that in the head by approximately 30-35 mmHg; (4) when the bypass roller pump was stopped. We also measured the concentration of halothane in the arterial blood of the bypass unit. In three animals, systemic metocurine was administered during bypass to detect the presence of venous contamination., Results: Baseline cerebral blood flow was 74 +/- 32 ml.100 g-1.min-1 (mean +/- SD). During bypass, cerebral blood flow originating from the systemic circulation was less than 1 ml.100 g-1.min-1, and isolation extended to the caudal medulla during periods 3 and 4, and to the first 1-cm segment of the spinal cord during period 2. The concentration of halothane in the oxygenator exhaust correlated reasonably well with the arterial halothane concentration (r = 0.82, P < 0.001). Systemic arterial metocurine concentrations peaked at 1 min (27 +/- 3.7 micrograms/ml) and decreased to 10.6 +/- 2.3 micrograms/ml at 10 min; head venous metocurine plasma concentrations gradually increased to 3.1 +/- 0.4 micrograms/ml at 10 min., Conclusions: This technique permits selective perfusion and delivery of inhaled anesthetics to the in situ goat brain, but is not adequate for selective delivery of fixed intravenous anesthetics.

The present study examined the postulate that the quotient of mean systemic arterial pressure and heart rate predicts the severity of myocardial ischemia during occlusion of the left anterior descending coronary artery. Studies were performed in open-chest fentanyl-anesthetized dogs before and during halothane (n = 8) or isoflurane (n = 8) anesthesia. The pressure-rate quotient (PRQ) decreased significantly in both groups during incremental increases in halothane or isoflurane to 68% and 57% of control values at 0.5 MAC and to 41% and 38% at 1.5 MAC for halothane and isoflurane, respectively. Myocardial lactate production was unchanged from the ischemic region, and no correlation between the PRQ and myocardial lactate production was observed. In contrast, heart rate correlated significantly (r = 0.376; P less than 0.05) with lactate production. The product of systolic systemic arterial pressure and heart rate (rate-pressure product) correlated with blood flow (r = 0.493; P less than 0.001) and with oxygen consumption (r = 0.571; P less than 0.001) in the normal myocardium. A weak correlation (r = 0.330; P less than 0.05) of rate-pressure product with myocardial lactate production from the ischemic region was observed. There were no correlations between the PRQ and myocardial lactate production from the ischemic region or indices of blood flow distribution (i.e., inner/outer ratio in the ischemic region or ischemic/normal ratio). The relationship of hemodynamic variables to measurements of regional myocardial metabolism was independent of background anesthetic agent of depth of anesthesia. The current data suggest that heart rate changes are weakly predictive of severity of myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

This study determined the effect of cardiopulmonary bypass (CPB) on canine enflurane minimum alveolar concentration (MAC). Fourteen dogs were anesthetized with enflurane in N2O and O2, and after tracheal intubation, the N2O was discontinued. Femoral arterial and pulmonary arterial catheters were placed, and MAC was determined with the tail-clamp method. CPB was initiated via the femoral artery-vein route, with additional venous return obtained from an external jugular vein. Partial CPB was used in the first 10 dogs. In 4 dogs, a membrane oxygenator (group 1) was used, and in the next 6 dogs a bubble oxygenator (group 2) was used. In 4 additional dogs (group 3), using bubble oxygenators, total CPB was achieved by occlusion of the pulmonary artery via a left thoracotomy. The CPB circuit was primed with Ringer's lactate, and circuit blood flows were 70-125 ml.kg-1.min-1, with mean arterial pressures maintained at 50-110 mmHg. MAC was determined again after termination of CPB. In 10 dogs, MAC was also measured during CPB. In 5 dogs MAC was measured after administration of protamine. MAC in all 14 dogs did not change (2.2 +/- 0.3 vs. 2.3 +/- 0.3). MAC remained constant in group 1 (2.4 +/- 0.3 vs. 2.3 +/- 0.4), group 2 (2.2 +/- 0.2 vs. 2.3 +/- 0.3), and group 3 (2.2 +/- 0.1 vs. 2.3 +/- 0.1). Similarly, MAC was unchanged during CPB (2.2 +/- 0.2 vs. 2.2 +/- 0.2) and after protamine (2.3 +/- 0.2 vs. 2.2 +/- 0.3). Temperature was 38.3 +/- 1.2 prebypass and 37.9 +/- 0.9 postbypass.(ABSTRACT TRUNCATED AT 250 WORDS)

Protamine sulfate (PS), used to neutralize the anticoagulant effect of heparin, is often associated with systemic hypotension. Whether this hypotension is secondary to a depression of myocardial function is not clear. The present study tested the hypothesis that systemic hypotension was accompanied by a depression in myocardial function and examined the possible role of histamine in mediating the cardiovascular response to PS. Seven conditioned dogs were chronically instrumented with pressure and ultrasonic dimension transducers. Studies were conducted under halothane anesthesia 7 to 10 days after instrumentation. Cardiac contractility was assessed using the slope, Ees, of the linear regression of the left ventricular end-systolic pressure-diameter relationship. Intravenous infusion of PS, 5 mg/kg, when given in periods of less than 30 seconds, decreased systemic arterial pressure by 45% (from 101 +/- to 54 +/- 5 mm Hg) without change in heart rate. Cardiac output decreased by 22% from control and the slope Ees decreased by 37% (from 14.5 +/- 1.2 to 8.7 +/- 1.4 mm Hg/mm). Systemic vascular resistance decreased by 34% (from 2581 +/- 121 to 1712 +/- 200 dyne.s.cm-5). The cardiovascular depression caused by PS was transient and could not be reproduced by a repeated dose given within a 60-minute period. Antagonists of histamine (diphenhydramine and cimetidine) could not attenuate the PS-induced cardiovascular depression. This depression was independent of preheparinization and did not occur when PS was infused slowly over a 2-minute period. The data clearly demonstrate negative inotropic and vasodilator effects of PS following rapid administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Fenoldopam, a selective dopamine1 receptor agonist, has been recommended for induced hypotension because it effectively lowers arterial blood pressure and improves renal perfusion. We examined cardiovascular functions during hypotension induced by fenoldopam or sodium nitroprusside. In eight halothane-anesthetized dogs, the left ventricle (LV) was instrumented with pressure and ultrasonic dimension transducers for the assessment of LV contractility using the analysis of the pressure-diameter relationship. Blood flow distribution was measured by radioactive microspheres. Doses of fenoldopam and nitroprusside were titrated to reduce mean arterial blood pressure to 60 mm Hg. After 40 min of hypotension, fenoldopam and nitroprusside caused similar increases in heart rate (17% +/- 4% vs 19% +/- 10%, respectively) and decreases in systemic vascular resistance (-24% +/- 5% vs -27% +/- 4%). Hypotension induced by fenoldopam was associated with higher LV end-diastolic pressure (4.4 +/- 0.6 vs 2.5 +/- 1.1 mm Hg) and end-systolic meridional wall stress (33.0 +/- 4.3 vs 17.8 +/- 2.1 g/cm2) when compared with nitroprusside. There were no significant changes in cardiac output and cardiac contractility as expressed by the slope (Ees) of the LV end-systolic pressure-diameter relationship, velocity of shortening of the diameter, and percentage of wall thickening of the LV. In contrast to nitroprusside, which decreased renal blood flow from 197 +/- 19 to 163 +/- 15 mL/min, renal blood flow increased during fenoldopam-induced hypotension from 187 +/- 20 to 239 +/- 18 mL/min. The increase in renal perfusion was similar in upper, middle, and lower regions of the kidney; however, it was more in the medulla compared with the cortex (37% +/- 17% vs 25% +/- 7%).(ABSTRACT TRUNCATED AT 250 WORDS)

A denervated, isolated canine hindlimb (HL) model was developed to minimize residual anesthetic contamination. To test the preparation, we determined the peripheral arterial vascular effects of atropine sulfate and the effect of the basal anesthetic on arterial resistance. In four dogs that were under halothane and oxygen anesthesia, the HL was prepared to allow either vascular isolation of the limb or continuity with the systemic circulation. During isolation the HL was perfused by roller pump at a preset flow rate through an infant oxygenator. Inspired gas fed to the oxygenator contained either 0%, 1.25%, or 2.5% halothane to determine that anesthetic's effect on HL arterial vascular resistance. No halothane (0%) was used in the oxygenator inflow during the atropine measurements. Vascular resistance was calculated from HL arterial pressure at constant flow. Halothane caused a significant stepwise fall in vascular resistance, with a decrease of 68% at 2.5% inspired concentration (p less than 0.01). Atropine produced a progressive attenuation of resistance that decreased by 18% after the 2.5 mg/kg dose (p less than 0.01). The model proved stable over time and demonstrated an apparent direct, dose-dependent vasodilating effect of both atropine and halothane in the canine HL muscle arterial bed.

The present study examines the postulate that isoflurane, in contrast to halothane, causes redistribution of blood flow away from an ischemic myocardial region through vasodilation of adjacent normally perfused myocardium. The study was performed in open-chest dogs anesthetized with fentanyl; ischemia was induced by occlusion of the left anterior descending coronary artery. At 0.6% alveolar concentration, isoflurane increased transmural blood flow to 125% of control values (P less than 0.05) in the normal region without concomitant changes in blood flow to the ischemic region or in the endocardial/epicardial flow ratio in the ischemic region. The evidence excludes either transmural steal or regional redistribution phenomena. Myocardial blood flow variables returned to control values at 1.8% isoflurane, and no blood flow redistribution effects were evident. In contrast, whereas halothane 0.4% caused no significant effect on myocardial blood flows, an alveolar concentration of 1.2% decreased transmural blood flow to normally perfused left ventricle to 70% of control (P less than 0.05). Regional myocardial oxygen consumption in the normal and ischemic areas decreased at higher alveolar concentrations and was unchanged at the lower concentrations for both agents. Myocardial lactate production from the ischemic region was unchanged with either agent, suggesting that, in terms of metabolic changes, neither agent worsened ischemia during sustained occlusion of the left anterior descending coronary artery. The present data show no evidence for worsening of myocardial ischemia with either isoflurane or halothane. Isoflurane causes a relatively greater increase in perfusion compared to myocardial oxygen consumption of normally perfused myocardium; nevertheless, sufficient coronary vascular reserve remains in the native collateral circulation so that myocardial metabolic supply-and-demand relationships during ischemia are not further compromised.

Small volumes (4-6 mL/kg) of 7.5% hypertonic saline solution (HTS) are reported to be effective for resuscitation from circulatory shock. When infused rapidly into either hypovolemic or normovolemic subjects, HTS can cause an immediate and severe hypotension before cardiovascular improvement. In the present study, we examined the hypothesis that the early hypotension produced by HTS was mediated by an acute and transient depression of cardiac contractility. left ventricular pressure and wall motions were measured simultaneously in 10 anesthetized dogs for the assessment of cardiac contractility. Infusion of HTS at 3 mL/kg in 1 min significantly decreased mean arterial blood pressure by 49%, from 95 +/- 4 to 51 +/- 5 mm Hg (P less than 0.05, mean +/- SEM) at 45 s after the onset of infusion. This initial decrease in arterial blood pressure was abrupt and transient (106 +/- 9 s). Concomitantly, cardiac output and coronary blood flow increased significantly from 2.8 +/- 1.0 to 3.9 +/- 1.1 L/min and from 23.7 +/- 5.3 to 49.8 +/- 4.7 mL/min, respectively. Although heart rate remained constant, systolic shortenings of left ventricular diameter and wall thickness increased from 5.6% +/- 0.5% to 7.8% +/- 0.5% and from 13.9% +/- 0.6% to 15.1% +/- 1.2%, respectively, indicating an improvement in cardiac contractility. This was confirmed by subsequent analysis of the left ventricular end-systolic pressure-diameter relationship. Systemic and pulmonary vascular resistance decreased by 60% and 27%, respectively. Despite an initial period of hypotension after rapid infusion of HTS, mean arterial blood pressure, cardiac output, and contractility were all significantly increased at 5 min after HTS infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

We examined the specific effects of 7.5% hypertonic saline (HTS) on myocardial performance and regional blood flow and compared the efficacies of HTS and lactated Ringer's solution (LR) for hypovolemic resuscitation. Studies were performed in anesthetized dogs subjected to rapid hemorrhage to decrease mean arterial pressure by 50% over 60 min. The animals were resuscitated with either HTS (n = 8) at 5 ml/kg or LR (n = 7) at a dose required for equivalent restoration of cardiac output. Cardiac contractility was assessed using the slope Ees of the left ventricular end-systolic pressure-diameter relationship and regional blood flow was measured using radioactive microspheres. At 10 min after resuscitation, mean arterial pressure increased from 45.1 +/- 2.5 to 77.7 +/- 3.2 mmHg with HTS and 50.9 +/- 2.5 to 80.1 +/- 3.2 mmHg with LR. Resuscitation with either fluid caused significant increases in heart rate and similar decreases in vascular resistance. Cardiac contractility (Ees) did not change significantly with LR, whereas with HTS, Ees increased from 14.8 +/- 0.9 during hemorrhage to 19.4 +/- 1.6 as compared with a baseline value of 13.4 +/- 1.5 mmHg/mm. Hemorrhage decreased blood flow to various organs by 50% to 70% of baseline. Except for better improvement in splenic and hepatic perfusion with HTS, similar restoration of blood flow to the heart, muscle, skin, kidney, and jejunum was observed at 10 min after resuscitation with either fluid. In this animal model of rapid and severe hemorrhagic shock, HTS given at approximately one-sixth the volume of LR was equally effective in providing temporary restoration of hemodynamic function.(ABSTRACT TRUNCATED AT 250 WORDS)

Under halothane anesthesia five dogs were prepared with both hindlimbs isolated from the systemic circulation to allow intermittent placement on extracorporeal perfusion at constant flow. One limb of each dog was surgically denervated. In this relatively anesthetic-free preparation, graded equivalent doses of alfentanil, fentanyl, and sufentanil were infused over 30 s, and vascular resistance was measured. Increasing opioid administration caused a progressive diminution in peripheral resistance. By the high dose level, alfentanil (500 micrograms/kg), fentanyl (50 micrograms/kg), and sufentanil (6 micrograms/kg) caused equal and significant decreases of 48%, 48%, and 44% in resistance, respectively. There was no difference among the opioids in effects on resistance at equivalent dosages. Neither pretreatment with naloxone nor denervation changed the response to the narcotics. We conclude that the three synthetic opioids produce vasodilation by direct action on the peripheral vascular smooth muscle.

We studied the effects of graded exposure to hyperbaric (1,875 mm Hg) oxygen therapy in an acute stroke model prepared by unilateral carotid artery interruption in gerbils. Pentobarbital alone, superoxide dismutase alone, two periods of hyperbaric oxygen alone, and each agent combined with hyperbaric oxygen were administered to investigate possible mechanisms of protection from cerebral ischemia. Survival rates and neurologic deficit scores over 5 days in all treated groups were compared with those in a control group. Survival rates in the groups subjected to 2 (63.9 +/- 4.0%) and 4 hours (70.1 +/- 5.2%) of hyperbaric oxygen alone were significantly higher than in the control group (53.6 +/- 4.2%). The group treated with pentobarbital alone also demonstrated increased survival (69.8 +/- 7.0%), but the combination of therapeutic regimens offered no apparent additive protection. By 5 days there were no differences in the neurologic deficit scores of the survivors in the groups. The toxic pulmonary effects of hyperbaric oxygen were assessed in a pilot LD50 study. The pressure used caused no mortality during 4 hours of exposure, and the calculated LD50 was 7.26 hours. This investigation demonstrates that graded doses of hyperbaric oxygen given after the insult increase survival in a gerbil model of stroke.

Malignant hyperthermia (MH) diagnostic biopsy centers across North America have not previously been standardized in regard to protocols and specific muscles. Recent standardization criteria prompted this study of the vastus and rectus abdominis muscles. This study evaluated changes in contracture tension after electrical stimulation of 271 bundles taken from the vastus (n = 16) and rectus abdominus (n = 19) muscle biopsies of normal individuals when exposed to tissue baths in the absence of and in the presence of caffeine (0.5, 1.0, 2.0, 4.0, 8.0, and 32.0 mM) alone, halothane (1% or 3%) alone, or the combination of halothane (1%) plus caffeine (0.25, 0.5, 1.0, 2.0, 4.0, and 32.0). Caffeine threshold concentration was that concentration of caffeine that produced a 7% increase in tension. Caffeine specific concentration (CSC) and halothane caffeine specific concentration (HCSC) were those concentrations of caffeine alone or of halothane plus caffeine that produced a 1 g increase in tension. The concentration of caffeine alone that increased the contracture tension by 7% averaged 6.7 +/- 0.3 mM for vastus, significantly greater than 4.1 +/- 0.2 mM for the rectus muscle biopsies. Caffeine specific concentration was significantly greater for vastus muscle (7.7 +/- 0.7 mM) than it was for rectus muscle (4.9 +/- 0.4 mM). Three percent halothane alone showed contractures in 3/41 vastus (all less than 0.5 g) and 18/54 rectus muscle bundles (8 greater than 0.5 g). Mean HCSC was statistically significantly greater for vastus muscle (1.9 +/- 0.2 mM) than for rectus muscle (1.2 +/- 0.2 mM).(ABSTRACT TRUNCATED AT 250 WORDS)

Intracranial pressure (ICP) was measured during alfentanil-induced rigidity in rats. Ten rats had arterial, central venous (CVP), and subdural cannulae inserted under halothane anesthesia. The animals were mechanically ventilated to achieve normocarbia (PCO2 = 42 +/- 1 mmHg, mean +/- SE). Following instrumentation, halothane was discontinued and alfentanil (125 mu/kg) administered iv during emergence from halothane anesthesia. In the five rats that developed somatic rigidity, ICP and CVP increased significantly above baseline (delta ICP 7.5 +/- 1.0 mmHg, delta CVP 5.9 +/- 1.3 mmHg). These variables returned to baseline when rigidity was abolished with metocurine. In five rats that did not become rigid, ICP and CVP did not change following alfentanil. These observations suggest that rigidity should be prevented when alfentanil, and, presumably, other opiates, are used in the anesthetic management of patients with ICP problems.

Alfentanil is an opioid that has been used both as a sole anesthetic and in conjunction with other inhalation anesthetics. However, its effects on myocardial performance and regional blood flow are not clearly known. Using sonomicrometry and radioactive microsphere techniques, we examined the hemodynamic responses to alfentanil when given as a loading dose (45 micrograms/kg) followed by continuous infusion (3 micrograms X kg-1 X min-1) in dogs anesthetized with halothane. Similar plasma levels of alfentanil were observed after the loading and infusion doses, and both techniques of administration produced a significant reduction in arterial pressure without change in global or regional function of the left ventricle. Although cardiac output and left ventricular end-diastolic pressure remained unchanged, heart rate and systemic vascular resistance decreased significantly after the loading dose and recovered slightly when alfentanil was infused continuously. Despite the systemic hypotension, alfentanil did not alter perfusion to the heart, brain, muscle, and skin; however, blood flow to the renal cortex and the arterial supply to the liver decreased by 25 and 60%, respectively. Reduction in blood flow to the kidneys and the liver suggests that alfentanil should be used with caution when normal function of these organs is in question.

To evaluate the influence of adenosine triphosphate (ATP)-induced vasodilation on myocardial performance and blood flow during aortic crossclamping (XC), ten dogs were instrumented to measure left ventricular (LV) pressure and dimensions. Regional LV function was assessed from the percentage of systolic shortening, whereas the slope of the linear regression of the LV end-systolic pressure-diameter relationship was used as an index of overall contractility. The regional blood flow distribution was measured from sequential injections of radioactive microspheres. Following XC, systemic arterial pressure proximal to the clamp (SAPa), LV end-diastolic pressure (LVEDP), LV end-systolic meridional wall stress (WS), and central venous pressure (CVP) increased significantly, whereas the cardiac index (CI) and heart rate did not change. After 30 minutes of ATP infusion (1 mg/kg/min) SAPa, LVEDP, WS, and CVP returned to control levels, CI increased significantly compared with XC alone, and vascular resistance fell below the control level. ATP produced a threefold increase in myocardial blood flow and shifted the intramural distribution in favor of the endocardial layer. In conclusion, our investigation of the effect of ATP on aortic XC in a canine model showed the drug to produce a smooth, predictable, and rapid reduction in left ventricular preload and afterload. This was accomplished with minimal changes in distal organ perfusion, some improvement in measured cardiac performance, and a large increase in myocardial blood flow.

The present study was undertaken to compare the hemodynamic effects of adenosine triphosphate (ATP) and sodium nitroprusside (NP) given in equieffective doses to induce hypotension during halothane anesthesia. Eight dogs, instrumented with pressure and ultrasonic dimension transducers for assessment of left ventricular (LV) performance, were given both NP and ATP. Regional blood flow was measured by radioactive microspheres. After 20 min of infusion, both drugs decreased systemic arterial pressure by 36% with minimal changes in cardiac index (CI), LV end-diastolic pressure, or heart rate. However, hypotension produced by ATP was associated with a greater CI (3.84 +/- 0.32 vs 2.97 +/- 0.35 L X min-1 X m-2) than was NP and also associated with a further decrease in systemic vascular resistance (14.4 +/- 1.4 vs 17.7 +/- 2.2 mm Hg X L-1 X min X m2). Left ventricular global function, measured by the slope of the linear regression line of the LV end-systolic pressure-diameter relation (Ees), did not change significantly after either drug. Blood flow to the coronary bed was significantly greater with ATP than with NP (231.6 +/- 30.6 vs 81.7 +/- 6.1 ml X min-1 X 100 g-1). Except for an increase in hepatic arterial blood flow with NP, neither ATP nor NP significantly altered blood flow to the brain, spinal cord, spleen, kidney, jejunum, muscle, and skin. Controlled hypotension by ATP was stable and rapidly reversible without rebound hypertension. The results of this study indicate that ATP is a rapidly acting, effective hypotensive agent that compares favorably with NP.

The present study was undertaken to examine cardiovascular function before and after either intravenous or intra-arterial infusion of hypertonic saline (7.5% NaCl) in halothane-anesthetized dogs. A high-fidelity micromanometer and ultrasonic dimension transducers were implanted to measure pressure and wall motion of the left ventricle (LV). Cardiac output (CO) was measured using an electromagnetic flowmeter and thermodilution. The slope (Ees) of the linear regression of the LV pressure-diameter relationship was used as an index of cardiac contractility. Intravenous infusion of hypertonic saline (3 ml/kg) increased mean arterial pressure (MAP, 104 +/- 6 to 116 +/- 6 mmHg), heart rate (HR, 124 +/- 21 to 140 +/- 13 bpm), CO (3.2 +/- 0.9 to 4.2 +/- 0.5 l/m) and Ees (11.6 +/- 2.1 to 14.8 +/- 1.9 mmHg/mm). Systemic vascular resistance (SVR) fell by 18%. The above responses were similar whether infusion was intravenous or intra-arterial into innervated or denervated hind limbs. While nerve blockade at T-4 (xylocaine) attenuated the changes in CO and SVR and completely prevented the tachycardia, the inotropic response remained intact. These studies suggest that the cardiac effects of hypertonic saline infusion are not mediated by pulmonary or peripheral osmoreceptors and the increased contractility may result from a direct myocardial effect of increased osmolality.