Search

Author(s): Niklas Nielsen [sup.1], Alain Cariou [sup.2] [sup.3], Christian Hassager [sup.4] Author Affiliations: (1) 0000 0001 0930 2361, grid.4514.4, Department of Clinical Sciences Lund, Anesthesia and Intensive Care, Lund University, [...]

Author(s): José Jalife Sudden cardiac arrest is a common cause of death in people with coronary artery disease, and also kills many young people who have heritable heart diseases. In [...]

Purpose Some of the neuroprotective effects of hydrogen sulfide (H.sub.2S) have been attributed to systemic hypometabolism and hypothermia. However, systemic metabolism may vary more dramatically than brain metabolism after cardiac arrest (CA). The authors investigated the effects of inhaled exogenous hydrogen sulfide on brain metabolism and neurological function in rabbits after CA and resuscitation. Methods Anesthetized rabbits were randomized into a sham group, a sham/H.sub.2S group, a CA group, and a CA/H.sub.2S group. Exogenous 80 ppm H.sub.2S was administered to the sham/H.sub.2S group and the CA/H.sub.2S group which suffered 3 min of untreated CA by asphyxia and resuscitation. Effects on brain metabolism (cerebral extraction of oxygen (CEO.sub.2), arterio-jugular venous difference of glucose [AJVD(glu)] and lactate clearance), S100B, viable neuron counts, neurological dysfunction score, and survival rate were evaluated. Results CEO.sub.2, AJVD(glu), and lactate increased significantly after CA. Inhalation of 80 ppm H.sub.2S significantly increased CEO.sub.2 (25.04 ± 7.11 vs. 16.72 ± 6.12 %) and decreased AJVD(glu) (0.77 ± 0.29 vs. 1.18 ± 0.38 mmol/L) and lactate (5.11 ± 0.43 vs. 6.01 ± 0.64 mmol/L) at 30 min after resuscitation when compared with the CA group (all P < 0.05). In addition, neurologic deficit scores, viable neuron counts, and survival rate were significantly better whereas S100B was decreased after H.sub.2S inhalation. Conclusions The present study reveals that inhalation of 80 ppm H.sub.2S reduced neurohistopathological damage and improves early neurological function after CA and resuscitation in rabbits. The increased CEO.sub.2 and decreased AJVD(glu) and enhanced lactate clearance may be involved in the protective effects., Author(s): Xia Wei [sup.1], Le Duan [sup.1], Liqun Bai [sup.1], Miaomiao Tian [sup.1], Wenzhi Li [sup.1], Bing Zhang [sup.1] Author Affiliations: (1) grid.412463.6, 0000000417626325, Department of Anesthesiology, Second Affiliated Hospital [...]

Three-dimensional (3D) optical coherence tomography (OCT) images of rat brain taken through the thinned skull were measured using quadrature fringe wide-field OCT (QF WF OCT) with a period of 10 min for total measurement time of 210 min stopping blood flow due to cardiac arrest, in order to investigate the potential of OCT to monitor tissue viability in brains. First, spatial resolution degradation was evaluated with QF WF OCT to demonstrate that the axial resolution was 390 [micro]m at a thickness of 1000 [micro]m. After cardiac arrest, the signal intensity in depth profiles increased 2.7 times compared with that before cardiac arrest. The ratio of signal intensity after euthanasia with an injection of pentobarbital sodium salt to that before sharply increased for 20 min, with stationary values of 2 to 4 overall. The trends of time variations of each position were similar. However, each stationary value depended on the 3D position. OCIS codes: 170.1610, 170.2655, 170.3880, 170.3890, 170.4500, 170.6935.

Humans with central lesions that augment sympathetic nerve activity are predisposed to cardiac arrhythmias, myocardial lesions, and sudden death. Previously, we showed that selectively killing neurons with neurokinin-1 receptors in the nucleus tractus solitarii (NTS) of rats attenuated the baroreflex and, in some animals, led to sudden unexplained death within ~2 wk. Interruption of arterial baroreflexes is known to increase sympathetic activity. Here we tested the hypothesis that lesions in the NTS lead to fatal cardiac arrhythmias and myocardial lesions. We studied electrocardiograms, echocardiograms, blood pressure, and heart rate in 14 adult male rats after bilateral microinjection into the NTS of stabilized substance P conjugated to the toxin saporin and compared the variables in five sham control rats and in five animals with toxin injected outside the NTS. Only injection of toxin into the NTS led to increased lability of arterial blood pressure, a sign of baroreflex interruption. Two animals treated with toxin died suddenly. All animals engaged in normal activity until, in two, rapid development of asystole and death over 6-8 min. Cardiac function when examined by echocardiography was normal, but pathologic examination of the heart revealed diffuse microscopic areas of acute coagulation necrosis in the myocardium in five animals, focal subacute necrosis in two animals, and both changes in one animal. This study supports the hypothesis that NTS lesions interrupting the baroreflex may induce cardiac arrhythmias and myocardial changes similar to those seen in humans with central lesions and may lead to sudden cardiac death. baroreflex; cardiac arrhythmia; heart injuries; sudden death; sympathetic nervous system

The aim of this study was to investigate effects of poly(ADP-ribose) polymerase (PARP) inhibition on mesenteric vascular function and metabolism in an experimental model of cardiopulmonary bypass (CPB) with cardiac arrest. Twelve anesthetized dogs underwent 90-min hypothermic CPB. After 60 min of cardiac arrest, reperfusion was started for 40 min following application of either saline vehicle (control, n = 6) or a potent PARP inhibitor, PJ-34 (10 mg/kg iv bolus and 0.5 mg * [kg.sup.1] * [min.sup.-1] infusion for 20 min, n = 6). PJ-34 led to better recovery of cardiac outpu (2.2 [+ or -] 0.1 vs. 1.8 [+ or -] 0.2 1/min in control) and mesenteric blood flow (175 [+ or -] 38 vs. 83 [+ or -] 4 ml/min, P < 0.05 vs. control) after reperfusion. The impaired vasodilator response of the superior mesenteric artery to acetylcholine, assessed in the control group after CPB (-32.8 [+ or -] 3.3 vs. -57.6 [+ or -] 6.6% at baseline, P < 0.05), was improved by PJ-34 (-50.3 [+ or -] 3.6 vs. -54.3 [+ or -] 4.1% at baseline, P < 0.05 vs. control). Although plasma nitrate/nitrite concentrations were not significantly different between groups, mesenteric nitric oxide synthase activity was increased in the PJ-34 group (P < 0.05). Moreover, the treated group showed a marked attenuation of mesenteric venous plasma myeloperoxidase levels after CPB compared with the control group (75 [+ or -] 1 vs. 135 [+ or -] 9 ng/ml, P < 0.05). Pharmacological PARP inhibition protects against development of post-CPB mesenteric vascular dysfunction by improving hemodynamics, restoring nitric oxide production, and reducing neutrophil adhesion. endothelial function; nitric oxide; neutrophil adhesion; hemodynamics

The interstitial fluid of the human myocardium was monitored in 13 patients undergoing aortic valve and/or bypass surgery before, during, and after hypothermic potassium cardioplegia. The regulation of glucose and lactate was studied after sampling with microdialysis. The following questions were addressed. 1) Is the rate of transcapillary diffusion the limiting step for myocardial uptake of glucose before or after cardioplegia? 2) Does cold potassium cardioplegia induce a critical deprivation of glucose and/or accumulation of lactate in the myocardium? Before cardioplegia, interstitial glucose was ~50% of the plasma level (P < 0.001). Interstitial glucose decreased significantly immediately after induction of cardioplegia and remained low (1.25 [+ or -] 0.25 mM) throughout cardioplegia. It was restored to precardioplegic levels 1 h after release of the aortic clamp. Interstitial glucose then decreased again at 25 and 35 h postoperatively to the levels observed during cardioplegia. Interstitial lactate decreased immediately after induction of cardioplegia but returned to basal level during the clamping period. At 25 and 35 h, interstitial lactate was significantly lower than before and during cardioplegia. Glucose transport over the capillary endothelium is considered rate limiting for its uptake in the working heart but not during cold potassium cardioplegia despite the glucose deprivation following perfusion of glucose-free cardioplegic solution. Lactate accumulated during cardioplegia but never reached exceedingly high interstitial levels. We conclude that microdialysis provides information that may be relevant for myocardial protection during open-heart surgery. myocardium; ischemia; microdialysis; surgery

The hypothesis is that chronic increases in left ventricular (LV) load induce oxidative stress and latent matrix metalloproteinase (MMP) is activated, allowing the heart to dilate in the absence of endothelial nitric oxide (NO) and thereby reduce filling pressure. To create volume overload, an arteriovenous (A-V) fistula was placed in male Sprague-Dawley rats. To decrease oxidative stress and apoptosis, 0.08 mg/ml nicotinamide (Nic) was administered in drinking water 2 days before surgery. The rats were divided into the following groups: 1) A-V fistula, 2) A-V fistula + Nic, 3) sham operated, 4) sham + Nic, and 5) control (unoperated); n = 6 rats/group. After 4 wk, hemodynamic parameters were measured in anesthetized rats. The heart was removed and weighed, and LV tissue homogeneates were prepared. A-V fistula caused an increase in heart weight, lung weight, and end-diastolic pressure compared with the sham group. The levels of malondialdehyde (MDA; a marker of oxidative stress) was 6.60 [+ or -] 0.23 ng/mg protein and NO was 6.87 [+ or -] 1.21 nmol/l in the LV of A-V fistula rats by spectrophometry. Nic treatment increased NO to 13.88 [+ or -] 2.5 nmol/l and decreased MDA to 3.54 [+ or -] 0.34 ng/mg protein (P = 0.005). Zymographic levels of MMP-2 were increased, as were protein levels of nitrotyrosine and collagen fragments by Western blot analysis. The inhibition of oxidative stress by Nic decreased nitrotyrosine content and MMP activity. The levels of tissue inhibitor of metalloproteinase-4 mRNA were decreased in A-V fistula rats and increased in A-V fistula rats treated with Nic by Northern blot analysis. TdT-mediated dUTP nick-end labeling-positive cells were increased in A-V fistula rats and decreased in fistula rats treated with Nic. Acetylcholine and nitroprusside responses in cardiac rings prepared from the above groups of rats suggest impaired endothelial-dependent cardiac relaxation. Treatment with Nic improves cardiac relaxation. The results suggest that an increase in the oxidative stress and generation of nitrotyrosine are, in part, responsible for the activation of metalloproteinase and decreased endocardial endothelial function in chronic LV volume overload. nitric oxide; malondialdehyde; collagen degradation; tissue inhibitor of metalloproteinase; arteriovenous fistula; nicotinamide; NADH oxidase; nitrotyrosine; TUNEL; cardiac ring; acetylcholine; nitroprusside; stretch; contraction; relaxation; heart failure

Byline: Alexandra Gendo (1), Ludwig Kramer (1), Michael Hafner (1), Georg-Christian Funk (1), Christian Zauner (1), Fritz Sterz (2), Michael Holzer (2), Edith Bauer (1), Christian Madl (1) Keywords: Sensory evoked potentials Cardiopulmonary resuscitation Postischemic metabolic and circulatory derangements Outcome prediction Abstract: Objective: To assess the validity of early sensory evoked potential (SEP) recording for reliable outcome prediction in comatose cardiac arrest survivors within 48 h after restoration of spontaneous circulation (ROSC). Design and setting: Prospective cohort study in a medical intensive care unit of a university hospital. Patients: Twenty-five comatose, mechanically ventilated patients following cardiopulmonary resuscitation Measurements and results: Median nerve short- and long-latency SEP were recorded 4, 12, 24, and 48 h after ROSC. Cortical N20 peak latency and cervicomedullary conduction time decreased (improved) significantly between 4, 12, and 24 h after resuscitation in 22 of the enrolled patients. There was no further change in short-latency SEP at 48 h. The cortical N70 peak was initially detectable in seven patients. The number of patients with increased N70 peak increased to 11 at 12 h and 14 at 24 h there was no further change at 48 h. Specificity of the N70 peak latency (critical cutoff 130 ms) increased from 0.43 at 4 h to 1.0 at 24 h after ROSC. Sensitivity decreased from 1.0 at 4 h to 0.83 at 24 h after ROSC. Conclusion: Within 24 h after ROSC there was a significant improvement in SEP. Therefore we recommend allowing a period of at least 24 h after cardiopulmonary resuscitation for obtaining a reliable prognosis based on SEP. Author Affiliation: (1) Department of Internal Medicine IV, Intensive Care Unit 13 H1, University of Vienna, Wahringer Gurtel 18-20, 1090 Vienna, Austria (2) Department of Emergency Medicine, University of Vienna, Wahringer Gurtel 18-20, 1090 Vienna, Austria Article History: Received Date: 01/11/2000 Accepted Date: 17/05/2001 Article note: Final revision received: 16 May 2001 Electronic Publication

Research demonstrates that the HF-1b transcription factor of cardiac conduction system and ventricular myocytes play a role in the sudden cardiac death in humans. Data reveal that the cardiovascular arrest is due to cardiac arrhythmogenesis brought about by a decrease and mislocalization of connexins and defects in the formation of ventricular Purkinje fibers.

A study was conducted to investigate the effects of the stimulation of the adenosine A3 receptor with the highly selective A3 agonist 2-chloro-N6-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (Cl-IB-MECA). It was believed that this reaction would reduce postischemic dysfunction and morphological injury in a neutrophil-free isolated perfused rat heart model through the activation of K(sub ATP) channels. Findings have indicated that cardioprotection afforded by A3-receptor stimulation may be partly regulated using K(sub ATP) channels.

Byline: S. Gando (1), S. Nanzaki (1), Y. Morimoto (1), S. Kobayashi (1), O. Kemmotsu (1) Keywords: Key words Cardiac arrest; Cardiopulmonary resuscitation; Selectin; Neutrophil; Endothelium Abstract: Objective: To investigate the relationship between cytokines and the inflammatory responses in patients with out-of-hospital cardiac arrest, we examined the changes of cytokines as well as alterations in the markers of neutrophil activation, platelet and endothelial activation, and endothelial injury. Design: Prospective, cohort study. Setting: General intensive care unit of a tertiary care center. Patients and participants: 26 out-of-hospital cardiac arrest patients were classified into two groups: those who achieved return of spontaneous circulation (ROSC) (n = 10) and those with no ROSC (n = 16). Eight normal healthy volunteers served as control subjects. Measurements and results: Serial levels of soluble L-selectin (sL-selectin), soluble P-selectin (sP-selectin), neutrophil elastase, and soluble thrombomodulin were measured during and after cardiopulmonary resuscitation (CPR). Serial levels of tumor necrosis factor [alpha] (TNF[alpha]) and interleukin-1[beta] (IL-1[beta]) were also measured. We could not find any elevations in either cytokine during the study period. In both groups, sP-selectin levels were significantly higher than those in control subjects from the time of arrival at the emergency department to 24 h after admission. sL-selectin levels in the two groups were markedly lower compared to those in control subjects at all sampling points. In patients with ROSC, cardiac arrest and CPR led to an increase in the levels of neutrophil elastase and soluble thrombomodulin that peaked 6 h or 24 h after arrival at the emergency department. No statistical differences in the levels of the two selectins, neutrophil elastase, and soluble thrombomodulin between the two groups were found during CPR. Conclusions: Out-of-hospital cardiac arrest and CPR induces platelet, neutrophil, and endothelial activation and is associated with endothelial injury. Inflammatory cytokines may not have an important role in human whole-body ischemia-reperfusion injury. Author Affiliation: (1) Department of Anesthesiology and Intensive Care, Hokkaido University School of Medicine, N15 W7, Kita-ku, Sapporo, 060 Japan e-mail: sgando@med.hokudai.ac.jp Tel. +81(11)716--1161 Fax +81(11)716--9666, JP Article note: Received: 2 November 1998 Final revision received: 3 March 1999 Accepted: 26 March 1999

Byline: Rudrashish. Haldar, Jasleen. Kaur, Sukhminder. Bajwa Nasocardiac reflex is a relatively less discussed variant of trigeminovagal reflex where the afferent arc of the reflex is represented by any of [...]

Sudden cardiac death during exercise is of concern to a large number of sports-minded people because cardiovascular disease is so prevalent in this country. Common causes of sudden cardiac death among athletes include atherosclerosis (plaque build-up in the arteries) in persons over 35 years old, and hypertrophic cardiomyopathy (enlarged heart with disease to the myocardium, middle layer of the walls of the heart), which is more common among younger individuals. A retrospective study of cases of exercise and non-exercise-related sudden cardiac deaths reported in the state of Maryland between 1981 and 1988 was performed. Subjects were between the ages of 14 and 40 years. The medical conditions most often associated with sudden death during exercise were examined. There were 656 non-exercise and 34 exercise-related deaths. In the exercise-related group, over 90 percent were men (31 of 34) and the average age was 26 years. Causes of death in this group were attributed to atherosclerosis (nine cases), hypertrophic cardiomyopathy (eight cases), malformed coronary arteries (four cases), ventricular hypertrophy (three cases), myocarditis (two cases), one case each of arrhythmogenic right ventricle and Kawasaki disease, and six unexplained cases. In the non-exercise-related group, over 75 percent were men (501 of 656) and the average age was 32 years. Severe atherosclerosis was more frequent in total non-exercise-related deaths (307 of 656), and hypertrophic cardiomyopathy was the cause of more exercise-related deaths (8 of 34). These results suggest that patients with hypertrophic cardiomyopathy have an increased risk of suffering sudden cardiac death during exercise. (Consumer Summary produced by Reliance Medical Information, Inc.)

People who recover from cardiac arrest are at risk of suffering a recurrent episode. A subset of this group (60 to 80 percent) exhibits abnormalities in heart function during electrocardiogram (ECG) testing; these patients respond well to medication that alleviates the abnormalities. This improvement appears to prevent recurrence of cardiac arrest. The remaining 20 to 40 percent of patients show no abnormalities during ECG testing; this group is thought to be at a particularly high risk for sudden cardiac death. Seventy-one survivors of a single episode of cardiac arrest were evaluated. During testing, 26 of these patients had no inducible ECG abnormalities, such as ventricular tachycardia (abnormally rapid patterns of contraction of the ventricle). After a 16-month follow-up, 11 of the 26 patients suffered recurrent cardiac arrest, and 10 of these patients died. Analysis of the clinical data pertaining to these patients revealed that several variables were more likely to be associated with recurrent cardiac arrest. Among the 11 patients who suffered a recurrence, 55 percent had dilated cardiomyopathy (a defect in the functioning of the heart muscle), and 64 percent experienced premature ventricular contractions. Twenty-four-hour ambulatory ECG-guided therapy (wearing a portable ECG machine) did not improve the survival rate for these patients. Further studies are needed to determine the optimal treatment strategy for this high-risk group of patients. (Consumer Summary produced by Reliance Medical Information, Inc.)

Heart attacks are caused by loss of circulation to the heart muscle. Abnormal contractions of the heart (''stunned myocardium'') often accompanies restored circulation following a heart attack, and this has been thought to be caused by generation of oxygen free radicals, which are very reactive charged oxygen molecules. The relationship between oxygen free radicals and damaged heart function during the diastolic (filling) and systolic (contracting) phases of heart action have been investigated. Infusion of chemically generated free radicals into the hearts of experimental animals did not cause ischemia (loss of blood flow) nor death of heart muscle cells. However, systolic function decreased by 40 percent, and this was reversed by free radical scavengers (proteins which destroy free radicals). Free radicals had no effect on diastolic function, and it appears likely that other mechanisms are responsible for the changes in diastole which follow heart attacks. (Consumer Summary produced by Reliance Medical Information, Inc.)

A study of 1,019 patients who were brought to a hospital in cardiac arrest in one year found that when the number of arrests was plotted against the hour of the day, the number of arrests increased steadily from 6 a.m. until it peaked at noon. Circadian rhythms, which are biological rhythms that fluctuate around a 24-hour period, have been found to influence heart attacks, angina, blood pressure and strokes. Furthermore, heart rate, the aggregation of platelets, and blood levels of hormones that regulate the heart and blood vessels all peak in the early morning hours. Treatments for heart disease may be more effective if they are given at specific times of the day., Objectives.--Published studies have indicated a circadian rhythm in the occurrence of sudden cardiac death. However, these studies have involved either retrospective analyses of death certificates or analyses of data collected during studies of pharmacologic agents in selected populations. Purpose.--To determine whether a circadian pattern be clearly demonstrated in a prospective study of out-of-hospital sudden cardiac death in a large, unselected population. Design.--All adult cases of sudden death of presumed primary cardiac cause from a large urban population were prospectively evaluated over a 12-month period. The incidence of sudden cardiac death was analyzed using harmonic regression of the data tabulated by hour of the day. Results.--During the year of study, 1019 consecutive primary cardiac arrests were analyzed. A significant circadian pattern was found (P

This review discusses cardiac hypertrophy in terms of hypertrophic signaling and novel antihypertrophic approaches for modulating myocardial growth without much affecting contractile function of the myocardial system. Animal and human models indicate that hypertrophy, in most instanes, is not a compensatory response to the mechanical load but a maladaptive process.

Considerable evidence to document the association of sleep apnoea and sudden cardiac death. In a study from the Oxford Center of Respiratory Medicine, it was demonstrated that in patients with [...]