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Aim: Improving prognosis with intravenous IgG (IVIG) has been ruled out in a large, multicenter, randomized controlled trial in patients with sepsis. However, its efficacy in the case of septic disseminated intravascular coagulation (DIC) has not been well studied. Results, materials & methods: We retrospectively evaluated the effects of IVIG on severity scores and 28-day survival in patients with septic DIC. A total of 80 patients with septic DIC were enrolled. Changes in infection-related markers, coagulation-related markers, severity scores and 28-day survival were compared between IVIG-treated and untreated groups. Discussion & conclusion: IVIG treatment significantly reduced the Sequential Organ Failure Assessment scores and DIC scores and increased platelet counts, but the 28-day mortality rate did not decrease significantly.

Procalcitonin (PCT) and presepsin (PSEP) are sepsis markers, but their diagnostic accuracy may be compromised in acute kidney injury (AKI). We evaluated their diagnostic accuracy in patients with/without AKI. This retrospective study comprised 91 patients with at least one criterion of systematic inflammatory response syndrome. AKI markers plasma neutrophil gelatinase-associated lipocalin (NGAL), plasma cystatin C (CysC), and estimated glomerular filtration rate (eGFR) were measured upon hospital admission and on days 1, 3, 5, and 7. Patients were divided into non-AKI and AKI groups. APACHE II severity scores were determined. PCT and PSEP levels were increased significantly in non-AKI and AKI patients with infection. NGAL, CysC, and eGFR in patients with infection were associated with PCT, PSEP, and APACHE II score, and levels of PCT and PSEP were correlated significantly with disease severity. PCT and PSEP are useful markers of bacterial infections in AKI but different thresholds should be applied.

This study was undertaken to analyze the association of type II secretory phospholipase A2 (sPLA2 -II) and surfactant protein D (SP-D) with the pulmonary oxygenation potential in patients with septic shock during polymyxin-B immobilized fiber-direct hemoperfusion (PMX-DHP). The study was conducted in 25 patients with acute lung injury (ALI) or acute respiratory distress syndrome (ARDS). PMX-DHP lowered the blood endotoxin level in all patients. Following PMX-DHP, there were decreases from day 0 → day 1 → day 2 in both the mean plasma sPLA2 -II level (340 → 260 → 189 ng/mL) and plasma SP-D level (483 → 363 → 252 ng/mL). The PaO2/FiO2 ratio (P/F ratio) rose (210 → 237 → 262) in all patients. Upon the onset of ALI or ARDS, there was a significant negative correlation between the sPLA2 -II level and the P/F ratio. Furthermore, there was a significant positive correlation between the sPLA2 -II and TNF-α levels. The results suggest that as the blood endotoxin levels were lowered by the PMX-DHP, the inflammatory reactions were suppressed, with suppressed formation of sPLA2 -II and improved pulmonary oxygenation potential. The results also suggested possible involvement of TNF-α in the production of sPLA2 -II.

Dexmedetomidine is a selective α2 adrenergic agonist. Although dexmedetomidine is widely used for sedation and analgesia, it frequently produces hypotension and bradycardia. The present study aimed to evaluate the effects of dexmedetomidine on cardiac function and coronary circulation using Langendorff-perfused guinea pig hearts. Coronary perfusion pressure (CPP) and left ventricular pressure (LVP) were continuously monitored, and electric field stimulation (EFS) was applied to stimulate sympathetic nerve terminals. Dexmedetomidine almost completely inhibited the EFS-induced increase in LVP at all ages. The effect of dexmedetomidine on coronary artery resistance varied according to postnatal age, i.e., dexmedetomidine had little effect on CPP in young hearts (8 weeks. The increase in CPP in adult hearts was inhibited by imiloxan, an α2B antagonist, and prazosin, an α1 antagonist. The results suggest that dexmedetomidine acts on α2 adrenergic receptors at sympathetic nerve terminals to suppress the release of norepinephrine. In addition, the findings suggest that dexmedetomidine directly affects α1 adrenoceptors and/or α2B adrenoceptors on coronary smooth muscles to increase CPP. The age-related changes in α adrenoceptor subtypes may be linked to the cardiodepressant effects of dexmedetomidine.

Non-traumatic rupture of the urinary bladder is termed “spontaneous rupture of the urinary bladder”. Although this disorder is relatively rare, when the bladder ruptures into the abdominal cavity, urine leaking into the abdominal cavity leads to the development of urinary peritonitis. We encountered seven patients with spontaneous rupture of the urinary bladder at our institution between 1987 and 2012. Six of these patients were women, all of whom had undergone surgery and radiotherapy to treat malignant uterine tumor. All seven patients suddenly developed abdominal pain and ascites. Urea nitrogen (UN) and creatinine (Cre) levels were greater in ascites than in the blood in all patients. Although all patients were treated conservatively, recurrence was identified in three patients. Recurrence was observed in only one of the four patients who received hyperbaric oxygen therapy. Conclusion: Hyperbaric oxygen therapy may be effective for recurrence of spontaneous rupture of the urinary bladder.

Although a number of studies have reported elevated levels of eicosanoids in acute lung injury with sepsis, the possibility that eicosanoids may act as risk and prognostic factors for sepsis patients who develop acute respiratory distress syndrome (ARDS) remains poorly studied. To clarify this aspect, we measured the levels of eicosanoids and used logistic regression analysis and receiver operating characteristic (ROC) curves to investigate whether eicosanoids could act as risk and prognostic factors for sepsis patients who develop ARDS. We conducted a casecontrol study comparing 13 sepsis patients with ARDS and 23 sepsis patients without ARDS. The plasma levels of leukotriene B4 (LTB4), 6-keto-prostaglandin F1α (6-keto-PGF1α) and thromboxane B2 (TXB2) were measured by radioimmunoassays as substitutes for the plasma levels of PGI2 and TXA2, which are unstable. The levels of eicosanoids in sepsis patients with ARDS were significantly higher than those in sepsis patients without ARDS. Logistic regression analysis revealed that LTB4 was the only risk factor for sepsis patients with ARDS (odds ratio, 1.10; P=0.02). The area under the ROC curve values for all eicosanoids were significantly greater than 0.5 (P

Aims Kampo medicine is based on the use of established formulations combining natural extracts with no “brand-name” products or corresponding “generic” formulation. Due to differences in manufacturing practices, products of different pharmaceutical companies may contain different concentrations of β-d-glucan and endotoxins. The aim of this study was to compare the concentrations of β-d-glucan and endotoxins in five Kampo extracts from four pharmaceutical companies. Methods Packages of Kampo extracts were dissolved in distilled water. β-d-Glucan and endotoxin concentrations were measured using high-sensitivity kinetic turbidimetric Limulus assay. Results All Kampo extracts examined in this study were found to contain detectable concentrations of β-d-glucan and endotoxins. Significant differences in the concentration of β-d-glucan and endotoxins (P = 0.0024 and P = 0.0013, respectively) were observed between products of different pharmaceutical companies. Conclusions High β-d-glucan and endotoxin contents were detected in Kampo extracts, with a large variability in the concentrations of both β-d-glucan and endotoxins among extracts from different pharmaceutical companies.

The ultra-short acting, selective β1-adrenergic antagonists landiolol and esmolol are widely used perioperatively; however, little is known about their acute direct actions on the heart. The current study utilized the Langendorff perfused heart system to measure changes in cardiac function and hemodynamics in response to each drug. Furthermore, electrophysiological analysis was performed on isolated ventricular myocytes. Direct application of esmolol significantly decreased systolic left ventricular pressure and heart rate at concentrations > 10 μM, while it dose-dependently increased coronary perfusion pressure. Esmolol also shortened the action potential duration (APD) in a concentration-dependent manner, an action maintained even when the delayed rectifier K+ current or ATP sensitive K+ current was blocked. Moreover, esmolol inhibited both the inward rectifier K+ current (IK1) and the L-type Ca2+ current (ICaL) and increased the outward current dose-dependently. In contrast, landiolol had minimal cardiac effects. In the Kyoto Model computer simulation, inhibition of either IK1 or ICaL alone failed to shorten the APD; however, an additional increase in the time-independent outward current caused shortening of the APD, equal to that induced by esmolol. In conclusion, esmolol directly inhibits cardiac performance significantly more so than landiolol, an effect revealed to be at least in part mediated by esmolol-induced APD shortening. Keywords:: esmolol, landiolol, Langendorff perfusion, patch clamp, coronary perfusion pressure

PURPOSE Laser scattering photometry (ESP) is a newly developed plasma endotoxin assay method using horseshoe crab amebocyte lysate (AL) that recognizes small particles produced by polymerization of coagulin under the stirring conditions at 1000rpm. We elucidated the effect of human serum album (HSA) in the ESP method. METHODS AL was dissolved with 630μL of the specimen and a 200-μL aliquot was used for ESP; this conventional protocol was regarded as the ESP630 method. The ESP210 method was also used, i. e. AL was dissolved with 210μL of the specimen and a 200-μL aliquot was used for ESP. RESULTS Water induced the agglutination, and HSA prolonged the agglutination time depending on its concentration especially in the ESP630 method. The water-induced agglutination was not inhibited by the addition of anti-factor C monoclonal antibody, and amidinophenyl benzoate hydrochloride, used as a clotting enzyme inhibitor, intensively inhibited the water-induced agglutination. Therefore, the water-induced agglutination was suggested to be a false-positive reaction to non-specific activation of the clotting enzyme. The HSA-induced prolongation of the reaction in the national health insurance-covered turbidimetric kinetic assay was not observed. CONCLUSION HSA or plasma protein seemed to affect the result, especially in the ESP630 method, and a non-specific reaction was found to occur in the ESP methods.

We present a 19-year-old man who excreted green urine after propofol infusion. The patient was admitted to our hospital for injuries sustained in a traffic accident and underwent surgery. After starting continuous infusion of propofol for postoperative sedation, his urine became dark green. Serum total bilirubin and urine bilirubin were both elevated. We believe that the green discoloration of the urine was caused by propofol infusion and was related to impaired enterohepatic circulation and extrahepatic glucuronidation in the kidneys.

The goal of the study was to examine the effects of sivelestat sodium hydrate (sivelestat), a neutrophil elastase inhibitor, on production of cytokines in granulocytes and monocytes, using flow cytometry after cytokine staining in whole blood culture. Blood samples were collected from healthy volunteers. Vehicle (control group), lipopolysaccharide (LPS) (LPS group), or LPS + sivelestat (sivelestat group) were added to the whole blood, followed by addition of a protein transport inhibitor in each group. After incubation, staining for cytokines retained in the cells was performed by addition of an anti-interleukin 8 (IL-8) or anti-tumor necrosis factor-α (TNF-α) antibody. The cells were then analyzed using flow cytometry. Granulocytic production of IL-8 induced by 1 ng/ml LPS was significantly (P

Objective: We measured the levels of soluble adhesion molecules in acute lung injury (ALI) patients and patients at risk of ALI, and then analyzed the correlations between the levels of the adhesion molecules and those of inflammatory cytokines to determine whether these factors are involved in the specific pathophysiology of ALI with sepsis. Methods: We conducted a case-control study comparing ALI (n = 13) and ALI-free (n = 14) patients with sepsis. Soluble adhesion molecules (soluble intracelluler adhesion molecule -1(sICAM-1), sE-selectin and soluble vascular cell adhesion molecule-1(sVCAM-1)), tumor necrosis factor-α(TNF-α) and interleukin-8 (IL-8) in the plasma were measured by enzyme-linked immunosorbent assays. Results: In the comparisons of the soluble adhesion molecule levels between ALI and ALI-free patients with sepsis, the sE-selectin level showed the most significant increase (P < 0.001), and was most strongly correlated with the TNF-α (P < 0.01) and IL-8 (P = 0.001) levels. sE-selectin was more specific factors for ALI, based on their greater areas under the receiver operating characteristic (ROC) curve (P < 0.01). Conclusion: Among the measured factors, sE-selectin appears to be involved in the specific pathophysiology of ALI with sepsis.

This study was undertaken to analyze the association of type II secretory phospholipase A

Few prospective studies have described the prognostic accuracy of presepsin for 28-day mortality during days 0 to 7, or its role in the diagnosis of disseminated intravascular coagulation (DIC) in patients with infection.We aimed to evaluate the clinical usefulness of presepsin levels by comparing infection markers such as procalcitonin, interleukin-6 and C-reactive protein, as well as markers of DIC such as fibrin degradation products (FDPs) and D-dimer, from days 0 to 7.A prospective, multicentre, observational study.Four medical institutions between June 2010 and June 2011.A total of 191 patients who fulfilled at least one of the systemic inflammatory response syndrome (SIRS) criteria were enrolled in the study.The presepsin levels were evaluated for their diagnostic accuracy in discriminating between SIRS and sepsis, the prognostic accuracy for 28-day mortality from days 0 to 7 and the diagnostic accuracy for DIC in patients with infection by comparison with other infection markers.The diagnostic accuracy for discriminating between SIRS and sepsis from combining the presepsin and procalcitonin measurements [area under the curve (AUC), 0.91; likelihood ratio, 4.96] was higher than that of presepsin (AUC, 0.89; likelihood ratio, 4.75) or procalcitonin (AUC, 0.85; likelihood ratio, 3.18) alone. Not only the correlation coefficient between the presepsin level and the sequential organ failure assessment (SOFA) score but also the prognostic accuracy of presepsin for 28-day mortality increased with the elapsed time, and both were highest at day 7. The diagnostic accuracy for DIC generated by combining presepsin and FDP (AUC, 0.84; likelihood ratio, 3.57) was higher than that of FDP (AUC, 0.82; likelihood ratio, 2.64) or presepsin (AUC, 0.80; likelihood ratio, 2.94) alone.The prognosis and severity of infection may be assessed more accurately by measuring the presepsin levels until day 7. Presepsin is a useful diagnostic tool for DIC with infection.

Non-invasive and real-time measures of neurological status after cardiac arrest are needed to be able to make an early determination of the postresuscitative outcome. We investigated whether the bispectral index (BIS) predicts the postresuscitative outcome in 10 patients with out-of-hospital cardiac arrest. We measured the BIS after return of spontaneous circulation (ROSC) in the emergency room and on admission to the intensive care unit (ICU). We determined the Glasgow Coma Scale (GCS) on admission to the emergency room and the ICU and the Glasgow Outcome Scale (GOS) on discharge from the ICU. The BIS increased after about 30 min of ROSC or reached a plateau in patients rated as achieving a good recovery or moderate disability, but it did not increase to >80 in patients rated as being in a permanent vegetative state/dead. The GCS on admission to the ICU was the same as that on admission to the emergency room. The BIS values were significantly lower in the nonsurviving group than in the surviving group. There was a positive correlation between the BIS on admission to the ICU and the GOS on discharge from the ICU. The BIS can thus be used to predict the postresuscitative outcome of patients with out-of-hospital cardiac arrest.

Dexmedetomidine is a potent and selective alpha-2 agonist, and is widely used for not only an adjunct to anesthesia but also sedation during mechanical ventilation in intensive care unit. It has been reported that, although the substance does not appear to have any direct effects on the myocardial contractility, it sometimes causes a decrease in heart rate and a dose-dependent decrease in arterial blood pressure and, in rare cases, leads to cardiac arrest or shock. However, detailed mechanisms remain uncertain. We hypothesized that effects of dexmedetomidine to coronary vasoactivity and cardiac function may differ depending on postnatal ages.

Whole-cell currents were recorded in single, spontaneously active cells dissociated from porcine sino-atrial node, and the conductance and gating properties of the delayed rectifier K+ current (IK) were investigated. The isolated cells exhibited spontaneous action potentials at a rate of 80.5 ± 5.4 min−1 (mean ± s.e.m., n = 11). Under Ca2+ current block, depolarization from −40 mV to various potentials activated a time-dependent outward current (IK). The activation curve of IK showed a half-activation potential (V½) of 20.5 ± 2.1 mV and a slope factor (S) of 16.4 ± 1.2 mV (n = 8). As the duration of the depolarizing pulse to either +10 or +60 mV was prolonged, the amplitude of the tail current increased in proportion to that of the activated outward current during depolarization. E4031 (2–5 μM), a selective blocker for the rapidly activating component of IK (IK,r), hardly affected IK, but chromanol 293B, a selective blocker for the slowly activating component (IK,s), inhibited IK with an IC50 of 8.79 μM. The reversal potential of IK was −75.2 ± 2.3 mV with 5.4 mM external and 150 mM internal K+. The time courses of activation and deactivation of IK were fitted by the sum of two exponential functions at various potentials. The relationship between the time constants and membrane potential showed a bell-shaped curve with a peak at around −10 mV for both fast and slow components. The results indicate that in porcine sino-atrial node cells IK is largely derived from IK,s and that IK,s plays a functional role in the slow diastolic depolarization. IK,s may, in part, account for the relatively slower heart rate of pigs than that of rabbit in which IK,r is a functionally dominant component of IK. Slow diastolic depolarization underlies the automaticity of the sino-atrial node (SAN) cells. Until recently, most ionic currents contributing to the slow diastolic depolarization have been identified and analysed extensively in both multicellular and single cell preparations (for review see Irisawa et al. 1993). The currents include the delayed rectifier K+ current (IK), the Na+-K+ pump current (Sakai et al. 1996), current due to the spontaneous opening of muscarinic K+ channels (Ito et al. 1994), L- and T-type Ca2+ currents (Hagiwara et al. 1988), hyperpolarization-activated cation current (If or Ih; DiFrancesco et al. 1986), background cation current (Hagiwara et al. 1992) and a dihydropyridine-sensitive sustained inward current (Guo et al. 1995). Using the conductance and gating parameters of individual current components, it is possible to reproduce the pacemaker activity in computer simulations (Yanagihara et al. 1980; Noble & Noble, 1984; Wilders et al. 1991). It should be noted, however, that most studies were carried out using rabbit hearts, and that the simulated action potentials only represent automaticity of the rabbit heart, the rate of which is approximately 200 beats min−1. It appears that there are substantial differences in current components among different species. For example, IK is largely attributed to the rapidly activating component of IK (IK,r) in rabbit SAN cells (Ito & Ono, 1995; Verheijck et al. 1995), whereas the slowly activating component of IK (IK,s) is a major component in guinea-pig SAN cells (Anumonwo et al. 1992). Since the conductance and gating properties of IK,r and IK,s are quite different (Sanguinetti & Jurkiewicz, 1991), their role in forming the spontaneous action potentials may differ depending on the species and heart rate. In the present study, we isolated single pacemaker cells from porcine hearts. The porcine heart rate, ranging from 60 to 80 beats min−1 in resting conditions, is much slower than that of rabbit. We show that the major component of IK in porcine heart is IK,s. The possible contribution of IK,s to the action potentials of porcine SAN cells will be discussed.

The hyperpolarization-activated cation current (If) was recorded in single pacemaker cells of the porcine sino-atrial node, and the effects of genistein, an isoflavone inhibitor of tyrosine-specific protein kinases was investigated by the whole-cell patch clamp technique. Genistein (20–500 μM) decreased If in a dose-dependent manner with an IC50 value of 62.3 μM and a maximum inhibition of 45.3%. The effect on If appeared without altering the half-activation potential (control, −88.3±2.8 mV; genistein, −87.0±1.8 mV) and the slope factor (control, 8.0±0.3 mV; genistein, 8.6±0.7 mV) of the steady-state activation curve. No significant voltage-dependency was detected in the fully-activated current-voltage relation measured by the double-pulse protocols. The inactive form of genistein analogue, daidzein (500 μM) or genistin (200 μM), were without effect. If was not affected by another tyrosine kinase inhibitor, tryphostin-47 (100 μM), but tyrphostin-25 (100–200 μM) suppressed If in an irreversible manner. Neither bath nor intracellular application of the tyrosine phosphatase inhibitor, orthovanadate, affected If, and subsequent application of genistein inhibited If significantly. These data indicate that the inhibition of If by genistein is not mediated through tyrosine kinase inhibition but through nonselective block of the If channels. Keywords: Porcine sino-atrial node, hyperpolarization-activated inward current, tyrosine kinase, genistein, tyrphostins, orthovanadate Introduction Although it is well established that protein tyrosine kinase (PTK) plays a primary role in regulating cellular growth and differentiation, recent studies have demonstrated that PTK can also modulate various ionic channels such as the cloned K+ channel (Huang et al., 1993), the NMDA receptor channel (Wang & Salter, 1994) and the cystic fibrosis trasmembrane regulator Cl− channel (Shuba et al., 1996). In the heart, the hyperpolarization-activated cation current (If) is normally recorded in sino-atrial node (SAN) cells, atrio-ventricular node cells and Purkinje fibres. The current plays a role of maintaining the less negative potential during diastole, thereby facilitating spontaneous activity of these cells (Irisawa et al., 1993). Recently, If of rabbit SAN cells was shown to be inhibited by genistein, a PTK inhibitor (Wu & Cohen, 1997), indicating that If channels might be regulated by tyrosine phosphorylation. On the other hand, genistein by itself has been shown to block various ionic channels including the voltage-gated K+ current of smooth muscle cells (Smirnov & Aaronson, 1995), L-type Ca2+ current in cardiac myocytes (Chiang et al., 1996) and cyclic AMP-dependent Cl− channel (Wang et al., 1998). Thus it is not yet clear whether or not If is regulated by tyrosine phosphorylation. To clarify the physiological importance of PTK in regulating If, it might be useful to examine the effects of tyrosine kinase inhibitors in different animal species. Since If plays a functional role in determining the heart rate, the contribution of If to the pacemaker potential and/or the extent of tyrosine phosphorylation of If channels might differ in various species. In the present study, therefore, we have isolated SAN cells of porcine hearts, which show spontaneous beating at a rate of approximately 80 min−1. We have shown that genistein inhibits If probably by nonselective block of the channels rather than through inhibiting PTK in porcine SAN cells.

Heart rate (HR) of mammalian species changes postnatally, i.e., HR of large animals including humans decreases, while HR in small animals such as mice and rats increases. To clarify cellular mechanisms underlying the postnatal HR changes, we performed in vivo HR measurement and electrophysiological analysis on sinoatrial node (SAN) cells in mice. The in vivo HR was ~320 beats min(-1) (bpm) immediately after birth, and increased with age to ~690 bpm at postnatal day 14. Under blockage of autonomic nervous systems, HR remained constant until postnatal day 5 and then increased day by day. The spontaneous beating rate of SAN preparation showed a similar postnatal change. The density of the L-type Ca(2+) current (LCC) was smaller in neonatal SAN cells than in adult cells, accompanied by a positive shift of voltage-dependent activation. Thus, the postnatal increase in HR is caused by both the increased sympathetic influence and the intrinsic activity of SAN cells. The different conductance and kinetics of LCC may be involved in the postnatal increase in pacemaker activity.

The purpose of this study was to investigate the relationship between the blood levels of interleukin (IL)-18 measured in the early stage of acute respiratory failure and the prognosis for patient survival. The study subjects were 38 patients with acute respiratory failure treated at our institution during the 4-year period from April 2004 to March 2008. The underlying clinical condition was defined as acute respiratory distress syndrome (ARDS; n = 12) or acute lung injury (ALI; n = 26). The serum levels of interleukin (IL)-18, IL-12, and tumor necrosis factor (TNF)-α were measured by enzyme-linked immunosorbent assays. The ARDS group showed significantly higher serum levels of IL-18, IL-12, and TNF-α even at an early stage after disease onset compared with the ALI group. A negative correlation was noted between the PaO2/FIO2 ratio (P/F ratio) and serum IL-18 level. Analysis of all 38 patients with ALI/ARDS revealed a 30-day mortality rate of 7.9 %, 60-day mortality rate of 15.8 %, and 90-day mortality rate of 18.4 %. The early-stage serum levels of IL-18, IL-12, and TNF-α were significantly higher in the non-survivors at 60 and 90 days, but not at 30 days, than in the corresponding survivors. The present data demonstrate an inverse correlation between serum IL-18 level and the P/F ratio, suggesting the possible involvement of IL-18 in the pathogenesis of respiratory failure in patients with ALI/ARDS. Early-stage serum IL-18, IL-12, and TNF-α levels appear to reflect the >60-day prognosis in patients with ALI/ARDS.

We previously reported a study of systemic inflammatory response syndrome (SIRS) cases in the Tohoku district of Japan in which the patients showed a 30-day mortality from acute lung injury/acute respiratory distress syndrome (ALI/ARDS) of about 20%. Cases in which chest X-ray findings did not meet ALI/ARDS criteria were diagnosed as acute hypoxemic respiratory failure (AHRF), but about 50% of these patients progressed to ALI/ARDS. The objective of this study was to verify the findings obtained in the earlier study and to gain further insights into the pathognomonic symptoms of AHRF associated with SIRS.A prospective cohort study was performed in SIRS patients admitted to the intensive care unit (ICU) with PaO(2)/fractional inspired oxygen (FIO(2))or = 300 mmHg. Patients were assigned to ALI or ARDS groups based on symptoms at ICU entry. Cases in which chest X-ray showed no infiltration shadows in bilateral lung fields were classified as AHRF.A total of 240 patients were enrolled in the study. The 30-day mortalities were 21.6% and 20.0% in the ALI and ARDS groups, respectively. Of the 88 AHRF patients, 49 progressed to ALI/ARDS, with progression occurring within 3 days after ICU entry in most cases; 39 patients recovered with no progression. Chest X-ray and computed tomography (CT) showed no findings indicating ALI/ARDS in 20 AHRF patients at ICU entry, but 7 of these patients progressed to ALI/ARDS.The mortality rates of ALI and ARDS were 21.6% and 20.5%, respectively. More than half of the AHRF patients progressed to ALI or ARDS. Some AHRF patients had normal findings on chest CT, but subsequently showed a bilateral shadow on a chest X-ray. This indicates that mild pathologic lesions may not show imaging abnormalities.

The use of sevoflurane in pediatric patients, which could enable a more rapid emergence and recovery, is complicated by a high incidence of postanesthetic agitation, probably due to residual sevoflurane during washout. The present study was designed to investigate whether administration of nitrous oxide (N2O) reduces sevoflurane concentration at awakening and suppresses postanesthetic agitation. The study enrolled 20 children classified as ASA physical status I. Anesthesia was induced with 5% sevoflurane and maintained with 2.5% end-tidal sevoflurane and N2O in oxygen. In the control group, sevoflurane and N2O were discontinued immediately after completion of surgery. In the N2O group, inspired N2O was replaced with oxygen after the bispectral index (BIS) had reached 80. The end-tidal concentrations of sevoflurane at awakening were significantly lower (P < 0.05) in the N2O group than in the control group. The BIS at awakening was higher (P < 0.01) in the N2O group than in the control group. The point scores of postanesthetic agitation were significantly lower (P < 0.01) in the N2O group than in the control group. Using N2O during washing out of sevoflurane may improve postanesthetic agitation at awakening in children.

In cardiac sino-atrial node (SAN) cells, time- and voltage-dependent changes in the gating of various ionic currents provide spontaneous, stable and repetitive firing of action potentials. To address the ionic nature of the species-dependent heart rate, action potentials and membrane currents were recorded in single cells dissociated from the porcine SAN, and compared with those from SAN cells of rabbits, guinea-pigs and mice. The porcine SAN cells exhibited spontaneous activity with a frequency of 60-80 min(-1), which was much slower than that of rabbit SAN cells. Under voltage clamp conditions, depolarization activated the L-type Ca2+ current (I(CaL)) followed by a gradual activation of the delayed rectifier K+ current (I(K)) while hyperpolarization activated the hyperpolarization-activated cation current (I(h)). It was found that the major component of I(K) in porcine SAN is the slowly activating I(K) (I(Ks)), in contrast to SAN cells of the rabbit and other species in which the rapid I(K) (I(Kr)) plays an active role in repolarization and the subsequent pacemaker depolarization. Replacement of rabbit I(Kr) with porcine I(Ks) and a slight modification in the gating parameters and amplitudes of other current systems in the 'Kyoto Model' gave an adequate reconstruction of spontaneous action potentials as well as of the voltage clamp recordings. We conclude that the density and the kinetics of I(K) contribute, in part, to the different heart rates of various species.