腺苷和芬太尼预处理减轻急性失血性休克兔心肌损伤

目的：观察腺苷和芬太尼预处理对急性失血性休克家兔心肌缺血损伤的影响。方法：24只家兔随机分为对照组（C组）、腺苷预处理组（A组）和芬太尼预处理组（F组）。按Wigger′s改良法制作家兔失血性休克模型。放血前15min各组分别给予等容量生理盐水、腺苷（1.5mg/kg）和芬太尼（25g/kg）。放血使平均动脉压（MAP）降至约40mmHg。持续监测MAP、左室压（LVP）、左室收缩压最大上升速率（＋dp/dtmax）和下降速率（-dp/dtmin）。放血前、放血后60min和90min抽血测定血清心肌肌钙蛋白I（cTn-I）浓度,实验结束时取心尖部组织行电镜检查。结果：各组放血后MAP、LVP、＋dp/dtmax和-dp/dtmin均明显下降,但A组和F组明显高于C组（P〈0.05或P〈0.01）。cTn-I在放血后60min和90min与放血前比较均明显增高（P〈0.01）,A组和F组增高程度低于C组（P〈0.01）,A组和F组之间差异无显著性（P〉0.05）。电镜检查发现A组和F组心肌损伤较C组减轻。结论：腺苷和芬太尼预处理均能减轻家兔急性失血性休克后的心肌损伤。     

Erythropoietin attenuates the tissue injury associated with hemorrhagic shock and myocardial ischemia

Here we investigate the effects of erythropoietin (EPO) on the tissue/organ injury caused by hemorrhagic shock (HS), endotoxic shock, and regional myocardial ischemia and reperfusion in anesthetized rats. Male Wistar rats were anesthetized with thiopental sodium (85 mg/kg i.p.) and subjected to hemorrhagic shock (HS; i.e., mean arterial blood pressure reduced to 45 mmHg for 90 min, followed by resuscitation with shed blood for 4 h), endotoxemia (for 6 h), or left anterior descending coronary artery occlusion (25 min) and reperfusion (2 h). HS and endotoxemia resulted in renal dysfunction and liver injury. Administration of EPO (300 IU/kg i.v., n = 10) before resuscitation abolished the renal dysfunction and liver injury in hemorrhagic, but not endotoxic, shock. HS also resulted in significant increases in the kidney of the activities of caspases 3, 8, and 9. This increase in caspase activity was not seen in HS rats treated with EPO. In cultured human proximal tubule cells, EPO concentration-dependently reduced the cell death and increase in caspase-3 activity caused by either ATP depletion (simulated ischemia) or hydrogen peroxide (oxidative stress). In the heart, administration of EPO (300 IU/kg i.v., n = 10) before reperfusion also caused a significant reduction in infarct size. In cultured rat cardiac myoblasts (H9C2 cells), EPO also reduced the increase in DNA fragmentation caused by either serum deprivation (simulated ischemia) or hydrogen peroxide (oxidative stress). We propose that the acute administration of EPO on reperfusion and/or resuscitation will reduce the tissue injury caused by ischemia-reperfusion of the heart (and other organs) and hemorrhagic shock.     

马桑内酯对锥体神经元三磷酸腺苷敏感钾通道的作用

背景：神经元异常放电的基础是细胞膜离子通道的激活与离子的跨膜运动。三磷酸腺苷敏感钾通道是将细胞电活动与代谢联系在一起的重要通道。三磷酸腺苷敏感钾通道是否参与癫痫的发病过程，马桑内酯是否具有调节三磷酸腺苷敏感钾通道的作用尚不清楚。 目的：了解致痫剂马桑内酯对大鼠海马锥体神经细胞膜三磷酸腺苷敏感钾通道的影响及三磷酸腺苷敏感钾通道在癫痫发病中的作用。 设计：随机对照实验。 单位：四川大学华西医院神经内科和四川大学华西基础医学与法医学院生理学教研室。 材料：实验于2000-05／12在泸州医学院完成。将Wistar乳鼠的培养的海马锥体神经元，随机分为正常对照组，四乙基胺组，二磷酸核苷组，马桑内酯组，电导与动力学组。 方法：Wistar乳鼠在麻醉和无菌条件下分离出海马组织，接种、培养24h后加入10μmol／L的阿糖胞苷，选择培养7-10d、生长良好、形态典型的锥体神经元进行膜片钳试验。正常对照组加入生理盐水；四乙基胺组加入5mmol／L氯化四乙基胺；二磷酸核苷组先加入30μmol/L的二磷酸核苷，后加入0．5mol／L的三磷酸腺苷；致痫组先加入1．0mL／L的马桑内酯，后加入1μmol／L的优降糖；对电导与动力学组，先调节钳制电压的大小，了解通道开放及通道形态，后加入马桑内酯。 主要观察指标：①观察神经元三磷酸腺苷敏感钾通道的活动及形态。（参观察不同钳制电压对通道活动的影响；了解二磷酸核苷、三磷酸腺苷和氯化四乙铵对通道的影响。②观察致痫剂马桑内酯对神经元细胞膜三磷酸腺苷敏感钾通道的激活作用及优降糖的影响。 结果：①对称性高钾溶液条件下，通道的翻转电位接近0mV。三磷酸腺苷敏感钾通道开放随着钳制电压绝对值的增大而增多，具有电压依赖性，该通道可被氯化四乙铵阻断。②其电流-电压（I-V）曲线可被直线拟合，电导值为（78．23&;#177;12．04）pS。③30μmol／L的二磷酸核苷可使通道开放增多，0．5mol／L的三磷酸腺苷可抑制通道活动。④1．0mL／L的马桑内酯诱导通道开放数量明显增多，1μmol／L的优降糖可抑制通道活动。⑤通道开放时间，致痫神经元T01为（1．754&;#177;0．060）ms，正常神经元为（1．733&;#177;0．046）ms，无显著性差异（n=25，t=0．147，P〉0．05）；而T02正常组为（2．441&;#177;0．265）ms，致痫组延长，为（10．446&;#177;0．579）ms（n=25,t=0．000，P〈0．01）。 结论：在马桑内酯诱导的癫痫发作中，三磷酸腺苷敏感钾通道开放的作用是降低动作电位频率、保护神经元，可能起一种负反馈调节作用。     

马桑内酯对锥体神经元三磷酸腺苷敏感钾通道的作用

背景神经元异常放电的基础是细胞膜离子通道的激活与离子的跨膜运动.三磷酸腺苷敏感钾通道是将细胞电活动与代谢联系在一起的重要通道.三磷酸腺苷敏感钾通道是否参与癫痫的发病过程,马桑内酯是否具有调节三磷酸腺苷敏感钾通道的作用尚不清楚.目的了解致痫剂马桑内酯对大鼠海马锥体神经细胞膜三磷酸腺苷敏感钾通道的影响及三磷酸腺苷敏感钾通道在癫痫发病中的作用.设计随机对照实验.单位四川大学华西医院神经内科和四川大学华西基础医学与法医学院生理学教研室.材料实验于2000-05/12在泸州医学院完成.将Wistar乳鼠的培养的海马锥体神经元,随机分为正常对照组,四乙基胺组,二磷酸核苷组,马桑内酯组,电导与动力学组.方法Wistar乳鼠在麻醉和无菌条件下分离出海马组织,接种、培养24 h后加入10 μmol/L的阿糖胞苷,选择培养7～10 d、生长良好、形态典型的锥体神经元进行膜片钳试验.正常对照组加入生理盐水;四乙基胺组加入5 mmol/L氯化四乙基胺;二磷酸核苷组先加入30 μmoL/L的二磷酸核苷,后加入0.5 mol/L的三磷酸腺苷;致痫组先加入1.0 mL/L的马桑内酯,后加入1 μmol/L的优降糖;对电导与动力学组,先调节钳制电压的大小,了解通道开放及通道形态,后加入马桑内酯.主要观察指标①观察神经元三磷酸腺苷敏感钾通道的活动及形态.②观察不同钳制电压对通道活动的影响;了解二磷酸核苷、三磷酸腺苷和氯化四乙铵对通道的影响.③观察致痫剂马桑内酯对神经元细胞膜三磷酸腺苷敏感钾通道的激活作用及优降糖的影响.结果①对称性高钾溶液条件下,通道的翻转电位接近0 mV.三磷酸腺苷敏感钾通道开放随着钳制电压绝对值的增大而增多,具有电压依赖性,该通道可被氯化四乙铵阻断.②其电流-电压(Ⅰ-Ⅴ)曲线可被直线拟合,电导值为(78.23±12.04)pS.③30μmol/L的二磷酸核苷可使通道开放增多,0.5 mol/L的三磷酸腺苷可抑制通道活动.④1.0mL/L的马桑内酯诱导通道开放数量明显增多,1μmol/L的优降糖可抑制通道活动.⑤通道开放时间,致痫神经元τ01为(1.754±0.060)ms,正常神经元为(1.733±0.046)ms,无显著性差异(n=25,t=0.147,P＞0.05);而τ02正常组为(2.441±0.265)ms,致痫组延长,为(10.446±0.579)ms(n=25,t=0.000,P＜0.01).结论在马桑内酯诱导的癫痫发作中,三磷酸腺苷敏感钾通道开放的作用是降低动作电位频率、保护神经元,可能起一种负反馈调节作用.     

Anesthetic influence on myocardial energy metabolism during hemorrhagic shock in rats

Twenty-eight male Wistar rats were used to assess the influence of inhalation anesthetics on myocardial energy metabolism during hemorrhage. They were anesthetized with pentobarbital and divided into four groups: a control group and three others which received 1.2% halothane, 2.2% enflurane or 1.4% isoflurane, respectively. Following a 15-min stabilization period, blood was gradually withdrawn over a 5-min period from a femoral artery. Systolic blood pressure was maintained at 40 mmHg for 30 min. Immediately after hemorrhage, the heart was removed and myocardial metabolites (ATP, ADP, AMP, lactate and glycogen) were measured by the enzymatic methods. Although no significant differences could be detected in ADP, AMP and lactate among the groups, there were significant increases of ATP content in rats receiving halothane and isoflurane when compared with the controls. There were also differences in myocardial glycogen content between the control group and those receiving isoflurane with those receiving halothane or enflurane. These results suggest that halothane or isoflurane may be more desirable than enflurane for maintenance of anesthesia during hypovolemia.     

Role of adenosine triphosphate-sensitive potassium channel inhibition in shock states: physiology and clinical implications

Shock states are associated with an impaired tissue oxygen supply-demand relationship and perturbations within the microcirculation, leading to global tissue hypoxia, finally resulting in multiple-organ failure or even death. Two of the most frequent causes of shock are acute hemorrhage and sepsis. Although the origin and the pathophysiology of hemorrhagic and septic shock are basically different, the involvement of adenosine triphosphate-sensitive potassium (KATP) channels, as an important regulator of vascular smooth muscles tone, plays a pivotal role under both conditions. Because the excessive activation of vascular KATP channels is a major cause of arterial hypotension and vascular hyporesponsiveness to catecholamines, the pharmacological inhibition of KATP channels may represent a goal-directed therapeutic option to stabilize the hemodynamic situation in shock states. Despite promising results of preclinical studies, the efficacy of this innovative therapeutic approach remains to be confirmed in the clinical setting. The differences in the species, the comorbidity, and the difficulty in determining the exact onset of shock in clinical practice and, thus, any duration-related alterations in vascular responses and KATP channel activation may explain the discrepancy between the results obtained from experimental and clinical studies. Currently, two of the most relevant problems related to effective KATP blockade in shock states are represented by (1) the dose itself (benefit-risk ratio) and (2) the route of administration (oral vs. i.v.). This review article critically elucidates the published in vivo studies on the role of KATP channel inhibition in both described shock forms and discusses the advantages and the potential pitfalls related to the treatment of human shock states.     

Protective effect of urinary trypsin inhibitor on myocardial mitochondria during hemorrhagic shock and reperfusion

OBJECTIVE: To examine the mitochondrial function in the myocardium after hemorrhagic shock and reperfusion and to evaluate the protective effect of urinary trypsin inhibitor (UTI) on mitochondria. DESIGN: Animal experiment. SETTING: University research laboratory. SUBJECTS: Wistar rats receiving 50,000 units/kg/hr of UTI (n = 27; UTI group) and control rats (n = 26; control group). INTERVENTIONS: Rats were subjected to low-perfusion ischemia with the left ventricular systolic pressure maintained at 50 mm Hg for 60 mins by bleeding, followed by a 60-min reperfusion by transfusion of shed blood. UTI was infused continuously from 10 mins before bleeding. Cardiac function was measured before bleeding, after bleeding, and after transfusion; at each determination point, the myocardial contents of adenosine triphosphate (ATP), creatine phosphate (P-Cr), pyruvate (Pyr), and lactate (Lac) were measured enzymatically. The cytosolic phosphorylation potential (PP) as well as the redox potential of the oxidized form of nicotinamide adenine dinucleotide/reduced form of nicotinamide adenine dinucleotide couple in mitochondria (Eh(NAD+/NADH)) and change of Gibbs free energy in ATP hydrolysis (deltaG(ATP hydrolysis) energy) were calculated. MEASUREMENTS AND MAIN RESULTS: Cardiac function decreased during hemorrhagic shock but improved significantly in the UTI group after transfusion compared with the control group. Lac and the Lac/Pyr ratio were significantly lower in the UTI group than in the control group after transfusion. ATP and P-Cr were significantly higher in the UTI group than in the control group after transfusion. PP (x10(3) M-1), Eh(NAD+/NADH) (x - 1 mV), and deltaG(ATP hydrolysis) (x - 1 kcal/mol) were 1.9 +/- 0.4, 266 +/- 4, and 9.7 +/- 0.2, respectively, in the control group and 4.0 +/- 0.9, 274 +/- 5 and 13.0 +/- 0.2, respectively, in the UTI group after transfusion (p <.001, p <.001, and p <.001, respectively). CONCLUSIONS: In reperfusion after hemorrhagic shock, oxidative phosphorylation in myocardial mitochondria is impaired and energy production remains reduced, even after reperfusion. UTI contributed to the recovery of cardiac function after reperfusion, probably by reducing the severity of mitochondrial dysfunction during a state of shock and by maintaining energy production.     

Splanchnic metabolism during gut ischemia and short-term endotoxin and hemorrhagic shock as evaluated by intravasal microdialysis

The splanchnic area is of considerable interest in different types of shock. To characterize the metabolic changes in the splanchnic region in response to different types of shock we used a model where shock-induced metabolic changes in the splanchnic region were studied by the use of intravasal microdialysis. 23 anesthetized domestic pigs were randomized into four groups: Group I, serving as controls (n = 5); Group II, mesenteric ischemia for 180 followed by 120 min of reperfusion (n = 5); Group III, endotoxin shock for 5 h (n = 5); and Group IV, hemorrhagic shock for 180 min followed by re-transfusion of shed blood (n = 8). Microdialysis catheters were placed in the left femoral artery, portal vein and a small ileal mesenteric vein. Samples of the perfusate were continuously collected in micro-vials and analyzed for glucose, lactate, pyruvate and glycerol. In gut ischemia and endotoxin shock the outflow-pattern of lactate, lactate/pyruvate ratio and glucose in the mesenteric vein differed significantly from controls and hemorrhage whereas an increase in glycerol was only noted in the ischemic group. The most prominent differences were detected in lactate/pyruvate ratio, a marker of tissue ischemia with the most pronounced changes during mesenteric ischemia/reperfusion. During endotoxin shock increases in microdialysate metabolites were only noted in the splanchnic region suggesting a specific vulnerability in the region. Studying the lactate/pyruvate ratio may provide additional information when interpreting increased blood lactate levels. In addition glycerol may prove to be a useful marker of splanchnic ischemia. Intravasal microdialysis represents a potentially useful method for monitoring regional metabolic events.     

Depletion of myocardial glucose is observed during endotoxemic but not hemorrhagic shock in a porcine model

Introduction

Metabolic dysfunction is one of the hallmarks of sepsis yet little is known about local changes in key organs such as the heart. The aim of this study was to compare myocardial metabolic changes by direct measurements of substrates, such as glucose, lactate and pyruvate, using microdialysis (MD) in in-vivo porcine endotoxemic and hemorrhagic shock. To assess whether these changes were specific to the heart, we simultaneously investigated substrate levels in skeletal muscle.

Methods

Twenty-six female pigs were randomized to three groups: control (C) n = 8, endotoxemic shock (E) n = 9 and hemorrhagic shock (H) n = 9. Interstitial myocardial pyruvate, lactate and glucose were measured using MD. Skeletal muscle MD was also performed in all three groups.

Results

Marked decreases in myocardial glucose were observed in the E group but not in the H group compared to controls (mean difference (CI) in mmol/L: C versus E -1.5(-2.2 to -0.8), P <0.001; H versus E -1.1(-1.8 to -0.4), P = 0.004; C versus H -0.4(-1.1 to 0.3), P = 0.282). Up to four-fold increases in myocardial pyruvate and three-fold increases in lactate were seen in both shock groups with no differences between the two types of shock. There was no evidence of myocardial anaerobic metabolism, with normal lactate:pyruvate (L:P) ratios seen in all animals regardless of the type of shock.In skeletal muscle, decreases in glucose concentrations were observed in the E group only (mean difference: C versus E -0.8(-1.4 to -0.3), P = 0.007). Although skeletal muscle lactate increased in both shock groups, this was accompanied by increases in pyruvate in the E group only (mean difference: C versus E 121(46 to 195), P = 0.003; H versus E 77(7 to 147), P = 0.032; C versus H 43(-30 to 43), P = 0.229). The L:P ratio was increased in skeletal muscle in response to hemorrhagic, but not endotoxemic, shock.

Conclusions

Endotoxemia, but not hemorrhage, induces a rapid decrease of myocardial glucose levels. Despite the decrease in glucose, myocardial lactate and pyruvate concentrations were elevated and not different than in hemorrhagic shock. In skeletal muscle, substrate patterns during endotoxemic shock mimicked those seen in myocardium. During hemorrhagic shock the skeletal muscle response was characterized by a lack of increase in pyruvate and higher L:P ratios.Hence, metabolic patterns in the myocardium during endotoxemic shock are different than those seen during hemorrhagic shock. Skeletal muscle and myocardium displayed similar substrate patterns during endotoxemic shock but differed during hemorrhagic shock.     

The relative contributions of myocardial wall thickness and ischemia to ultrasonic myocardial integrated backscatter during experimental ischemia

The purpose of this study was to assess the empirical relationship between myocardial integrated backscatter (IB) and myocardial wall thickness (WT) in normal myocardium. A second object was to estimate the additional contribution to acute ischemic integrated backscatter levels given this relationship. Myocardial IB measurements and simultaneous myocardial WT measurements were made in 16 open-chested pigs with intact coronary circulation (normal myocardium) and 10 min after the flow in the left anterior descending coronary artery had been reduced to 20% of its baseline value (ischemic myocardium). Measurements were made 50 times during one cardiac cycle and averaged over 10 cardiac cycles. IB and WT measurements were normalized with respect to the nonischemic end-diastolic values. The relationship between IB and WT in normal myocardium was estimated in every individual pig by simple linear regression. Estimates of IB during ischemia were calculated on the basis of this relationship and the ischemic WT measurements. Differences of the estimator and the actual measurement made during ischemia depict the actual contribution of the state of acute ischemia, without the influence of WT. The slope of the relationship between IB and WT during normal myocardial contraction ranged from -0.16 to 0.03 dB/% (mean = -0.036 dB/%, SD = 0.06 dB/%). The additional contribution of ischemia ranged from -3.84 to 5.56 dB (mean = 0.31 dB, SD = 2.72 dB). It was concluded that the average contribution of ischemia to IB measurements is insignificant if the IB dependency on WT is removed from the data and that the higher level of ischemic IB measurements can be explained by the decrease in wall thickness during ischemia and not by the ischemia itself.     

低血容量性休克大鼠全身氧动力学的变化研究

目的：研究低血容量性休克时全身氧动力学的变化特点。方法：按４ｍｌ／ｋｇ,每隔０．５分次从静脉放血,观察大鼠休克过程中全身氧供给（ＤＯ２）,氧消耗（ＶＯ２）和氧摄取率（ＥｘｔＯ２）的变化。结果：失血后１．５小时血红蛋白浓度开始显著降低,心率明显加快,失血２．０小时平均动脉压明显下降,此时ＤＯ２亦开始进行性下降,由于ＥｘｔＯ２出现代偿升高,ＶＯ２维持相对不变;     

Redistribution of cardiac output during hemorrhagic shock in sheep

OBJECTIVE: Our goal was to evaluate the robustness of one of the assumptions used by esophageal Doppler monitors to compute systemic stroke volume and cardiac output; i.e., a constant flow proportion between supra-aortic vessels and descending aorta. For this purpose, we measured ascending and descending aortic blood flows during acute hemorrhage in anesthetized ewes. DESIGN: Prospective, experimental study. SETTING: Animal research facility. SUBJECTS: Adult ewes. INTERVENTIONS: Anesthetized animals were implemented with an aortic pressure transducer and two ultrasound transit time flowmeters placed around ascending and descending aorta, respectively. After baseline measurements, three incremental blood withdrawals were followed by progressive blood restitution in three similar steps. MEASUREMENTS AND MAIN RESULTS: Ascending and descending aortic blood flows were reduced in a proportional manner after hemorrhage (-48% and -46%, respectively; p < .05 vs. baseline). Following blood restitution, flows were not fully restored, but ascending aortic flow was reduced by 27% with respect to initial control values while descending aortic flow was only 15% below. The agreement between ascending aortic flow and cardiac output calculated as descending aortic flow divided by 0.7 was characterized by a bias of 0.07 L/min and limits of agreement of +1.24 L/min and -1.10 L/min. CONCLUSIONS: Minor blood flow redistribution between supra-aortic and descending aortic territories was seen only following blood restitution but not during hemorrhage in these anesthetized ewes. This observation supports the robustness of the assumption of constant flow proportion used by the esophageal Doppler monitor to calculate systemic stroke volume from descending aortic flow measurements.     

Technique to prevent limb ischemia during peripheral cannulation for extracorporeal membrane oxygenation

Prolonged extracorporeal support using femoral cannulation may cause limb ischemia. A technique is described using antegrade, retrograde arterial perfusion and venous drainage to prevent limb ischemia.     

热休克蛋白70对严重创伤休克后肝脏的作用

目的 探讨热休克蛋白70（HSP70）对严重创伤休克后肝脏作用.方法 成年Wistar大鼠,采用双侧股骨骨折伴失血性休克致严重创伤模型,动态观察伤后8 h大鼠肝组织HSP70、血清肝功能生化指标、肝脏病理等变化.HSP70表达测定采用免疫印迹法,并进行计算机图像分析.结果 伤后HSP70在肝组织中表达迅速增加,6 h达到峰值,伤后8 h仍维持较高水平;创伤合并休克后,HSP70表达高峰提前至伤后4 h,持续表达至伤后6 h后逐渐下降,死亡前在肝组织中仍有少量表达.创伤休克后血清ALT、TB伤后4 h开始明显增高（P＜0.01）,白蛋白下降（P＜0.01）.肝脏镜下创伤休克后6 h肝窦内出现较多炎性细胞浸润.结论 在创伤休克早期,HSP70可能参与了肝组织细胞抗损伤机制的启动,但随着休克时间的延长,HSP70的过高持续表达,则可能对肝脏造成损害.HSP70在创伤休克后肝保护与肝损害过程中可能发挥双重作用.     

Diagnosis of myocardial ischemia during ventricular pacing

Discordant ST elevation > 5 mm was recently described as an electrocardiographic sign with good specificity and moderate sensitivity for the diagnosis of acute myocardial infarction during right ventricular pacing. This report shows that the same sign may occur transiently during myocardial ischemia and also serve as a diagnostic marker.     

Plasma and myocardial visfatin expression changes are associated with therapeutic hypothermia protection during murine hemorrhagic shock/resuscitation

Aim

Cytokine production during hemorrhagic shock (HS) could affect cardiac function during the hours after resuscitation. Visfatin is a recently described protein that functions both as a proinflammatory plasma cytokine and an intracellular enzyme within the nicotinamide adenine dinucleotide (NAD⁺) salvage pathway. We developed a mouse model of HS to study the effect of therapeutic hypothermia (TH) on hemodynamic outcomes and associated plasma and tissue visfatin content.

Methods

Mice were bled and maintained at a mean arterial pressure (MAP) of 35 mmHg. After 30 min, animals (n = 52) were randomized to normothermia (NT, 37 ± 0.5 °C) or TH (33 ± 0.5 °C) followed by rewarming at 60 min following resuscitation. After 90 min of HS (S90), mice were resuscitated and monitored for 180 min (R180). Visfatin, interleukin 6 (IL-6), keratinocyte-derived chemokine (KC), tumor necrosis factor-alpha (TNF-α), and myoglobin were measured by ELISA.

Results

Compared to NT, TH animals exhibited improved R180 survival (23/26 [88.5%] vs. 13/26 [50%]; p = 0.001). Plasma visfatin, IL-6, KC, and TNF-α increased by S90 in both groups (p < 0.05). TH attenuated S90 plasma visfatin and, after rewarming, decreased R180 plasma IL-6, KC, and myoglobin (p < 0.05) relative to NT. Heart and gut KC increased at S90 while IL-6 increases were delayed until R180 (p < 0.05). NT produced sustained elevations of myocardial KC but decreased visfatin by R180, effects abrogated by TH (p < 0.05).

Conclusions

In a mouse model of HS, TH improves hemodynamics and alters plasma and tissue proinflammatory cytokines including the novel cytokine visfatin. TH modulation of cytokines may attenuate cardiac dysfunction following HS.