乌司他丁对大鼠全肝缺血-再灌注肺损伤的保护作用

目的 观察乌司他丁对大鼠全肝缺血-再灌注(I-R)肺损伤的保护作用.方法 24只SD大鼠随机分为全肝缺血-再灌注组(I-R组)、乌司他丁组(U组)及假手术对照组(C组),每组8只.检测支气管肺泡灌洗液(BALF)中总蛋白含量、肺组织干/湿质量比(D/W)、肺组织髓过氧化物酶(MPO)及超氧化物歧化酶(SOD)含量,并以逆转录聚合酶链式反应(RT-PCR)方法检测三组大鼠肺组织基质金属蛋白酶(MMP)14 mRNA的相对表达量.结果 与U组和C组比较,I-R组大鼠肺组织BALF总蛋白和MPO含量明显增高,肺组织D/W和SOD显著降低.MMP14 mRNA相对表达量显著增高(P<0.05).结论 乌司他丁可减轻全肝I-R肺损伤;抑制肺组织MMP14 mRNA的表达可能是其机制之一.     

肢体缺血/再灌注致急性肺损伤的研究现状

肢体缺血,再灌注是临床常见的一种病理生理过程,再灌注损伤不仅存在于局部缺血组织,尚可进一步引发远隔器官肺的损伤,现就肢体缺血/再灌注(limb ischemin-reperfusion,LIR)致急性肺损伤(acute lung injury,ALI)的病理生理机制和防治措施作一综述.     

肢体缺血/再灌注致急性肺损伤的研究现状

肢体缺血,再灌注是临床常见的一种病理生理过程,再灌注损伤不仅存在于局部缺血组织,尚可进一步引发远隔器官肺的损伤,现就肢体缺血/再灌注(limb ischemin-reperfusion,LIR)致急性肺损伤(acute lung injury,ALI)的病理生理机制和防治措施作一综述.     

肢体缺血/再灌注致急性肺损伤的研究现状

肢体缺血,再灌注是临床常见的一种病理生理过程,再灌注损伤不仅存在于局部缺血组织,尚可进一步引发远隔器官肺的损伤,现就肢体缺血/再灌注(limb ischemin-reperfusion,LIR)致急性肺损伤(acute lung injury,ALI)的病理生理机制和防治措施作一综述.     

肢体缺血/再灌注致急性肺损伤的研究现状

肢体缺血,再灌注是临床常见的一种病理生理过程,再灌注损伤不仅存在于局部缺血组织,尚可进一步引发远隔器官肺的损伤,现就肢体缺血/再灌注(limb ischemin-reperfusion,LIR)致急性肺损伤(acute lung injury,ALI)的病理生理机制和防治措施作一综述.     

肢体缺血/再灌注致急性肺损伤的研究现状

肢体缺血,再灌注是临床常见的一种病理生理过程,再灌注损伤不仅存在于局部缺血组织,尚可进一步引发远隔器官肺的损伤,现就肢体缺血/再灌注(limb ischemin-reperfusion,LIR)致急性肺损伤(acute lung injury,ALI)的病理生理机制和防治措施作一综述.     

肢体缺血/再灌注致急性肺损伤的研究现状

肢体缺血,再灌注是临床常见的一种病理生理过程,再灌注损伤不仅存在于局部缺血组织,尚可进一步引发远隔器官肺的损伤,现就肢体缺血/再灌注(limb ischemin-reperfusion,LIR)致急性肺损伤(acute lung injury,ALI)的病理生理机制和防治措施作一综述.     

肢体缺血/再灌注致急性肺损伤的研究现状

肢体缺血,再灌注是临床常见的一种病理生理过程,再灌注损伤不仅存在于局部缺血组织,尚可进一步引发远隔器官肺的损伤,现就肢体缺血/再灌注(limb ischemin-reperfusion,LIR)致急性肺损伤(acute lung injury,ALI)的病理生理机制和防治措施作一综述.     

肢体缺血/再灌注致急性肺损伤的研究现状

肢体缺血,再灌注是临床常见的一种病理生理过程,再灌注损伤不仅存在于局部缺血组织,尚可进一步引发远隔器官肺的损伤,现就肢体缺血/再灌注(limb ischemin-reperfusion,LIR)致急性肺损伤(acute lung injury,ALI)的病理生理机制和防治措施作一综述.     

肢体缺血/再灌注致急性肺损伤的研究现状

肢体缺血,再灌注是临床常见的一种病理生理过程,再灌注损伤不仅存在于局部缺血组织,尚可进一步引发远隔器官肺的损伤,现就肢体缺血/再灌注(limb ischemin-reperfusion,LIR)致急性肺损伤(acute lung injury,ALI)的病理生理机制和防治措施作一综述.     

Protective effects of propofol against ischemia/reperfusion injury in rat kidneys

Aim: The purpose of this study was to investigate and compare the efficiency of propofol in the reduction of injury induced by free radicals in a rat model of renal ischemia/reperfusion (I/R). Method: Twenty-four Wistar rats were divided into four groups in our study. Rats in the sham group underwent laparotomy and were made to wait for 120 min without ischemia. Rats in the control group were given nothing with ischemia–reperfusion. Rats in the I/R groups were given propofol (25 mg/kg) and 10% intralipid (250 mg/kg) ip, respectively, 15 min before the ischemia for 60 min followed by reperfusion for 60 min. The kidney tissues of the rats were taken under anesthesia at the end of the reperfusion period. Evaluation of biochemical malondialdehyde (MDA), superoxide dismutase, and catalase activities and histopathological analysis were performed with these samples. Results: I/R significantly increased MDA levels (p < 0.05). Histopathological findings of the control group confirmed that there was renal impairment by tubular cell swelling, interstitial edema, medullary congestion, and tubular dilatation. MDA levels were lower in the propofol group compared to control group (p < 0.05). In the propofol group, the level of histopathological scores is significantly decreased than control and intralipid groups in ischemia–reperfusion. Conclusion: Our results demonstrate that I/R injury was significantly reduced in the presence of propofol. The protective effects of propofol may be due to their antioxidant properties. These results may indicate that propofol anesthesia protects against functional, biochemical, and morphological damage better than control in renal I/R injury.     

瘦素在肝缺血/再灌注致肾损伤中作用的研究

目的：研究瘦素（Leptin）在肝缺血/再灌注（I/R）后肾组织中的表达变化,探讨其与肝I/R介导的肾损伤的关系。方法：建立大鼠70%肝I/R模型,设立假手术和缺血60min后再灌注60、150、240、360min组,观察肾脏的病理学变化,检测各组血清尿酸、总抗氧化能力,肾Leptin蛋白及其mRNA表达的变化。结果：与假手术组比较,缺血60min/再灌注150min及再灌注240min组血清尿酸显著升高,以再灌注240min升高最为显著;再灌注240min和360min组血清总抗氧化能力显著升高,以再灌注240min升高最为显著;再灌注150、240和360min组肾Leptin蛋白表达显著升高,再灌注60、240、360min组肾LeptinmRNA表达显著升高,而再灌注150min组LeptinmRNA显著降低。病理学观察提示肝I/R早期的肾损伤较重而后期显著减轻。结论：Leptin在肝I/R后肾组织内的表达变化与肾损伤密切相关,提示它可能作为一种保护因子对抗肝I/R介导的肾损伤。     

The role of HMGB-1 on the development of necrosis during hepatic ischemia and hepatic ischemia/reperfusion injury in mice

BACKGROUND: High-mobility group 1 (HMGB-1) is a late mediator of endotoxin lethality in mice. The release of HMGB-1 is delayed compared to other proinflammatory cytokines that mediate shock and tissue injury. The purpose of this study was to investigate the role of HMGB-1 levels in response to hepatic ischemia, hepatic I/R injury, and the relationship between changes in HMGB-1 and other cytokines. MATERIALS AND METHODS: Three murine models were employed: our robust model of segmental hepatic warm ischemia (SHWI), a model of partial hepatic ischemia/reperfusion injury (PHIRI), and a model of total hepatic ischemia/reperfusion injury (THIRI). Over a 48-h period following ischemic insult and reperfusion using these models, serum HMGB-1 concentrations, concentrations of HMGB-1 in ischemic and nonischemic lobes, and serum concentrations of TNF-alpha and IL-6 levels were determined in mice. An anti-HMGB-1 antibody treatment was used in SHWI and THIRI to evaluate what aspects of response to ischemia and reperfusion were potentially mediated by HMGB-1. RESULTS: Hepatic HMGB-1 tissue concentrations exhibited biphasic changes in SHWI mice, which were increased in the ischemic lobes relative to nonischemic lobes at 12 h but decreased relative to nonischemic lobes at 24 h after ischemic insult. These results suggested that HMGB-1 was released into the systemic circulation by necrotic cells over the first 12 h but this process may be complete by 24 h postischemia. By 6 to 12 h after SHWI, serum TNF-alpha began to increase significantly and continued to increase for 18 h, followed by a sudden decline. Similarly, serum IL-6 increased over 1-3 h after SHWI and then decreased over the next 6 h. Treatment with an anti-HMGB-1 antibody significantly prolonged survival time in SHWI and THIRI. CONCLUSIONS: HMGB-1 plays a significant role in the response to hepatic ischemia and hepatic ischemia/reperfusion injury. The present study demonstrated a time-dependent production of HMGB-1 following hepatic warm ischemia in mice. The inherent HMGB-1 in ischemic areas was exhausted and HMGB-1 may be released by necrotic cells. HMGB-1 activation is involved in immediate proinflammatory stress response to I/R and anti-HMGB-1 antibody treatment remarkably improved survival. We demonstrated that systemic HMGB-1 accumulation was measured at an earlier phase of the hepatic ischemia and ischemia/reperfusion injury model than LPS-induced endotoxemia.     

七氟醚对肺缺血／再灌注损伤的保护机制

背景七氟醚作为一种较理想的吸入麻醉药,被广泛应用于临床,实验表明七氟醚对肺缺血／再灌注损伤（ischemia／reperfusion injury,I／RI）具有保护作用。目的通过分析近年的研究总结七氟醚对肺I／RI的保护机制。内容七氟醚通过减轻肺通透性、抑制炎症反应、减轻脂质过氧化反应、抑制细胞凋亡、减轻细胞内钙离子超载等发挥肺I／RI的保护作用。趋势应进一步探讨七氟醚对肺的保护作用,加强对七氟醚的临床应用研究,为实际临床工作提供可靠的依据。     

阿片类药物减轻急性缺血/再灌注损伤及相关机制

背景 缺血预处理对于器官缺血/再灌注损伤（ischemia/reperfusion injury,I/RI）具有强大的保护作用,但其临床应用受到时机以及伦理学的限制.近年来有研究发现阿片类药物预处理以及后处理对组织器官I/RI同样具有保护作用,其既不损伤器官又能产生与缺血预处理相同的效果,是更为可行的治疗措施. 目的 在将阿片类药物处理推广至临床应用前,仍需进行更多大规模的临床研究.拟就阿片类处理减轻I/RI的发展过程及其作用机制进行探讨. 内容 阿片类药物处理I/RI的几种方式及其机制. 趋向 阿片类药物处理比较其他损伤性处理方式更易操作,且对I/RI同样具有保护作用,有望成为日后治疗的热点之一.     

Role of leukotrienes on hepatic ischemia/reperfusion injury in rats

BACKGROUND: Leukotrienes (LT), composed of cysteinyl LT (cLT; LTC(4), LTD(4), and LTE(4)) and LTB(4), are potent lipid mediators enhancing the vascular permeability and recruitment of neutrophils, which are common features of hepatic ischemia/reperfusion (I/R) injury. The aim of this study was to investigate whether LT can mediate the liver and lung injuries following hepatic I/R. MATERIALS AND METHODS: Sprague-Dawley rats were subjected to 90 min of partial hepatic ischemia followed by 3, 12, and 24 h of reperfusion. In the hepatic and pulmonary tissues, LT content and the mRNA expression of LT-synthesis enzymes, 5-lypoxygenase (5-LO), LTC(4) synthase (LTC(4)-S), and LTA(4) hydrolase (LTA(4)-H) were measured. Tissue injuries were assessed by plasma ALT, histological examination, and wet-to-dry tissue weight ratios. RESULTS: The cLT content in the hepatic tissue after 12 and 24 h reperfusion was increased 4- to 5-fold compared to controls and this was accompanied by the enhancement of hepatic edema and plasma ALT elevation. There were no significant changes in the mRNA expression of LT-synthesis enzymes in both tissues. LTB(4) levels were not increased despite a significant neutrophil infiltration in both tissues. CONCLUSIONS: These data suggest that cLT are generated in the liver during the reperfusion period and may contribute to the development of hepatic edema and exert cytotoxicity. Factors other than LTB(4) may contribute to neutrophil infiltration.     

小剂量氯胺酮对心肺转流后肺损伤的保护作用

目的观察应用小剂量氯胺酮对心肺转流(CPB)后肺损伤的影响。方法30例二尖瓣置换手术病人随机均分为氯胺酮组(K组)和对照组(C组),两组麻醉方法相同。K组于麻醉诱导后和CPB开始前分别缓慢静注氯胺酮1mg/kg;C组静注同等容量的生理盐水。于手术开始前(T0)、CPB停止即刻(T1)、2h(T2)、12h(T3)记录气道峰压(Ppeak)、气道平台压(Pplautue),通过Flow-Directed漂浮导管测定平均肺动脉压(MPAP)、肺毛细血管楔压(PCWP)、心输出量(CO),计算肺血管阻力(PVR),同时抽取动脉血、混合静脉血测动脉血气、血常规、肿瘤坏死因子α(TNF-α)、白细胞介素1(IL-1)、血清可溶性细胞间黏附分子-1(sICAM-1)及中性粒细胞表面CD11b、CD18的表达。结果CPB后两组病人的所测各项指标均明显升高(P<0.05),但K组显著低于C组(P<0.05),CPB后C组中性粒细胞在肺组织中的浸润明显高于K组,CD11b、CD18表达较高的中性粒细胞容易浸润于肺组织中。结论CPB中应用小剂量氯胺酮可以减轻全身性炎症反应和缺血-再灌注损伤导致的肺组织损伤,对肺功能有显著的保护作用。     

肢体缺血预处理减轻肝缺血/再灌注损伤的研究进展

背景 肝缺血/再灌注损伤(hepatic ischemia/reperfusion injury,HI/RI)是肝外科手术及肝移植中常见的病理生理现象,是术后肝功能衰竭和移植物无功能的主要原因.研究表明肢体缺血预处理(limb ischemia preconditioning,LIPC)可减轻HI/RI,具体机制仍不清楚.目的 通过综述LIPC减轻HI/R1的可能机制,为临床减轻HI/RI提供新的思路.内容 介绍HI/RI机制及LIPC减轻HI/RI的可能作用机制.趋向 LIPC作为减轻HI/RI的措施具有重大的临床应用价值.     

七氟醚对心肌缺血/再灌注损伤的临床研究进展

背景 七氟醚的心肌保护作用得到广泛关注,大量基础研究表明七氟醚对心肌缺血/再灌注损伤(myocardial ischemia/reperfusion injury,MI/RI)具有确切的保护作用.然而,临床中关于七氟醚具有心肌保护作用的结论尚未完全统一.目的 通过总结近年的研究进展对七氟醚的心肌保护作用进行阐述.内容 不同心脏手术及非心脏手术中七氟醚药物处理的心肌保护效果.趋向 今后仍需加强对七氟醚心肌保护作用的临床研究,为围手术期患者的心肌保护提供更为可靠的理论依据.     

电针对脑缺血/再灌注损伤的神经保护的研究进展

背景 中国针灸用于中风等神经系统疾病的治疗有悠久的历史和丰富的临床经验.电针是传统针灸与现代电学技术相结合的治疗方式,它对脑缺血/再灌注损伤(ischemia/reperfusion injury,I/RI)的病理演变有重要影响.目的 探讨电针的神经保护及其机制.内容 依照脑I/RI的病理生理机制,分析与总结电针对脑I/RI的保护作用及其机制. 趋向 电针在运用补充与替代疗法预防、治疗或辅助治疗脑I/RI方面有良好的发展前景.