缺血预处理对肾脏缺血再灌注损伤保护作用的研究进展

肾缺血再灌注损伤导致急性缺血性肾衰竭在临床上十分常见.研究显示缺血预处理对肾缺血再灌注损伤具有保护作用.近年来关于肾缺血预处理作用机制的报道较多,本文就缺血预处理对肾缺血再灌注损伤保护作用的研究现状作一综述.     

缺血预处理在肝脏外科中的应用

近年来缺血预处理已经从动物实验阶段走向临床应用，但其如何保护肝脏拮抗热缺血再灌注损伤或移植肝在保存过程中冷缺血损伤的机制还未完全明确，在肝脏外科临床的应用中也还存在不同观点。文中就缺血预处理在肝脏外科临床中的应用情况作一综述。     

缺血预处理改善骨骼肌缺血再灌注损伤的实验研究

缺血预处理改善骨骼肌缺血再灌注损伤的实验研究冯亚高闽坤山＊邓素雅＊＊汪功久骨骼肌缺血再灌注损伤是临床常见的病理过程。然而到目前为止仍没有一种十分有效的防治方法应用于临床。１９８６年Ｍｕｒｒｙ等〔１〕首次应用缺血预处理方法即短时间重复缺血、间断再灌注改...     

缺血预处理对肾脏缺血再灌注损伤保护作用的研究进展

肾缺血再灌注损伤导致急性缺血性肾衰竭在临床上十分常见。研究显示缺血预处 理对肾缺血再灌注损伤具有保护作用。近年来关于肾缺血预处理作用机制的报道较多,本文就缺 血预处理对肾缺血再灌注损伤保护作用的研究现状作一综述。     

缺血预处理的概念及其在临床上的应用

缺血预处理是近年来提出的新概念。本文就缺血预处理的意义、病理生理机制及研究现状进行综述，认为缺血处理可显著减轻缺血灌注引起的组织损伤，增强组织对缺血的耐受性，具有广泛的临床应用价值。     

缺血预处理在肠缺血/再灌注损伤中的研究进展

缺血预处理是近年来提出的一种新的肠缺血/再灌注损伤的保护方法,即使在小肠长时间缺血/再灌注之前,进行一次或多次短暂的缺血,再灌注过程.研究表明缺血预处理对小肠缺血/再灌注损伤具有保护作用,但机制复杂,尚未明确.现就缺血预处理在肠缺血,再灌注损伤中的研究进展作一综述.     

缺血预处理研究现状及其在骨骼肌缺血再灌注损伤中的进展

骨骼肌缺血再灌注损伤临床上甚为常见。至今仍无十分有效的防治方法。最近 ,缺血预处理 (ｉｓ ｃｈｅｍｉｃｐｒｅｏｎｄｉｔｉｏｉｎｇ)提高组织缺血耐受性的现象颇受关注[1,2 ] 。本文就缺血预处理的进展及其在骨骼肌缺血再灌注损伤中的应用综述如下。缺血预处理的概念首先由Ｍｕｒｒｙ在心肌缺血再灌注损伤研究中提出。 1981年和 1986年Ｒｅｉｍｅｒ等[3 ,4 ] 发现短暂重复缺血并未引起组织ＡＴＰ相应减少 ,同时注意到连续 4次间断 10ｍｉｎ心肌缺血 ,7只试验狗中仅有 1例发生心肌坏死。 1986年Ｍｕｒｒｙ等[5]首次采用 4次间断 5ｍｉｎ…     

心肌缺血后处理研究新进展

急性心肌梗死目前是临床致残和致死的主要原因，其根本解决方法就是恢复心肌的正常血液供应。随着经皮冠状动脉腔内成形术、冠状动脉溶栓术和冠状动脉旁路移植术的广泛应用，心脏缺血，再灌注损伤越来越受到关注。1986年Murry等首先在犬心模型中发现缺血预处理现象，此后的大量研究证实可以应用预处理对抗缺血，再灌注损伤。2003年Zhao等首先在犬心模型中发现缺血后处理现象，并认为可以减轻再灌注损伤。现就有关研究作一综述。[第一段]     

缺血后处理和缺血预处理对兔脊髓缺血再灌注损伤的保护作用

缺血预处理及后处理可减轻心肌缺血再灌注损伤，但对脊髓缺血再灌注损伤的作用有待进一步探讨。本研究拟观察缺血预处理、缺血后处理及二者联合应用对兔脊髓缺血再灌注损伤的保护作用。     

远处缺血预处理减轻肾上腹主动脉阻断后肾脏损伤的实验研究

急性肾功能衰竭 (acuterenalfailure, ARF)是腹主动脉瘤破裂修补术及肾上腹主动脉瘤术后的严重并发症。经典的缺血预处理 (ischemicpreconditioning, IPC)及远处缺血预处理(remoteischemicpreconditioning, RIP)作为一种内源性抗缺血再灌注损伤 (ischemiareperfusioninjury, IR     

Advantage of ischemic preconditioning for hepatic resection in pigs

BACKGROUND: Ischemic preconditioning (IP) and intermittent inflow occlusion (IO) have provided beneficial outcomes in hepatic resection. However, comparison of these two procedures against warm hepatic ischemia-reperfusion injury has not been studied enough. MATERIALS AND METHODS: Pigs that had undergone 65% hepatectomy were subjected to Control (120 min continuous ischemia, n = 6), IP (10 min ischemia and 10 min reperfusion, followed by 120 min continuous ischemia, n = 6), and IO (120 min ischemia in the form of eight successive periods of 15 min ischemia and 5 min reperfusion, n = 6). We evaluated hepatocyte injury by aspartate aminotransferase, lactate dehydrogenase and hepaplastin test, hepatic microcirculation by hepatic tissue blood flow (HTBF) and endothelin (ET)-1, inflammatory response by tumor necrosis factor-alpha (TNF-alpha), and histopathology after reperfusion. RESULTS: IP prevented hepatocyte injury, HTBF disturbance, and hepatocyte necrosis in histopathology as well as IO. These two groups showed significantly better outcomes than Control. IP produced significantly less ET-1 and TNF-alpha than IO. CONCLUSIONS: IP ameliorated hepatic warm ischemia-reperfusion injury. Furthermore, IP gained more advantages in preventing chemokine production such as ET-1 and inflammatory response over IO. IP could take the place of IO for hepatectomy.     

Ischemic preconditioning attenuates the lipid peroxidation and remote lung injury in the rat model of unilateral lower limb ischemia reperfusion

BACKGROUND: Ischemia and reperfusion of the skeletal muscle tissue may cause remote lung injury. We aimed to evaluate the protective effect of ischemic preconditioning (IP) on the lung during unilateral lower limb ischemia reperfusion (IR). METHODS: Four groups of rats were used in this study: (i) the sham group (sham, n = 6) served as time controls, they remained anesthetized for the whole duration of the study; (ii) the ischemia and reperfusion group (IR, n = 10) underwent 4 h of left lower limb ischemia followed by 2 h of reperfusion; (iii) the ischemic preconditioning group (IP, n = 10), the left lower limbs of rats were exposed to three cycles of IP (10 min of ischemia followed by 10 min of reperfusion); and (iv) the ischemic preconditioning plus ischemia reperfusion group (IP/IR, n = 10) underwent IP followed by IR as in the IP and IR groups. Plasma and tissue samples were taken at the end of the study period for determination of lung tissue myeloperoxidase activity (MPO) and polymorphonuclear leukocyte count (PMNL), histological lung injury score and plasma thiobarbituric acid reactive substances (TBARS) level. RESULTS: PMNL count and MPO activity in the lung tissue, and plasma TBARS level were higher in the IR group compared with other groups while there were no differences between the sham and the IP and between the sham and the IP/IR groups. Histological lung injury score was higher in the IR group than in the IP/IR and sham groups. The plasma TBARS level in the IP group was significantly lower than in the IP/IR group. CONCLUSION: IP pretreatment reduces lipid peroxidation and lung injury caused by lower limb IR.     

缺血后处理对兔睾丸缺血再灌注的影响

目的:探讨缺血后处理对不同缺血程度的兔睾丸缺血再灌注损伤的作用。方法:42只雄性大白兔随机分成对照组、缺血组(R1、R2、R3组)、后处理组(P1、P2、P3组),每组6只。缺血组、后处理组在超声监测下制成睾丸不同缺血程度模型:R1、P1组睾丸回声均匀,血流轻度减少;R2、P2组睾丸回声增粗,血流明显减少;R3、P3组睾丸出现片状或放射状低回声,血流信号消失。出现上述图像变化后,缺血组给予直接灌流,后处理组于恢复灌流前给予后处理措施,即再灌注30s/缺血30s,反复3次。再灌注前进行超声造影,3d后测定各组组织丙二醛(MDA)、超氧化物歧化酶(SOD)含量。HE染色后光镜下观察睾丸组织和病理学改变,并行Johnsen's评分和凋亡指数分析;电镜下观察睾丸组织超微结构。结果:再灌注前各造影参数速度参数(β)、峰值时间(TTP)、峰值基础强度差(PBD)、峰值减半时间(DT/2),R1与P1组比较均无显著差异(P>0.05)、R2与P2组比较均无显著差异(P>0.05)、R3与P3组无显影。MDA含量:R1与P1组比较有显著差异(P<0.05),R2与P2组比较有显著差异(P<0.05),R3与P3组比较无显著差异(P>0.05)。SOD活性:R1与P1组比较有显著差异(P<0.05),R2与P2组比较有显著差异(P<0.05),R3与P3组比较无显著差异(P>0.05)。Johnsen's评分:R1与P1组比较有显著差异(P<0.05),R2与P2组比较无显著差异(P>0.05),R3与P3组比较无显著差异(P>0.05)。凋亡指数:R1与P1组比较有显著差异(P<0.05),R2与P2组比较无显著差异(P>0.05),R3与P3组比较无显著差异(P>0.05)。电镜:P1组超微结构损伤程度较R1组轻,R2与P2组超微结构无明显差异,R3与P3组超微结构无明显差异。结论:缺血后处理可以减轻睾丸缺血再灌注损伤,但是受到缺血程度的影响,并且在病理学和生化学上的表现不一致。     

Clinical course linkage among different priapism subtypes: Dilemma in the management strategies

Objectives: Priapism is a rare condition whose management differs according to the etiology. We report the clinical course of three forms of priapism to assess the feasibility and safety of recent management strategies. Methods: The study included eight patients complaining of persistent erection for ≥4 h who were treated in our institution between January 1996 and July 2007. Results: Overall, we categorized 12 cases of priapism in eight patients divided as follows: five cases of ischemic priapism (IP), three of stuttering priapism (SP), and four of non‐ischemic priapism (NIP). Two of five IP patients needed a shunt procedure, which led to the subsequent erectile dysfunction. The other three were treated successfully with a corporal injection of sympathomimetic agents and subsequently suffered from SP. One of the three SP patients suffered from mimicked NIP with increased arterial blood flow during the initial treatment for IP. Four of the NIP patients including the mimicked one achieved complete detumescence, through arterial embolization in two and conservative management in two. Conclusions: Current management seems effective and safe in the short‐term. However, the long‐term outcome of the treatment for IP is still disappointing. Careful long‐term observation is needed for an appropriate management.     

单次与多次缺血后处理对肺缺血再灌注损伤的实验研究

目的观察不同周期的缺血后处理（IP）对肺缺血再灌注损伤（LIRI）的影响，寻找具有最佳肺保护功能的IP周期和时机，并探讨IP对LIRI作用的机制，为临床提供实验依据。方法48只Wistar大鼠随机分为6组，每组8只。对照组、缺血再灌注（IR）组、IP-Ⅰ-IP-Ⅳ组，测定肺组织湿／干重比（W／D）、丙二醛（MDA）含量、一氧化氮合酶（NOS）、超微量Na^＋-K^＋-ATP酶活性，并在光镜下观察肺组织结构变化。结果IP-Ⅱ、IPⅢ组相比，差异无统计学意义（P〉0．05）；但较IR组、IP－Ⅰ、IP－Ⅳ组的MDA含量明显降低，Na^＋-K^＋-ATP酶活性明显升高（P〈0．05）。光镜下可见IP-Ⅱ、IP-Ⅲ组肺泡和支气管壁充血水肿较IR组和IP-Ⅰ、Ⅳ组明显减轻。结论IP对大鼠LIRI具有保护作用，尤其以给予Ⅱ、Ⅲ周期的30S再灌、30s停灌的IP具有较好的肺保护效果，并推测在缺血后立即给予2-3min的IP肺保护效果好。其机制可能与抑制活性氧自由基（ROS）和iNOS的生成，诱导Na^＋-K^＋-ATP酶活性升高有关。     

热休克蛋白70对肝硬化大鼠肝脏缺血再灌注损伤保护作用的研究

目的 探讨热休克蛋白70（HSP70）对肝硬化大鼠肝脏缺血再灌注损伤的保护作用。方法Wistar雄性大鼠用四氯化碳皮下注射制成肝硬化模型。分两组:IP组（缺血预处理组）,用 Pringle’s法阻断肝门15min后,恢复血供,关腹;C组（对照组）,只予以开、关腹。48h后,再次阻断肝门30min,恢复血供。用Western blotting法检测IP后6、24、48h肝组织中HSP70的表达水平;测再灌注1h血清生化酶（ALT、AST、LDH）水平;计算术后一周生存率,并行肝脏病理组织学检查。结果 IP组在缺血预处理后24-48hHSP70表达显著增强,呈高水平;而C组中在各时点HSP70均无表达增强。再灌注1h,IP组的ALT、AST、LDH水平显著低于C组（P<0.01或P<0.05,n=7）。术后一周生存率IP组（93.10％,n=29）明显高于C组（73.33％,n=30）（P<0.05）。缺血再灌注后1h,IP组的肝细胞损伤明显轻于C组。结论 HSP70能够减轻肝硬化大鼠肝脏缺血再灌注损伤,提高术后生存率。     

Ischemic preconditioning in solid organ transplantation: from experimental to clinics

This study reviews the current understanding of ischemic preconditioning (IP) in experimental and clinical setting, and the mechanisms that mediate the complex processes involved as a tool to protect against ischemia and reperfusion (I/R) injury, but is not intended as a complete literature review of preconditioning. IP has been mainly elucidated in cardiac ischemia. Recent reports confirm the efficacy of pre- and postconditioning in cardiac surgery and percutaneous coronary interventions in humans. IP utilizes endogenous as well as distant mechanisms in skeletal muscle, liver, lung, kidney, intestine and brain in animal models to convey varying degrees of protection from I/R injury. Specifically, preconditioned tissues exhibit altered energy metabolism, better electrolyte homeostasis and genetic reorganization, as well as less oxygen-free radicals and activated neutrophils release, reduced apoptosis and better microcirculatory perfusion. To date, there are few human studies, but recent trials suggest that human liver, lung and skeletal muscle acquire protection after IP. Present data address the potential therapeutic application of IP in the prevention of I/R damage specially aimed at clinical transplantation. IP is ubiquitous but more research is required to fully translate these findings to the clinical arena.     

Ischaemic preconditioning protects against ischaemia/reperfusion injury: emerging concepts.

INTRODUCTION: Ischaemic preconditioning (IP) has emerged as a powerful method of ameliorating ischaemia/reperfusion (I/R) injury to the myocardium. This review investigates whether this phenomenon is universally applicable in modulating I/R injury to other tissues. METHODS: A Medline search was conducted to identify both animal and human studies that described IP-induced protection from I/R injury in a variety of non-cardiac organ systems. Particular emphasis was placed on elucidation of underlying physiological concepts. RESULTS AND CONCLUSIONS: IP utilises endogenous mechanisms in skeletal muscle, liver, lung, kidney, intestine and brain in animal models to convey varying degrees of protection from I/R injury. To date there are few human studies, but recent reports suggest that human liver, lung and skeletal muscle acquire similar protection after IP. Specifically, preconditioned tissues exhibit reduced energy requirements, altered energy metabolism, better electrolyte homeostasis and genetic re-organisation, giving rise to the concept of 'ischaemia tolerance'. IP also induces 'reperfusion tolerance' with less reactive oxygen species and activated neutrophils released, reduced apoptosis and better microcirculatory perfusion compared to non-preconditioned tissue. Systemic I/R injury is also diminished by preconditioning. IP is ubiquitous but more research is required to fully translate these findings to the clinical arena.     

远端分流术治疗缺血性阴茎异常勃起随访分析

目的:回顾本院收治的缺血性阴茎异常勃起(IP)的临床资料和随访结果,为合理治疗IP提供依据。方法:分析自2004年至2010年收治的IP的临床资料,并通过电话和门诊就诊的方式随访。结果:8例IP就诊前均在外院接受过不同方式的减压治疗,失败后转入本院。年龄平均34.5岁,缺血时间平均84.5 h(36¹32 h)。在本院行阴茎海绵体穿刺抽吸冲洗后完全疲软1例,部分疲软7例;进一步行Al-Ghorab分流术,成功2例,失败5例。对失败者施行T型分流术,5例完全疲软。成功随访5例,2例中度ED,3例完全性ED。与中度ED相比,完全性ED者缺血时间较长。结论:减压治疗失败后,早期尝试T型分流术可提高IP治疗的成功率。     

不同预处理对大鼠肝移植供肝保护作用的探讨

目的 通过应用缺血、加热等多种手段对大鼠供肝进行移植术前的预处理,比较各种预处理方法对大鼠肝移植供肝缺血再灌注损伤的保护作用. 方法 将SD大鼠50只,随机分为5组:半肝缺血预处理组、脾脏缺血预处理组、热休克预处理组、热休克+缺血预处理组及手术对照组,分别进行肝脏预处理后行模拟原位肝移植术,术后检测胆汁流量,术后24 h检测血清ALT,AST,ALP水平并观察肝脏形态学变化. 结果 半肝缺血预处理组、热休克预处理组移植后胆汁分泌量多于对照组,血清ALT,AST水平明显低于对照组(P<0.05);热休克+缺血预处理组的血清ALT水平低于对照组(P<0.05),胆汁分泌量及血清AST与对照组没有显著差异;脾脏缺血预处理组的胆汁分泌量多于对照组,血清ALT水平低于对照组(P<0.05). 结论 肝脏缺血预处理初始阶段保护作用最明显,将缺血及热休克预处理两种方法联合处理大鼠时,其保护作用弱于单独缺血或单独热休克的预处理方法;脾脏缺血预处理也具有保护肝脏的作用.