雷米芬太尼预处理对大鼠局灶性脑缺血-再灌注损伤的保护作用

目的观察雷米芬太尼预处理对大鼠局灶性脑缺血再灌注损伤的保护作用。方法23只雄性大鼠,随机分为两组。雷米芬太尼预处理(R)组(n=13)经股静脉注入雷米芬太尼(0.6μg·kg-1·min-1),每次5min输注,连续3次,中间间隔5min;盐水对照(C)组(n=10)经股静脉注入盐水,每次5min输注,连续3次,中间间隔5min;30min后,所有动物用右侧颈内动脉尼龙线线栓法致大脑中动脉阻闭120min,然后拔出尼龙线恢复再灌注。观察再灌注后24h神经功能障碍改变并评分。再灌注24h时处死动物,取大脑行2,3,5triphenyltetrazolium(TTC)染色以计算脑梗死容积百分比。结果缺血再灌注后动物均表现一定神经功能障碍,再灌注24h内C组神经功能障碍逐渐加重,R组则呈减轻趋势;再灌注24h时神经功能障碍评分(NDS)R组明显低于C组(P<0.05);再灌注24h时脑梗死容积百分比,R组明显小于C组(P<0.01)。结论雷米芬太尼预处理对大鼠局灶性脑缺血再灌注损伤可产生保护作用。     

福辛普利预处理对缺氧复氧期豚鼠心室肌细胞Na+/Ca2+交换电流的影响

目的:观察福辛普利晚期预处理对缺氧复氧心室肌细胞Na /Ca2 交换电流的影响。方法:应用全细胞膜片钳方法,记录观察酶解的成年豚鼠心室肌细胞Na /Ca2 交换电流在缺氧复氧期的变化。结果:缺氧复氧明显增加心肌Na /Ca2 交换电流,在-100mV和 60mV时较对照组分别增加41.05%及32.75%,福辛普利预处理后可明显抑制缺氧复氧心肌Na /Ca2 交换电流,在-100mV和 60mV时分别减少17.90%及14.20%,有助于减少钙内流,减轻钙超载。结论:福辛普利预处理可抑制缺氧复氧心肌Na /Ca2 交换电流逆向转运。     

异氟醚预处理对心脏瓣膜置换术病人血清一氧化氮与肌钙蛋白Ⅰ的影响

目的探讨异氟醚预处理对心肌缺血-再灌注损伤的保护效应及机制。方法择期行心脏瓣膜置换术的风湿性心脏瓣膜病病人32例,随机分为异氟醚组和对照组,每组16例。异氟醚组以1.5%~2%异氟醚吸入复合芬太尼维持麻醉,心肺转流(CPB)开始前洗脱10min,CPB后以芬太尼维持麻醉;对照组以芬太尼维持麻醉。分别于麻醉前(T0)、CPB前(T1)、CPB30min(T2)、术后8h(T3)、24h(T4)抽取中心静脉血测定一氧化氮(NO)、NO合酶(NOS)与心肌肌钙蛋白I(cTnI)浓度。结果两组病人T0时NO、NOS与cTnI浓度差异无显著意义;异氟醚组T1、T2时NO、NOS浓度明显高于对照组(P<0·05),T3、T4时cTnI浓度明显低于对照组(P<0·05)。结论异氟醚具有心肌预适应作用,其机制可能与增加NO释放有关。     

核转录因子NF-κＢ参与单磷酰脂A预处理的延迟保护作用

目的：探讨核转录因子NF-κB在单磷酰脂A预处理的延迟阶段的作用。 方法： 建立大鼠心肌缺血/再灌注（I/R）损伤模型。分别应用单磷酰脂A（MLA）、NF-κB的特异性抑制剂DDTC加MLA预处理心脏, 24 h对心脏进行较长时间缺血再灌注，检测心肌梗死范围、LDH释放及心肌细胞凋亡率。另外分组检测MLA预处理0 min、15 min、30 min、60 min、NF-κB抑制剂DDTC加MLA预处理后30 min时NF-κB活性。 结果: MLA预处理减小再灌注心肌梗死范围、降低血浆LDH活性、减少细胞凋亡(P<0.05 vs I/R)。同MLA预处理组相比， DDTC+MLA组心肌梗死范围增大、LDH活性增高, 细胞凋亡增加(P<0.05)。与预处理前相比，NF-κB活性在预处理后15 min明显升高、30 min达到高峰、60 min下降(P<0.01)。与MLA预处理后15 min、30 min、60 min相比， DDTC加MLA预处理后30 min时,NF-κB活性明显降低(P<0.01)，而与MLA预处理0 min无显著差别(P＞0.05)。 结论: (1) MLA预处理对24 h后缺血/再灌注心肌有保护作用。(2) 核转录因子NF-κB参与心肌预处理后的延迟保护作用，MLA预处理后NF-κB快速的核转移并激活可能是药物预处理延迟保护作用的重要机制之一。     

心肌缺血/再灌注前处置时血浆一氧化氮的变化及意义

目的：在兔心肌缺血／再灌注前处置模型的基础上，了解NO在心肌缺血前处置中所起的作用及意义。方法：采用免麻醉后开胸结扎左冠状动脉降支，反复结扎（缺血）10分钟，放开（再灌）5分钟，最后结扎30分钟再灌20分钟造成缺血／再灌注前处置模型后，对比观察了各组动物血浆中NO、TXB2、6－K－PGF1α、SOD和MDA浓度的变化，以及各组动物球结膜微循环及心肌病理学的变化。结果：前处置组血浆NO、6－K－PGF1α、SOD浓度显著高于缺血／再灌注组，而MDA、TXB2浓度明显低于缺血／再灌注组。前处置组心肌超微结构损伤明显轻于缺血／再灌注组，球结膜微循环基本正常。结论：心肌缺血前处置可增加心血管内皮细胞合成NO，而NO具有减轻心肌缺血／再灌注损伤、改善微循环障碍的作用。     

微量去甲肾上腺素预处理对大鼠心肌延迟性保护效应的实验研究

目的 :通过在体大鼠心肌缺血 /再灌注 (I/R)模型探讨去甲肾上腺素预处理对I/R心肌的延迟性保护作用。方法 :将实验动物分为假手术、I/R和去甲肾上腺素预处理 (NEPC) 3组 ,分别测定心肌梗塞面积、左室功能 ,观察心肌超微结构及血清肌酸激酶 (CK)及乳酸脱氢酶 (LDH)活性的变化。结果 :预先注入去甲肾上腺素能明显减小I/R所致的心肌梗塞面积 ,改善左室功能 ,保护心肌超微结构 ,增强细胞稳定性减少细胞内蛋白酶的漏出。结论 :去甲肾上腺素预处理可介导延迟性心肌保护效应 ,鉴于该法简便且无明显创伤更易于临床推广应用。     

1，6—二磷酸果糖预处理对离体大鼠心肌缺血再灌注损伤的保护作用

目的:观察1,6-二磷酸果糖(FDP)预处理对离体大鼠心肌缺血再灌注损伤的保护作用。方法:随机分成两组应用Iangendorff灌注装置用Krehs-Ring(K-R)液和K-R液加FDP5mmol·L~(1)对大鼠心脏进行缺血前预处理10分钟,缺血20分钟和再灌注20分钟实验,观察每期左室舒张未期压(LVEDP)、心肌组织内二醛(MDA)含量、超氧歧化物酶(SOD)的活性。Wistar大鼠心脏48个,每8个一组进行对照组和FDP组对比观察。结果:在缺血前期FDP组LVEDP和MDA无明显差异,缺血期FDP组MDA变化与对照组比较明显下降(P<0.01),再灌注期FDP组LVEDP和MDA明显下降(P<0.05),在FDP组SOD活性明显增高(P<0.01)。结论:FDP预处理具有提高大鼠心肌耐缺氧力,对大鼠心肌缺血再灌注损伤具有保护作用,该保护作用的机制可能与清除氧自由基功能有关。     

Involvement of capsaicin-sensitive sensory nerves in early and delayed cardioprotection induced by a brief ischaemia of the small intestine

Early cardioprotection can be achieved by a brief ischaemia of noncardiac tissues. Our study examined whether a brief ischaemia of the small intestine induces both early and delayed cardioprotection in the rabbit and assessed the possible mechanism involved in the activation of capsaicin-sensitive sensory nerves. The plasma concentration of creatine kinase (CK) and infarct size (necrotic zone/left ventricular zone) after 30 min coronary artery occlusion and 180 min reperfusion were determined in rabbits. Infarct size was 35.5±6.8% in the control non-preconditioned group. Preconditioning induced by a brief period of 10-min small intestine ischaemia significantly reduced infarct size (6.5±1.9%, P<0.01 vs. the control non-preconditioned group) and decreased CK release (3092±236 and 1094±117 U/l for myocardial ischaemia-reperfusion and preconditioning plus myocardial ischemia-reperfusion, respectively, P<0.01), and the protection was partly abolished by pretreatment with capsaicin (50 mg/kg, s.c.) 4 days before the experiments. A brief period of anterior mesenteric artery occlusion caused an increase in the plasma level of calcitonin gene-related peptide-like immunoreactivity (CGRP-LI), an effect which was abolished by pretreatment with capsaicin. Similar protection was shown in the animals subjected to a brief period of anterior mesenteric artery occlusion 24 h before coronary artery occlusion, and this delayed protection was also abolished partly by pretreatment with capsaicin. Capsaicin treatment (50 mg/kg, s.c.) alone also protected the ischa-emic myocardium. The results suggest that brief ischaemia of the small intestine induces both early and delayed protection against reperfusion-induced myocardial injury, and the effects are, at least partly, related to the activation of capsaicin-sensitive sensory nerves. Received: 13 August 1998 / Accepted: 4 January 1999     

Use of tactile stiffness to detect fatigue in the latissimus dorsi muscle

In clinical settings, no method has been established to examine the fatigue of a latissimus dorsi muscle (LDM) preconditioned for cardiomyoplasty. We examined the feasibility of measuring muscle stiffness (tactile stiffness) to evaluate muscle fatigue in situ using our tactile sensor. We stimulated canine LDM with burst pacing and monitored both stiffness and tension to determine their relationship. In both dissected LDM and LDM in situ, the decrements of these parameters during burst pacing were compared between preconditioned and unconditioned LDM. In measurement in situ, the sensor probe was placed on the LDM through a small incision. Strong statistical correlation was shown between stiffness and tension (r = 0.935). In decrements of stiffness in situ, there were statistically significant differences between preconditioned and unconditioned LDM. Our tactile sensor system can provide an efficient method for evaluating fatigue of muscles in situ without measuring muscle tension.