异搏定对急性缺氧复合失血性休克狗心泵功能的影响

13只健康雄性家犬,在模拟4000m高原低压舱内,复制失血性休克,低血压(5.38kPa)维持1小时,于失血后60、70、80min给药组(n=6)和对照组(n=7)动物分别静注异搏定0.15mg/kg和等量葡萄糖水,于90min将失血全部输回。     

Effects of Sympathetic Denervation and Dexamethasone on Pial Microvascular Pressure in Acute Hypoxic Rabbits

To determine the effects of sympathetic denervation and dexamethasone on the individualcerebral vascular pressure profile during hypoxia, the authors measured the pial microvascular pres-sure in 24 anesthetized rabbits with a servo-null system. At a simulated altitude of 4000 meters, inthe intact group, the mean pressure in pial arterioles of 50-70 μm in diameter decreased markedly.The ratio of pressure drop between the upstream and downstream of the arteriole measured in-creased markedly, and the blood flow in the internal carotid artery was nearly doubled of the nor-mal. The pial arteriolar pressures of both the denervated and dexamethasone groups were significantlyhigher than that of the intact group, but were not different from their prehypoxic values. The ratioof pressure drop between the upstream and downstream of the denervated and dexamethasonegroups remained unchanged, and much lower than that of the intact group, These results lead tothe following conclusions: (1) Sympathetic nerves and dexamethasone exert no effect on thelongitudinal distribution of cerebro-vascular pressure in rabbits during normoxia, normocapnia andnormotension.(2) During hypoxia, pressure drop increases in the upstream arteries and/or decreasesin the downstream vessels of the microvascular pressure measured site (arterioles 50- 70 μm in diame-ter) partly due to the activation of the sympathetic nerve. (3) Dexamethasone can prevent theredistribution of cerebrovascular pressure induced by hypoxia, which can partly explained the ac-tion of dexamethasone in preventing high altitude sickness.     

急性缺氧大鼠的心输出量和局部血流量

以~(99m)Tc标记蟾蜍红细胞(~(99m)Tc-RBC)作为生物微球,用参考血样本方法(RSM)测定急性缺氧大鼠的心输出量(CO)和局部血流量(LBF)。大鼠在麻醉条件下进行人工通气,用10%O~2—90%N_2混合气体通气20分钟造成急性缺氧,左心室内注入~(99m)Tc-RBC 4～6万,从股动脉收集参考血样本(RS)测定CO和LBF,实验结果表明,在人工通气条件下,急性缺氧使大鼠的心率(HR)减慢、CO降低,和以冠状血流和脑血流增加及内脏血流减少为主的血流重新分配。     

缺氧家兔组织钙调蛋白水平及钙调蛋白拮抗剂对血流动力学的影响

为观察钙调蛋白(CaM)在缺氧所致的肺动脉高压等血流动力学改变中的作用,我们采用环核苷酸磷酸二脂酶的方法测定了缺氧家兔肺动脉、肺和心肌组织CaM水平,观察了脂质体包裹的CaM拮抗剂三氟啦嗪(TFP)对缺氧动物血流动力学的影响。结果表明:1.缺氧(模拟4000m高原10～11天)家兔肺动脉、肺和心肌组织CaM活性量水平与平原对照值无显著差异,CaM在上述实验条件下改变不甚显著;2.在模拟4000m高原为缺氧家兔注入脂质体包裹的TFP后,Ppa无显著改变,PVR有增高趋势,而观察45分钟末动物肺动脉的CaM活性受到显著抑制,说明缺氧性肺动脉压增高不一定依赖于CaM;3.家兔肺循环和体循环对缺氧反应不同,在模拟4000m高原,脂质体包裹的TFP对缺氧动物的肺、体循环的血流动力学影响也不同,提示;肺循环与体循环血管平滑肌收缩的调节机制不尽一致。     

慢性心力衰竭合并贫血患者采用左卡尼汀联合促红细胞生成素治疗的临床效果分析

目的探讨左卡尼汀联合促红细胞生成素治疗慢性心力衰竭合并贫血的临床治疗效果。方法将我院收治的86例慢性心力衰竭合并贫血患者作为对象,根据对比实验方法分为观察组与参考组,各为43例,给予观察组左卡尼汀联合促红细胞生成素治疗,给予参考组单纯左卡尼汀注射液治疗,观察两组患者临床治疗效果,记录患者治疗期间不良反应发生情况。结果观察组治疗血清FFA含量、血红蛋白含量均出现明显改善(P<0.05);观察组患者红细胞膜Na+-K+ATP酶的活性改善明显优于参考组(P<0.05);两组患者治疗期间不良反应发生率比较无统计学意义(P>0.05)。结论左卡尼汀联合促红细胞生成素治疗慢性心力衰竭合并贫血有助于纠正贫血现象,促进患者心功能的改善,安全性高,可推广使用。     

视神经急性损伤后Long Evans大鼠闪光视觉诱发电位的实验研究

目的探索视神经急性损伤后Long Evans大鼠闪光视觉诱发电位(F-VEP).方法使用AVE8000自动视觉电生理系统,检测正常及视神经急性损伤后Long Evans大鼠F-VEP.结果测出了正常Long Evans大鼠F-VEP潜伏时和振幅值;检测了视神经急性不完全损伤后F-VEP,其特点为潜伏时延迟,振幅值降低,与正常相比有显著性差异;视神经横断后F-VEP波形呈熄灭型.结论 Long Evans鼠视神经损伤模型可用于观察视神经保护效应的研究,F-VEP是客观反映视神经功能的简便而有效的方法.     

创伤性膈疝26例外科治疗体会

目的:探讨创伤性膈疝的诊断与治疗方法。方法:回顾性分析1995年~2004年收治的26例创伤性膈疝患者,对其诊治方法和并发症进行总结评价。结果:全组开放性伤17例,闭合性伤9例。18例合并其他脏器损伤。行剖胸探查14例,剖腹探查8例,同时剖胸剖腹探查3例,胸腔镜检查修补1例。术后死亡l例,发生并发症6例(23.1%)。结论:早期诊断和手术治疗;是减少并发症的根本措施。     

法洛四联症合并左肺动脉起源异常一例

病例资料 患者，女．10岁，曾在外院以先天性心脏病法洛四联症入院，欲行根冶术，术中发现左肺动脉起源有异常．故未能实施手术。1个月后患者来我院就诊。查体：口唇发绀，杵状指趾。胸骨左缘3～4肋间可闻及Ⅳ级收缩期杂音,心前区可触及震颤。X线平片示：右侧肺血少，左捌肺血多，主动脉增宽．右心室增大。