失血性休克再灌注复苏后血浆降钙素基因相关肽的变化

探讨失血性休克再灌注复苏后血浆中降钙素基因相关肽（ＣＧＲＰ）改变的意义，早期使用磷脂酶Ａ２（ＰＬＡ２）阻断剂、抗氧化剂对ＣＧＲＰ的影响及其与ＰＬＡ２激活、氧自由基产生的关系。家兔失血性休克维持６０分钟后回输自体血液及平衡盐液，血浆中ＣＧＲＰ逐渐升高，复苏后６小时达顶点，同出血前比较有显著性差异（Ｐ＜０．０５）；ＰＬＡ２阻断剂氯喹及ＭＥ８１０１、抗氧化剂黄芪酮于失血后复苏前使用可明显抑制复苏后血浆中ＣＧＲＰ的增高；同时，复苏后家兔平均动脉压（ＭＡＰ）和血ｐＨ值逐渐下降，与ＣＧＲＰ变化没有明显相关（ｒ＝０．００４０和ｒ＝０．０４３５）；假手术造成血浆ＣＧＲＰ水平复苏后逐渐上升，同术前比较差异同样显著（Ｐ＜０．０５），但并不伴随ＭＡＰ和ｐＨ值的下降，氯喹、ＭＥ８１０１及黄芪酮纠正酸中毒、维持血压稳定的作用与抑制ＣＧＲＰ并无明显相关。结果提示：家兔失血性休克后再灌注复苏过程中血浆ＣＧＲＰ水平的上升可能不是ｐＨ值和ＭＡＰ下降的重要因素；ＰＬＡ２阻断剂和抗氧化剂并非通过抑制ＣＧＲＰ上升而产生抗酸中毒及稳定循环血压的作用     

茶色素对缺血性心脑血管病血浆ET及CGRP的影响

目的：探讨茶色素对缺血性心脑血管病患血浆内皮素（ＥＴ）、降钙素基因相关肽（ＣＧＲＰ）的影响。方法：用放射免疫分析法检测３２例缺血性心脑血管病患茶色素治疗前后血浆ＥＴ、ＣＧＲＰ含量的变化。结果：治疗后治疗前比较。血浆ＥＴ及Ｅ／Ｃ比值显降低（Ｐ〈０．０１）,血浆ＣＧＲＰ显升向（Ｐ〈０．０１）。结论：茶色素有明确的降低ＥＴ、升高ＣＧＲＰ的作用。     

实验性脑出血大鼠急性期血浆内皮素和降钙素基因相关肽含量变化的研究

目的：探讨血浆内皮素（ＥＴ）和降钙素基因相关肽（ＣＧＲＰ）在实验性脑出血大鼠急性期中的变化规律,初步分析其在脑出血急性期中的病理生理意义。方法：用Ｎａｔｈ 法复制脑出血大鼠模型,放射免疫法动态测定急性期血浆ＥＴ及ＣＧＲＰ含量,电镜下观察脑组织超微结构变化。结果：实验组血浆ＥＴ 含量在各观察点均明显高于对照组（４ 小时Ｐ＜ ０．０５,１２ 小时与７ 日Ｐ均＜ ０．０１,２４ 小时与７２ 小时Ｐ均＜ ０．００１）,７ 日时间点实验组与正常组比较差异非常显著（Ｐ＜ ０．０１）。实验组血浆ＣＧＲＰ含量在各时间点亦明显高于对照组（４ 小时及７ 日Ｐ 均＜ ０．０５,１２、２４ 和７２ 小时Ｐ均＜ ０．０１）,７ 日时间点与正常组比较有显著性差异（Ｐ＜ ０．０５）。结论：血浆ＥＴ 及ＣＧＲＰ在脑出血急性期均升高,其变化规律基本一致,与脑损伤程度呈正相关,提示二者对脑出血急性期的病理演变过程有重要意义     

乌拉地尔对高血压患者血浆降钙素基因相关肽与内皮素含量的影响

目的探讨新型降压药乌拉地尔（ＵＲＡ）对高血压患者血浆降钙素基因相关肽（ＣＧＲＰ）和内皮素（ＥＴ）含量的影响。方法采用放射免疫方法测定１５例高血压患者ＵＲＡ治疗前后血浆ＣＧＲＰ和ＥＴ含量变化。结果高血压患者血浆ＣＧＲＰ明显低于正常对照组（Ｐ＜００１）。血浆ＥＴ及ＥＴ／ＣＧＲＰ明显高于正常对照组（Ｐ＜００１）。经静脉ＵＲＡ治疗后５ｍｉｎ,高血压患者血浆ＣＧＲＰ明显升高（Ｐ＜００１）,ＥＴ及ＥＴ／ＣＧＲＰ则明显降低（Ｐ＜００１）。结论ＣＧＲＰ与ＥＴ共同在高血压发病过程中起重要作用。ＵＲＡ可明显提高人体内ＣＧＲＰ水平,在降低血压的同时对ＥＴ有明显的拮抗效应。     

血浆内皮素及降钙素基因相关肽在急性脑血管病时的变化

目的 探讨血浆内皮素（ＥＴ）及降钙素基因相关肽（ＣＧＲＰ）水平在急性脑血管病（ＡＣＶＤ）时的变化。方法 以４９例急性脑硬塞（ＡＣＩ）和３８例脑出血（ＡＣＨ）为对象与４１名健康志愿者为对照,采用放免法测定血浆ＥＴ及ＣＧＲＰ水平。结果 两组患者血浆ＥＴ水平明显高于对照组（Ｐ〈０．００１）;ＡＣＩ患者血浆ＣＧＲＰ水平明显低于对照组（Ｐ〈０．００１）,ＡＣＨ患者血浆ＣＧＲＰ水平明显高于对照组（Ｐ〈０．００     

山莨菪碱对家兔全脑缺血再灌注脑组织TXA2和PGI2代谢的影响

目的 探讨山莨菪碱对家兔全脑缺血再灌注期间脑组织ＴＸＡ２和ＰＧＩ２代谢的影响。方法 ４０只家兔随机分为假手术组、缺血组、缺血再灌注组、治疗组、采用“闭塞双侧颈总动脉和椎动脉＋体循环低血压法”建立全脑缺血再灌注损伤模型。缺血２０ｍｉｎ,再灌注２ｈ,通过放免法测定脑组织ＴＸＢ２、６－ｋｅｔｏ－ＰＧＦα含量及其比值。结果 缺血组脑组织ＴＸＢ２、６－ｋｅｔｏ－ＰＧＦ１α含量明显高于假手术组（Ｐ〈０．０１,Ｐ〈０．０５）;再灌注组脑组织ＴＸＢ２、ＴＸＢ２／６－ｋｅｔｏ－ＰＧＦ１α比值明显高于缺血组（Ｐ〈０．０１）;而治疗组脑组织ＴＸＢ２及ＴＸＢ２／６－ｋｅｔｏ－ＰＧＦ１α比值较缺血再灌注组显著降低（Ｐ〈０．０１）。结论 脑缺血再灌注损伤与ＴＸＡ２／ＰＧＩ２比例失调有关;山莨菪碱具有抑制ＴＸＡ２合成,调节ＴＸＡ２－ＰＧＩ２     

茶色素对缺血性脑血管病血浆ET,CGRP,TXB_2和6-k-PGF_(1α)的影响

目的探讨茶色素（ＴＰ）治疗缺血性脑血管病患者的意义。方法观察ＴＰ对缺血性脑血管病患者（５５例）治疗前后血浆内皮素（ＥＴ）、降钙素基因相关肽（ＣＧＲＰ）、血栓素Ｂ２（ＴＸＢ２）和６ 酮 前列腺素Ｆ１α（６ ｋ ＰＧＦ１α）含量的变化。结果ＴＰ能明显降低ＥＴ、ＴＸＢ２水平（Ｐ＜０．０１，＜０．０５），升高ＣＧＲＰ含量（Ｐ＜０．０１）。结论ＴＰ能有效地降低缺血性脑血管病患者ＥＴ、ＴＸＢ２水平，升高ＣＧＲＰ含量，调整Ｅ／Ｔ、Ｔ／Ｋ失衡。因而对防治缺血性脑血管病具有重要意义     

急性出血性脑血管病并发多脏器功能失常综合征患者血浆内皮素-1及降钙素基因相关肽水平的观察

目的：探讨血浆内皮素１（ＥＴ１）和降钙素基因相关肽（ＣＧＲＰ）在急性出血性脑血管病（ＡＨＣＶＤ）并发多脏器功能失常综合征（ＭＯＤＳ）发病中的作用。方法：采用放射免疫法分别测定２１例ＡＨＣＶＤ合并ＭＯＤＳ患者（ＭＯＤＳ组）、２０例ＡＨＣＶＤ患者（ＡＨＣＶＤ组）及３０例正常人（正常对照组）血浆中ＥＴ１和ＣＧＲＰ水平。结果：ＭＯＤＳ组及ＡＨＣＶＤ组血浆ＥＴ１水平明显高于正常对照组（Ｐ均＜０．０１），ＭＯＤＳ组ＥＴ１水平又明显高于ＡＨＣＶＤ组（Ｐ＜０．０１）。ＡＨＣＶＤ组血浆ＣＧＲＰ水平高于正常对照组，但无显著性差异（Ｐ＞０．０５）。而ＭＯＤＳ组血浆ＣＧＲＰ水平明显低于正常对照组，ＥＴ１／ＣＧＲＰ（Ｅ／Ｃ）比值明显高于ＡＨＣＶＤ组及正常对照组（Ｐ均＜０．０１）。结论：血浆ＥＴ１水平升高、ＣＧＲＰ水平降低、Ｅ／Ｃ比值严重失衡与ＭＯＤＳ的发生相关；检测血浆ＥＴ１和ＣＧＲＰ水平对评估ＡＨＣＶＤ患者预后有一定意义     

醒胸注射液抗脑缺血再灌注损伤作用的实验研究

目的 探讨醒脑静注射液９ＸＮＪＩ）对脑缺血灌注操作的防治作用及其机理。方法 制备家兔ＣＩＲＩ模型,随机分为对照组和ＸＮＪＩ组,动态观察血浆及脑组织一氧化氮（ＮＯ）水平、内皮素９ＥＴ）含量、丙二醛（ＭＤＡ）浓度、超氧化物歧化酶（ＳＯＤ）活性及脑超微结构的变化。结果 脑缺血再灌注期间,血浆和脑组织ＮＯ水平及ＳＯＤ活性明显下降（Ｐ〈０．０５和Ｐ〈０．０１）,ＥＴ及ＭＤＡ含量显著升高（Ｐ〈０．０５和Ｐ〈０     

降钙素基因相关肽对心脏局部肾素—血管紧张素系统的作用

为探讨降钙素基因相关肽（ＣＧＲＰ）对心脏局部肾素－血管紧张素系统（ＲＡＳ）的作用。我们用离体大鼠心脏缺血／再灌注（Ｉ／Ｒ）模型以放免法测定血管紧张素Ⅱ（ＡＴⅡ）的含量,观察ＣＧＲＰ对Ｉ／Ｒ损伤时心脏局部ＲＡＳ的影响,并以血管紧张素转换酶抑制剂（ＡＣＥＩ）作为对照,结果：（１）离体心脏经Ｉ／Ｒ损伤后,心肌组织及灌流液中ＡＴⅡ含量均较对照组显著升高（Ｐ〈０．０１）;（２）ＣＧＲＰ和ＡＣＥＩ都能拮抗缺血     

Two-stage resuscitation of the cat brain after prolonged cardiac arrest

Following prolonged cardiac arrest, reperfusion of the brain is endangered by the low blood perfusion pressure during the early resuscitation phase. In order to avoid low perfusion brain injury, a two-stage resuscitation protocol was applied to cats submitted to 30 min potassium chloride induced cardiac arrest: first, the heart was resuscitated, followed — after stabilisation of blood pressure — by recirculation of the brain. During cardiac resuscitation the brain was disconnected from the general circulation by inflating a pneumatic cuff around the neck. The results were compared with the outcome of conventional one-stage resuscitation following 15 min cardiac arrest. Cardiac resuscitation was successful in 5 out of 8 animals with 15 min and in 6 out of 13 animals with 30 min cardiac arrest. In successfully resuscitated animals of both groups, brain energy metabolism recovered to normal within 3 h although two-stage resuscitation increased brain ischemia time to 37–61 min. Twostage resuscitation, in consequence, is a promising approach for revival of the brain after prolonged cardiac arrest.     

内皮细胞功能紊乱在肝缺血-再灌注损伤中的作用及左旋精氨酸的干预

目的　探讨内皮细胞功能紊乱在肝缺血—再灌注损伤中的作用及左旋精氨酸对其的影响。方法　实验兔和肝癌手术患者均随机分为肝缺血—再灌注组 (n =10和n =6 )和肝缺血—再灌注 +左旋精氨酸治疗组 (n =10和n =6 ) ;分别取缺血前、缺血 4 5min(兔 )或 2 5min(患者 )和再灌注 4 5min(兔 )或 2 5min(患者 )共 3个时相点 ,用放射免疫法测定血浆透明质酸(HA) ,赖氏法检测谷丙转氨酶 (ALT)。结果　肝缺血—再灌注期间 ,实验兔和肝癌手术患者血浆HA、ALT明显升高 ,尤以再灌注 4 5min(兔 )或 2 5min(患者 )为著 (P <0 0 5或P <0 0 1)。左旋精氨酸可逆转上述指标 ,缺血时兔HA和ALT虽降低 ,但均P>0 0 5 ;患者HA虽降低 ,但P >0 0 5 ,而ALTP <0 0 1。再灌注时兔HA和ALT明显降低 ,均P <0 0 1;患者HA和ALT也显著下降 ,均P <0 0 1。结论　内皮细胞功能紊乱在肝缺血—再灌注损伤发生、发展中起重要的作用 ,左旋精氨酸通过保护内皮细胞而减轻肝缺血—再灌注损伤。     

高血糖促使心肺复苏后大鼠脑组织大量中性粒细胞浸润

目的 探讨高血糖加重大鼠全脑缺血-再灌注损伤的可能机制。方法 建立大鼠心肺复苏模型,以髓过氧化物酶作为中性粒细胞活性的观察指标,观测高血糖对心肺复苏后大鼠24h及72h脑组织中的中性粒细胞活性影响。结果 正常血糖组大鼠脑组织中几乎无髓过氧化物酶阳性细胞表达,而高血糖组大鼠在复苏后24、72h的中性粒细胞活性明显增高。结论 高血糖促使中性粒细胞在缺血后的全脑中早期大量浸润,是加重全脑缺血一再灌注损伤的重要因素。     

Normoxic ventilation during resuscitation and outcome from asphyxial cardiac arrest in rats

The formation of reactive oxygen species during reperfusion is one trigger for neuronal injury after global cerebral ischemia. Because formation of reactive oxygen species requires delivery of molecular oxygen to ischemic tissue, restricting inspired oxygen during reperfusion may decrease neurological damage. This study examined whether ventilation with room air rather than pure oxygen during resuscitation would improve neurological recovery after cardiac arrest in rats. Adult, male rats were subjected to 8 min of asphyxia resulting in cardiac arrest. During resuscitation, rats were ventilated either with hyperoxia (FiO2 = 1.0) or normoxia (FiO2 = 0.21, room air). Neurobehavioral deficits were scored daily for 72 h after resuscitation, after which brains were collected for histology. Normoxia decreased arterial oxygen content. Other physiological parameters and mortality did not differ between groups. All surviving rats exhibited behavioral and histological signs of brain damage. Neurological deficit scores did not differ between normoxia and hyperoxia conditions at any time point. The number of ischemic neurons in the hippocampus also did not differ between groups. These data indicate neither benefit nor detriment of reducing inspired oxygen concentration during resuscitation from asphyxial cardiac arrest in rats.     

经皮氧饱和度监测在院外心脏骤停患者心肺脑复苏中的应用

目的探讨经皮氧饱和度(SpO2)监测在院外心脏骤停患者心肺脑复苏中的意义。方法 394例院外心脏骤停患者分成两组,监测组221例患者入院后立即进行心肺脑复苏,同时予以SpO2监测并观察波形为指导持续胸外按压;未监测组173例患者入院后立即进行心肺脑复苏,但未予以SpO2监测;两组比较心、脑肺复苏成功率及心跳骤停持续时间、自主心跳恢复时间和脑缺血缺氧时间。结果监测组心肺复苏成功117例(52.94%)与未监测组心肺复苏成功72例(41.62%)比较,差异有统计学意义(χ2=4.98,P<0.05),监测组脑复苏成功14例(6.33%)与未监测组脑复苏成功6例(3.47%)比较,差异无统计学意义(χ2=1.66,P>0.05)。监测组的心跳骤停持续时间(43.93±23.33)min短于未监测组(52.92±26.28)min,自主心跳恢复时间(22.13±18.72)min亦短于未监测组(29.09±21.40)min,差异均有统计学意义(t分别=2.45、2.35,P均<0.05);而两组脑缺血缺氧时间比较,差异无统计学意义(t=1.16,P>0.05)。结论在经皮SpO2监测指导下进行胸外按压有助于提高胸外按压的有效性,从而提高心肺复苏的成功率。     

心肺复苏犬血TNF及ET含量变化的实验研究

目的 :探讨复苏犬血肿瘤坏死因子 (TNF)和内皮素 (ET)在复苏前后含量的变化规律及意义。方法 :电击致犬室颤 ,15 min后行标准复苏 ,测量心脏停跳 15 min,复苏后 0 .5 h、2 h、4 h血 TNF及 ET的含量。结果 :与正常组相比 ,心脏停跳 15 min时 ,血 TNF含量即显著升高 (P<0 .0 1) ,复苏后 30 min,血 ET含量亦明显升高 (P<0 .0 1) ,TNF及ET含量于复苏后 2 h达最高 ;各实验组与相应对照组相比与上述结果相似。结论 :复苏前后血 ET、TNF含量变化可能是机体在急剧缺血再灌注后出现的一种强烈的自身应激调节机制 ,在复苏后的病理生理过程中起重要作用     

Soluble epoxide hydrolase gene deletion reduces survival after cardiac arrest and cardiopulmonary resuscitation

The P450 eicosanoids epoxyeicosatrienoic acids (EETs) are produced by cytochrome P450 arachidonic acid epoxygenases and metabolized through multiple pathways, including soluble epoxide hydrolase (sEH). Pharmacological inhibition and gene deletion of sEH protect against ischemia/reperfusion injury in brain and heart, and against hypertension-related end-organ damage in kidney. We tested the hypothesis that sEH gene deletion improves survival, recovery of renal function and pathologic ischemic renal damage following transient whole-body ischemia induced by cardiac arrest (CA) and resuscitation. Mice with targeted deletion of sEH (sEH knockout, sEHKO) and C57Bl/6 wild-type control mice were subjected to 10-min CA, followed by cardiopulmonary resuscitation (CPR). Survival in wild-type mice was 93% and 80% at 10 min and 24 h after CA/CPR (n=15). Unexpectedly, survival in sEHKO mice was significantly lower than WT. Only 56% of sEHKO mice survived for 10 min (n=15, p=0.014 compared to WT) and no mice survived for 24 h after CA/CPR (p<0.0001 versus WT). We conclude that sEH plays an important role in cardiovascular regulation, and that reduced sEH levels or function reduces survival from cardiac arrest.     

Mild hypothermia alone or in combination with anesthetic post-conditioning reduces expression of inflammatory cytokines in the cerebral cortex of pigs after cardiopulmonary resuscitation

Introduction  

Hypothermia improves survival and neurological recovery after cardiac arrest. Pro-inflammatory cytokines have been implicated in focal cerebral ischemia/reperfusion injury. It is unknown whether cardiac arrest also triggers the release of cerebral inflammatory molecules, and whether therapeutic hypothermia alters this inflammatory response. This study sought to examine whether hypothermia or the combination of hypothermia with anesthetic post-conditioning with sevoflurane affect cerebral inflammatory response after cardiopulmonary resuscitation.     

心肺复苏犬心肌及血浆内皮素含量变化的实验研究

目的:研究复苏犬心肌组织及血浆内皮素(endothelin,E T)含量的变化规律及意义。方法:电击致犬室颤、心跳呼吸骤停,15m in后进行标准复苏,观察心脏停跳15m in、复苏后0.5h、2h、4h时心肌组织及血E T含量。结果:复苏后0.5h心肌组织及血浆E T含量较对照组明显升高(P<0.01),复苏后2h血浆E T含量达最高,心肌组织E T含量持续升高至复苏后4h(P<0.01)。结论:复苏后心肌组织及血中E T含量变化可能是机体在急剧缺血再灌注后出现的一种强烈的自身应激调节机制,与复苏后的心肌损伤及血流动力学不稳定有关。     

Resuscitation of the rabbit brain after acute complete ischemia lasting up to one hour: pathophysiological and pathomorphological observations

This study was conducted to investigate the degree of insult from arrest of cerebral blood flow leading to total brain ischemia, as a model for brain resuscitation studies in rabbits. In normothermic rabbits under light barbiturate anesthesia, cerebral blood flow was completely arrested for 5, 10, 15, 20, 30, 45 and 60 min by intrathoracic occlusion of the brachiocephalic trunk, the left subclavian and both internal thoracic arteries. Arterial blood pressure, arterial pH, arterial blood gases, cerebral blood flow, intracranial pressure, hematocrit and end tidal CO2 were monitored and recorded before, during and for 8 h after reperfusion. Disappearance and return of spontaneous EEG activity, vasomotor and respiratory centers were also recorded. During ischemia, the EEG was suppressed within 15 s and vasomotor and respiratory centers within 3-6 min. In all animals with 5, 10, 15 and 20 min cerebral ischemia bioelectric activity of brain cortex, vasomotor and respiratory centers returned upon recirculation. In about 50% animals with 30, 45 and 60 min ischemia recovery of basic brain function did not occur. After different periods of ischemia, histopathologic lesions were located mostly in the frontal cortex and hippocampus with ischemic neuronal change as the most frequent structural change. Brain cell necrosis was seen after successful resuscitation. This study indicates the feasibility of an ischemic insult in rabbits for use in resuscitation studies.