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1.
心脏停跳复苏后将脑温降低至30~32℃时,测定脑组织PGI2及TXA2含量。结果表明:全脑中度低温可明显抑制TXA2的产生,而PGI2含量无明显变化。提示中度低温能早期有效地抑制脑内花生四烯酸环氧酶途径代谢,减轻缺血后脑损伤。  相似文献   

2.
目的和方法用硫代巴比妥酸比色法和放免方法检测缺血再灌注家兔心肌丙二醛(MDA)及血浆血栓素A2(TXA2)、前列环素(PGI2)浓度变化,探讨氧自由基(OFR)与TXA2、PGI2在心肌缺血再灌注损伤中的作用.结果与对照组比较缺血及再灌注组心肌组织MDA明显升高,心肌组织含水量增加,再灌注组血浆TXA2浓度及TXA2/PGI2比值高于对照组,TXA2与心肌组织MDA含量呈正相关(r=0.73,P<0.05).结论OFR与TXA2/PGI2 平衡失调相互作用,可能共同参与心肌缺血再灌注损伤的发生.丹参可减轻上述的变化.  相似文献   

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观察缺维生素E大鼠,正常对照及缺维生素E后补充维生素E大鼠体内TXA2和PGI2含量的变化。结果表明。缺维生素E大鼠体内TXA2含量明显增高;PGI2含量显著降低。这种改变可能与缺E造成的脂质过氧化物(LPO)有关。  相似文献   

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目的观察奥德金对急性心肌梗死的疗效.方法急性心肌梗死病人75例,分析奥德金治疗前后血浆血栓素(TXA2)和前列腺素(PGI2)指标的变化以及与对照组、溶栓组之间指标变化的比较.结果奥德金治疗后与治疗前相比TXA2明显减少,PGI2明显增加,PGI2/TXA2明显上升(P<0.01);奥德金组与溶栓组相比,TXA2明显减少(P<0.01),PGI2明显增加(P<0.01),PGI2/TXA2明显上升(P<0.05).结论奥德金治疗急性心梗有效.  相似文献   

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气功对两种证型高血压患者TXB2及6—keto—PGf1α的影响   总被引:1,自引:0,他引:1  
采用气功及心痛定治疗45列肝阳上亢及阴虚阳亢型高血压患者,观察各组TXB26-K-PGF1α,及TXB2/6-X-PGF1α值,结果显示:气功能治疗组中,肝阳上亢型,阴虚阳亢型及心痛定组TXB2及TXB2/6-K-PGF1α值均明显下降,而6-K-PGF1α明显上升,TXB2及6-K-PGF1α含量变化组间差别无统计学意义,提示气功和心痛定对高血压患者的血浆TXB2及6-K-PGF1α均具有调节作  相似文献   

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Hyperlipemia rabbit models established with high cholesterol and fat diet were treated vith directmoxibustion and medicinal cake-separated moxibustion. The post-treatment plasma 6-keto-prostaglandin F_(1α)(6-keto-PGF_(1α)) and thromboxane B2 (TXB_2) contents were determined by radioimmunoassay. Resultsindicated that the plasma 6-keto-PGF_(1α) content significantly increased,the TXB_2 level decreased (P<0.05)and the TXB_2 /6-keto-PGF_(1α) ratio also decreased (P<0.01) in the medicinal cake-separated moxibustiongroup as compared with those in the model group respectively,but there was no significant differencebetween the medicinal cake-separated moxibustion group and the direct moxibustion group (P>0.05),suggesting that both the medicinal cake-separated moxibustion and direct moxibustion can regulate theplasma 6-keto-PGF_(1α) and TXB_2 contents,and the TXB_2/6-keto-PGF_(1α) ratio with similar actions,and have acertain protective action on endothelial cells of the aorta in the rabbit of hyperlipemia  相似文献   

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目的研究不同程度亚低温对大鼠心肺复苏(CPR)后脑组织凋亡的影响。方法利用窒息法制作心肺复苏模型,SD大鼠
15只,随机分为对照组(正常体温)、34 ℃低温组、32 ℃低温组,每组各5只。对照组在CPR后置于室温25 ℃下常规治疗;34 ℃低
温组(34+/-0.2 ℃)和32 ℃低温组(32+/-0.2 ℃)在CPR 0.5 h后分别给予亚低温治疗。各组大鼠均于CPR后12 h取脑组织,免疫
组化法测定大脑皮层caspase-3蛋白表达,Western blotting测定Bcl-2、Bax表达,同时观察各组脑组织病理变化。结果与常温
组相比,低温组神经元caspase-3 表达均明显减弱(P<0.05),其中32 ℃低温组caspase-3 表达减弱更加明显(P<0.05);低温组
Bcl-2表达明显增强(P<0.05),32 ℃低温组的Bcl-2蛋白表达比34 ℃低温组表达更强;3组大鼠神经元凋亡蛋白bax的表达无明
显差异。结论亚低温可能通过降低caspase-3蛋白的表达、增强Bcl-2的表达,从而抑制脑细胞凋亡减轻脑损伤,32 ℃亚低温治
疗比34 ℃更能起到脑保护的作用。
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Thepathophysiologicalmechanismsofischemicbraindamagevaryaftercardiacarrest (CA)andcardiopulmo nary cerebralresuscitation .ThesemechanismsconsistoftheprimaryinsultofCA (completetemporaryglobalbrainischemia)andsecondaryderangementsduringandafterreperfusion reoxygenation (ie ,postischemic anoxicenceph alopathy ,alsocalledcerebralpostresuscitationsyndrome) .AfterCA ,intheprevioushealthyorganism ,cerebraloxy gen (O2 )deliverymaybereduceddespitecontrolledarteri alnormotensionandnormoxemia .Atthes…  相似文献   

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犬心脏停搏复苏后脑氧供需变化及高血压性再灌流的影响   总被引:1,自引:0,他引:1  
目的观察犬心脏停搏(cardiac arrest,CA)复苏后再灌流期间脑氧代谢情况变化及高血压性再灌流的影响.方法建立犬电击引起室颤(ventricularfibriHation,VF)性CA 8 min后开胸心肺复苏(CPR)模型,动物随机分两组:正常血压性再灌流(NT)组(n=6),高血压性再灌流(HT)组(n=6),在自主循环恢复(ROSC)后,MAP在NT组维持于CA前基础值水平,而HT组维持于基础值的110%~115%.取动脉血及脑矢状窦血行血气分析,观察CA前及CA再灌流后30、60、120、240 min的脑动脉-矢状窦氧含量差(ca-ssDO2)及矢状窦氧分压(PssO2)变化.结果与基础值比较,CA后再灌流30min,NT组Ca-ssDO2显著下降(P<0.05),PsO2显著升高(P<0.01),直至再灌流240 min,Ca-ssDO2升高显著(P<0.01),PssO2下降显著(P<0.01).两组间比较,再灌流30min,HT组Ca-ssDO2下降显著(P<0.01),PssO2升高显著(P<0.01),但此后4 h内两组脑氧代谢值差别不显著(P>0.05).结论CA复苏后脑氧供需关系失衡,高血压性再灌流进一步增加CA后早期脑氧供应.  相似文献   

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目的:寻找肾上腺素用于心肺复苏的最佳剂量。方法:选择成年杂种犬60条,随机分为6组,造成心梗模型后致颤,分别给予0.02、0.05、0.075、0.1、0.2、0.3mg/kg体重的肾上腺素进行心肺复苏,比较心肺复苏的成功率,恢复自主循环的时间及自主循环恢复1min后血流动力学指标的变化;并以电镜技术观察肾上腺素对心肌组织的影响。结果:0.075mg/kg和0.1mg/kg体重组复苏的成功率明显高于其他各组(P<0.05),且此两组自主循环的恢复时间明显短于其他各组(P<0.05);各组复苏1min后血流动力学指标的变化:随着剂量的增加,收缩压、舒张压、左室收缩末压逐渐增加,但心输出量和冠脉血流量却在0.075mg/kg体重组达最高,与其他各组比较P值均<0.05,超过0.1mg/kg心输出量和冠脉血流量不再继续增加;电镜所见:各组非梗塞区的心肌组织只有轻微改变,与所用的肾上腺素的剂量无关。结论:犬心肺复苏过程中应用0.075mg/kg和0.1mg/kg体重的肾上腺素为最佳剂量  相似文献   

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目的:研究心脏停跳复苏犬脑组织、外周血红细胞Na+-K+-ATP酶活性的变化,探讨复苏后脑损伤的病理生理变化及外周血红细胞Na+-K+-ATP酶活性与脑组织Na+-K+-ATP酶活性之间的相关关系.方法:采用犬室颤心跳呼吸骤停模型,进行标准心肺复苏,分别观察室颤前、心脏停跳10 min及复苏后30、120、240 min的脑组织、外周血红细胞Na+-K+-ATP酶活性变化.结果:心脏停跳10 min及复苏后30、120、240 min的脑组织、外周血红细胞Na+-K+-ATP酶活性均较室颤前有明显降低,并且外周血红细胞Na+-K+-ATP酶活性与脑组织Na+-K+-ATP酶活性之间存在着显著的相关关系.结论:复苏后脑组织Na+-K+-ATP酶活性降低,可能参与了脑组织损伤的病理生理过程,作为复苏后脑组织损伤的监测指标有一定价值.  相似文献   

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Y Z Zhang  X F Yan 《中西医结合杂志》1990,10(11):669-71, 645
The authors examined the influences of nifedipine and Paeonia lactiflora (PL) on plasma LPO, TXB2 and 6-keto-PGF1 alpha in cholesterol-fed rabbits. In this study, oral administration of nifedipine (15 mg/kg per day) and PL (0.5 g/kg per day) with 2% cholesterol diet for 15 weeks caused 60.75% and 74.24% reduction in the lesion area of aorta respectively. The levels of plasma LPO, TXB2, cholesterol, phospholipid and calcium of the intimalmedia of the aorta in the treated groups were significantly lower than those in the control group, but the level of 6-keto-PGF1 alpha in the treated groups was significantly higher. The durations of TXB2 elevation and 6-keto-PGF1 alpha reduction were delayed. The ratio of TXB2/6-keto-PGF1 alpha tended to balance. The ratio of TXB2/6-keto-PGF1 alpha was significantly positive correlation with the percentage of lesion area of the aorta. It is demonstrated that calcium metabolism plays an important role in thromboxane, prostaglandin, and LPO synthesis. In conclusion, the inhibition of LPO production and the regulation of TXA2-PGI2 balance may be one of the mechanisms of anti-atherogenesis of calcium antagonists and PL.  相似文献   

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In the femoral head necrosis model rabbit induced by endotoxin combined with methylprenisolone, the dynamical changes of plasma TXB2 and 6-keto-PGF1αcontents were observed. As a result, microscopic examination showed that in the model group, bone trabeculae became fine, empty bone lacunae increased,and osteoblasts in number decreased; the ratio of TXB2 and 6-keto-PGF1α was out of balance, and these changes worsened gradually with the lapse of time; Compound Sheng Mai Cheng Gu Capsules (复方生脉成骨胶囊) could reverse femoral head necrosis, protect the vascular endothelial cells, recover the balance of TXB2 and 6-keto-PGF1α. It is concluded that the hormone-induced femoral head necrosis is closely related with blood stasis, and that the Chinese drugs for activating blood circulation and removing blood stasis can prevent the femoral head from development of necrosis.  相似文献   

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