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At the same time, the contents of myocardial Ca2+ and MDA were decreased significantly as well as the activities of myocardial SOD and GSH-Px increased markedly. Conclusion: CASI is of protective effect on myocardial ischemia-reperfusion arrhythmia, which may be related to scavenging the oxygen free radicals and Ca2+ overload formed during reperfusion.

CASI对大鼠心肌缺血再灌注心律失常具有明显保护作用,其机制可能与提高心肌组织的抗氧化酶活性,减少自由基及Ca2+超负荷对心肌的氧化损伤有关。

Objective To observe the effect of Cornu Cervi on the change of VEGF after the acute damage of myocardium in animal model of myocardial ischemia, and inquired into the mechanism of the protective effect on myocardium cell.

目的观察鹿茸提取物对心肌缺血动物模型心肌损伤急性期后血管内皮生长因子变化的的影响,并探讨其对心肌细胞保护作用的机制。

SHEN-FU Injection can accelerate the resume of myocardial function during ischemia-reperfusion, countermine arrhythmias after reperfusion, reduce the myocardial infarct size.

可以促进缺血再灌注心肌收缩和舒张功能的恢复,降低再灌注心律失常的发生率,缩小心肌梗死范围,减轻心肌组织的超微结构损伤性改变。

The effects of IR and IP on hemodynamics, epicardial electrography, myocardial infarct size, cardiomyocytic apoptosis and gene proteins involving apoptosis (Fas, Bcl-2 and Bax) are observed in aneasthetized rabbit myocardium.

在麻醉家兔心肌IR模型上,观察IR和IP对血流动力学、心外膜电图、心肌梗死范围、心肌细胞凋亡和凋亡相关调控基因蛋白(Fas、Bcl-2、Bax等)的影响。

The effects of myocardial ischemia-reperfusion and RIP on hemodynamics, epicardial electrography, myocardial infarct size, cardiomyocytic apoptosis and gene proteins involving apoptosis (Fas, Bcl-2 and Bax) are observed in aneasthetized rabbit myocardium.

在麻醉家兔心肌IR(myocardial ischemia-reperfusion,MIR)模型上,观察MIR和肾脏IP(renal ischemic preconditioning,RIP)对血流动力学、心外膜电图、心肌梗死范围、心肌细胞凋亡和凋亡相关调控基因蛋白(Fas、Bcl-2、Bax等)的影响。

Results:By short term stimulating,the vitality of blood serum enzyme increased and the change of ultrastruucture showed the hypermetabolism of cardiac muscles;with the state of high stress prologing,the vitality of blood serum enzyme decreased gradually;the damage ...

结果:随应激状态时间延长、强度增加,血清心肌酶(LD H、HBD H、C K、GO T)活力短时间刺激升高,然后逐渐下降,心肌超微结构短期刺激为代谢亢进的变化,以后呈逐渐加重的损伤性改变。结论:高应激状态能够引起大鼠心肌损伤。

The results suggest that CGRP has effects of protecting the myocardial injury induced by isoproterenol, correcting the imbalance between MDA and SOD level, inhibiting the stronger lipid hyperoxide reaction, preventing the myocardial enzyme leak from injuried cardiomyocyte and antagonizing arrhythmia in rats.

静脉用CGRP治疗异丙肾上腺素所致大鼠心肌损伤,能纠正MDA和SOD的失衡,抑制过强脂质过氧化反应,并保护心肌细胞,防止心肌酶漏出,拮抗心律失常。

Results (1)LVMI gradually increased from 5d to 30d in OG (P<0.01);(2)Counts of intracardiac bFGF immune reaction and bFGF mRNA expression were increased at 5d, were essentially normalized at 30d;(3) Intracardial ACE activity, angiotensin II concentration, ACE protein and ACE mRNA expression were progressively risen from 0.5 h or 4 h to 30 d;(4)LVMI was positively correlated with the level of ACE protein and ACE mRNA expression following 5d.

2OG中心肌bFGF免疫反应特异性染色强度增加,半定量显示5天升高(P<0.05),30天基本恢复正常(P>0.05);bFGF mRNA表达1天升高(P<0.05),其后类似bFGF。(3)心肌血管紧张素转换酶活性和血管紧张素Ⅱ水平在术后0.5小时即升高(P<0.05),4小时明显增高(P<0.01),峰值在30天;心肌ACE蛋白及ACE mRNA表达均在术后4小时明显增高(P<0.05或<0.01),其后逐渐升高,峰值在30天;5天及其后,LVMI与ACE蛋白及ACE mRNA表达数量呈正相关。

Result: After treatment of the left ventricular with DD, vs aorta-contricted model group, NO content, cNOS and Na+-K+-ATPase, Ca2+-ATPase activity were significantly increased, the content of AngII in left ventricle and serum and iNOS activity and the ratio of HW/BW, LVI, MD were significantly reduced.

结果:与模型组比较DD能显著提高心肌组织NO含量和结构型NOS,Na+-K+-ATPase,Ca2+-ATPase活性;降低心肌组织诱生型NOS活性;抑制血浆及心肌组织AngⅡ和胶原的产生;减轻心脏质量参数及MD。

Acute myocardial infarction is a common cause for sudden and unexpected death. However, it is difficult to detect the myocardial changes in medico-legal practice with traditional macroscopic examination or routine histological stains when the sudden death occurs in the hyper-acute phase of infarction (<3h).

急性心肌梗死是引起猝死的常见原因,然而,在法医实践中,对于心肌梗死的超急性期(<3小时)发生死亡的心脏用传统的肉眼观察或常规组织学检查的方法很难发现心肌的形态学改变从而提供客观的诊断依据。

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