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左心室舒张压升高所诱导的心肌牵张可使正常血压大鼠和自发性高血压大鼠的离体灌注心脏产生预处理。

Myocardial stretch induced by increased left ventricular diastolic pressure preconditions isolated perfused hearts of normotensive and spontaneously hypertensive rats.

作者信息

Nakagawa C, Asayama J, Katamura M, Matoba S, Keira N, Kawahara A, Tsuruyama K, Tanaka T, Kobara M, Akashi K, Ohta B, Tatsumi T, Nakagawa M

机构信息

Second Department of Medicine, Kyoto Prefectural University of Medicine, Japan.

出版信息

Basic Res Cardiol. 1997 Dec;92(6):410-6. doi: 10.1007/BF00796215.

Abstract

OBJECTIVE

The aim of our study was to determine whether myocardial stretch (non-ischemic stress) could precondition isolated perfused hearts of both normotensive Wister-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR).

METHODS

The perfused hearts in Langendorff mode were subjected to 30 min of global no-flow ischemia followed by 30 min of reperfusion. Left ventricular developed pressure (LVDP) and end-diastolic pressure (LVEDP) were measured. In the control group, LVEDP was set at 10 mmHg. In the stretch group, LVEDP was increased to 30 or 60 mmHg for 5 min before 30 min of ischemia. In the ischemic preconditioning group, the hearts were exposed to two cycles of a 5-min period of ischemia before 30 min of ischemia. Myocardial lactate contents were measured at the baseline and at the end of the 60 mmHg stretch.

RESULTS

Hemodynamic parameters of LVDP and LVEDP at 30 min of reperfusion improved in the stretch group (LVEDP of 60 mmHg) and the ischemic preconditioning group. Coronary flow did not decrease during the stretch. Recovery of the coronary flow during reperfusion was better in the stretch and ischemic preconditioning groups. Postischemic contractile function was better in WKY rats than in SHR. Myocardial lactate contents at the end of 60 mmHg stretch were negligible.

CONCLUSIONS

Myocardial stretch induced by increasing LVEDP preconditioned isolated perfused hearts of both WKY rats and SHR, via mechanisms not involving myocardial ischemia during stretch.

摘要

目的

我们研究的目的是确定心肌牵张(非缺血性应激)是否能对正常血压的Wistar-Kyoto(WKY)大鼠和自发性高血压大鼠(SHR)的离体灌注心脏起到预处理作用。

方法

采用Langendorff模式灌注心脏,使其经历30分钟的全心无血流缺血,随后再灌注30分钟。测量左心室舒张末压(LVEDP)和左心室发展压(LVDP)。对照组中,LVEDP设定为10 mmHg。牵张组在缺血30分钟前,将LVEDP升高至30或60 mmHg并维持5分钟。缺血预处理组在缺血30分钟前,使心脏经历两个5分钟的缺血周期。在基线和60 mmHg牵张结束时测量心肌乳酸含量。

结果

牵张组(LVEDP为60 mmHg)和缺血预处理组在再灌注30分钟时的LVDP和LVEDP血流动力学参数得到改善。牵张过程中冠状动脉血流未减少。牵张组和缺血预处理组在再灌注期间冠状动脉血流的恢复情况更好。缺血后收缩功能在WKY大鼠中比在SHR中更好。60 mmHg牵张结束时的心肌乳酸含量可忽略不计。

结论

通过增加LVEDP诱导的心肌牵张,对WKY大鼠和SHR的离体灌注心脏起到预处理作用,其机制不涉及牵张期间的心肌缺血。

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