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腺苷和双嘧达莫模拟缺血预处理的作用。

Adenosine and dipyridamole mimic the effects of ischemic preconditioning.

作者信息

Mosca S M, Gelpi R J, Cingolani H E

机构信息

Centro de Investigaciones Cardiovasculares Universidad Nacional de La Plata 60 y 120, Argentina.

出版信息

J Mol Cell Cardiol. 1994 Oct;26(10):1403-9. doi: 10.1006/jmcc.1994.1158.

Abstract

The effects of preconditioning, adenosine and dipyridamole in protecting the systolic and diastolic alterations of myocardial stunning in rabbit hearts were studied. Isovolumic left ventricular developed pressure (LVDP), and end diastolic pressure (LVEDP) were measured. The time constant of relaxation (T) was calculated. Isolated rabbit hearts were subject to 15 min of global ischemia (37 degrees C) followed by 30 min of reperfusion. LVDP and LVEDP stabilized to 55 +/- 5% and 320 +/- 28% of control values respectively (stunned group) T increased early in reperfusion (from 48.2 +/- 3.9 to 97.2 +/- 10 ms P < 0.05) but returned to control value late in reperfusion. When hearts were preconditioned by a single cycle of 5 min of ischemia LVDP and LVEDP stabilized at 89 +/- 3% and 162 +/- 34% of preischemic values respectively (P < 0.05 with respect to stunned group). The change in T was attenuated (62 +/- 6 ms at 5 min of reperfusion, P < 0.05 with respect to stunned group). Hearts treated either with adenosine (800 micrograms/min) or the nucleoside transport blocker dipyridamole (4 micrograms/min) previously to the ischemia, recovered their LVDP to 86 +/- 1% and 82 +/- 3% of preischemic values, respectively (P < 0.05 with respect to stunned group). Adenosine and dipyridamole also attenuated the increase in LVEDP (195 +/- 12% and 197 +/- 10% respectively, P < 0.05 with respect to stunned group).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

研究了预处理、腺苷和双嘧达莫对兔心脏心肌顿抑时收缩和舒张改变的保护作用。测量了左心室等容收缩压(LVDP)和舒张末期压力(LVEDP)。计算了舒张时间常数(T)。将离体兔心脏进行15分钟的全心缺血(37℃),随后再灌注30分钟。LVDP和LVEDP分别稳定在对照值的55±5%和320±28%(顿抑组)。T在再灌注早期增加(从48.2±3.9毫秒增至97.2±10毫秒,P<0.05),但在再灌注后期恢复到对照值。当心脏通过5分钟缺血的单个周期进行预处理时,LVDP和LVEDP分别稳定在缺血前值的89±3%和162±34%(相对于顿抑组P<0.05)。T的变化减弱(再灌注5分钟时为62±6毫秒,相对于顿抑组P<0.05)。在缺血前用腺苷(800微克/分钟)或核苷转运阻滞剂双嘧达莫(4微克/分钟)处理的心脏,其LVDP分别恢复到缺血前值的86±1%和82±3%(相对于顿抑组P<0.05)。腺苷和双嘧达莫也减弱了LVEDP的增加(分别为195±12%和197±10%,相对于顿抑组P<0.05)。(摘要截短于250字)

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