模拟缺血时离体犬浦肯野纤维对肾上腺素能刺激电生理反应的发育差异。

A Fenrich, M Hamra
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引用次数: 1

摘要

肾上腺素能反应的发育差异可能导致细胞对缺血反应的年龄相关变化。标准微电极技术用于分离的幼犬和成年犬浦肯野纤维,以确定模拟缺血([K+]o = 10 mM, pH 6.7, pO2 < 25 mM Hg)单独或肾上腺素能刺激对自发跳动的浦肯野纤维的节律性活动以及节律性浦肯野纤维的跨膜电位和延迟后去极化(基本周期长度= 800-300 ms)的影响。使用的肾上腺素激动剂是苯肾上腺素(5 × 10(-8) M)和异丙肾上腺素(1 × 10(-6) M)。在所有自动纤维研究中,成人(-96 +/- 1 mV, n = 37)和年轻人(-98 +/- 1 mV, n = 36)的对照最大舒张电位在两组缺血期间都达到-62 +/- 1 mV,再灌注时又回到-96 +/- 2 mV。单独缺血时节律活动的发生率(以百分比表示)在两个年龄段相似:成人22%;年轻,25%。成人缺血时伴有苯肾上腺素过量的异位活动发生率为63%,可被吡唑嗪(1 × 10(-6) M)阻断,但不能被普萘洛尔(2 × 10(-7) M)阻断;年轻人的发病率为25%。异丙肾上腺素引起86%的年轻纤维和17%的成年纤维异位节律(p < 0.05)。在再灌注时,单纯缺血或缺血+肾上腺素刺激的成年人恢复到控制节律较慢。节律纤维对缺血或再灌注的跨膜电位反应无年龄相关差异,两组在800、500或300 ms起搏中断时均未出现去极化延迟。这些数据表明,肾上腺素能反应的年龄相关差异改变了细胞对缺血性损伤的反应。在某种程度上,异位搏动可能引发异常节律,这些对肾上腺素能激动剂敏感性的差异可能导致缺血期间致心律失常电位的发育差异。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Developmental differences in the electrophysiological response of isolated canine Purkinje fibers to adrenergic stimulation during simulated ischemia.

Developmental differences in adrenergic responsiveness may cause age-related changes in the cellular response to ischemia. Standard microelectrode techniques were used in isolated young and adult canine Purkinje fibers to determine the effect of simulated ischemia ([K+]o = 10 mM, pH 6.7, pO2 < 25 mm Hg) alone or with adrenergic stimulation on the rhythmic activity in spontaneously beating Purkinje fibers and on transmembrane potentials and delayed afterdepolarizations in paced Purkinje fibers (basic cycle length = 800-300 ms). The adrenergic agonists used were phenylephrine (5 x 10(-8) M) and isoproterenol (1 x 10(-6) M). For all automatic fibers studied, the control maximum diastolic potential in adults (-96 +/- 1 mV, n = 37) and in the young (-98 +/- 1 mV, n = 36) went to -62 +/- 1 mV during ischemia in both groups and returned to -96 +/- 2 mV with reperfusion. The incidence of rhythmic activity (expressed as percent) during ischemia alone was similar at both ages: adults, 22%; young, 25%. The incidence of ectopic activity with phenylephrine superfusion during ischemia for adults was 63%, an effect blocked by prazosin (1 x 10(-6) M) but not by propranolol (2 x 10(-7) M); the incidence for the young was 25%. Isoproterenol caused ectopic rhythms in 86% of young fibers and 17% of adult fibers (p < 0.05 young vs. adult). During reperfusion the return to control rhythm was slower in adults after ischemia alone or ischemia + alpha-adrenergic stimulation with phenylephrine. There were no age-related differences in the transmembrane potential response of paced fibers to ischemia or reperfusion, and there were no delayed afterdepolarizations with interruption of pacing at 800, 500, or 300 ms in either group. These data suggest that age-related differences in adrenergic responses alter the cellular response to an ischemic insult. To the extent that an ectopic beat may initiate an abnormal rhythm, these differences in sensitivity to adrenergic agonists may lead to developmental differences in arrhythmogenic potential during ischemia.

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