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儿茶酚胺可诱导腺苷受体介导的心肌保护作用,但不参与家兔的缺血预处理。

Catecholamines can induce adenosine receptor-mediated protection of the myocardium but do not participate in ischemic preconditioning in the rabbit.

作者信息

Thornton J D, Daly J F, Cohen M V, Yang X M, Downey J M

机构信息

Department of Physiology, University of South Alabama, Mobile 36688.

出版信息

Circ Res. 1993 Oct;73(4):649-55. doi: 10.1161/01.res.73.4.649.

Abstract

The role of catecholamines in ischemic preconditioning is unclear. Accordingly, the effects of tyramine-induced norepinephrine release and alpha 1-receptor blockade were examined. Ischemic preconditioning with a 5-minute coronary occlusion 10 minutes before a 30-minute ischemic interval resulted in only 7.7 +/- 3.1% infarction of the risk area, significantly less than that in control rabbits with isolated 30-minute coronary occlusions (34.4 +/- 3.2%, P < .01). Intravenous infusion of tyramine 10 minutes before 30 minutes of ischemia also protected the heart from infarction to an extent similar to that seen with ischemic preconditioning (6.9 +/- 2.4% infarction). This protection observed with tyramine infusion was eliminated by alpha 1-receptor blockade with BE 2254 (36.8 +/- 2.6% infarction) but was unaffected by beta-blockade with propranolol (10.5 +/- 2.4% infarction). Furthermore, the protection was unaffected when the tyramine-induced hypertension was attenuated by allowing blood to flow into a volume reservoir (3.9 +/- 0.8% infarction, P < .01 vs control value). The nonselective adenosine-receptor blocker PD 115,199 also eliminated tyramine-induced protection (40.2 +/- 5.6% infarction), indicating that adenosine is involved in adrenergic-mediated protection. BE 2254 could not block ischemic preconditioning (3.9 +/- 1.1% infarction, P < .01 vs control value). Therefore, catecholamine release before prolonged ischemia can protect the heart from infarction via the alpha 1-receptor, but adenosine receptor stimulation is also involved. alpha-Adrenergic stimulation does not appear to be critical to the protection observed after ischemic preconditioning.

摘要

儿茶酚胺在缺血预处理中的作用尚不清楚。因此,研究了酪胺诱导的去甲肾上腺素释放及α1受体阻断的作用。在30分钟缺血期前10分钟进行5分钟冠状动脉闭塞的缺血预处理,导致危险区域梗死率仅为7.7±3.1%,显著低于单纯30分钟冠状动脉闭塞的对照兔(34.4±3.2%,P<.01)。在30分钟缺血前10分钟静脉输注酪胺也能在一定程度上保护心脏免受梗死,其效果与缺血预处理相似(梗死率6.9±2.4%)。输注酪胺后观察到的这种保护作用被α1受体阻断剂BE 2254消除(梗死率36.8±2.6%),但不受普萘洛尔β受体阻断的影响(梗死率10.5±2.4%)。此外,当通过让血液流入容量储存器来减轻酪胺诱导的高血压时,保护作用不受影响(梗死率3.9±0.8%,与对照值相比P<.01)。非选择性腺苷受体阻断剂PD 115,199也消除了酪胺诱导的保护作用(梗死率40.2±5.6%),表明腺苷参与了肾上腺素能介导的保护作用。BE 2254不能阻断缺血预处理(梗死率3.9±1.1%,与对照值相比P<.01)。因此,长时间缺血前的儿茶酚胺释放可通过α1受体保护心脏免受梗死,但也涉及腺苷受体刺激。α肾上腺素能刺激似乎对缺血预处理后观察到的保护作用并不关键。

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