Catecholamines can induce adenosine receptor-mediated protection of the myocardium but do not participate in ischemic preconditioning in the rabbit.
Catecholamines can induce adenosine receptor-mediated protection of the myocardium but do not participate in ischemic preconditioning in the rabbit.
复制标题
儿茶酚胺可以诱导腺苷受体介导的心肌保护，但不参与兔子的缺血预适应。
DOI：
10.1161/01.res.73.4.649
复制
发表时间：
1993
影响因子：
20.1
通讯作者：
Downey,JM
中科院分区：
文献类型：
--
作者：
Thornton,JD;Daly,JF;Cohen,MV;Yang,XM;Downey,JM
儿茶酚胺在缺血预适应中的作用尚不清楚。因此，我们观察了酪胺诱导的去甲肾上腺素释放和α1受体阻断的作用。缺血30min前10min阻断冠脉5min的缺血预适应，仅有7.7+/-3.1%的梗死灶发生，显著少于对照组(34.4+/-3.2%，P<；.01)。在缺血30分钟前10分钟静脉注射酪胺也可以保护心脏免受梗塞的影响，其程度类似于缺血预适应(6.9+/-2.4%的梗塞)。这种保护作用可被BE 2254的α1受体阻断剂(36.8+/-2.6%)所消除，但不能被心得安(10.5+/-2.4%)的β-受体阻滞剂所影响。此外，当酪胺诱导的高血压通过允许血液流入容量储存库(3.9+/-0.8%的梗塞，P<；.01比控制值)而减弱时，这种保护作用不受影响。非选择性腺苷受体阻滞剂PD 115,199也消除了酪胺诱导的保护(40.2+/-5.6%梗死)，表明腺苷参与了肾上腺素能介导的保护。BE_(2254)不能阻断缺血预适应(3.9+/-1.1%梗死灶，P<；.01 vs对照组)。因此，在长时间缺血前释放儿茶酚胺可以通过α1受体保护心脏免受梗塞，但腺苷受体的刺激也参与其中。α-肾上腺素能刺激似乎不是缺血预适应后观察到的保护的关键。
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.