Dowell R T
Am J Physiol. 1979 Nov;237(5):C195-9. doi: 10.1152/ajpcell.1979.237.5.C195.
A previous study has shown that chronic chemical sympathectomy brought about by 6-hydroxydopamine injections results in a dpression in myocardial contractile function which is accompanied by reduced myofibrillar ATPase activity. To determine whether chronic beta-adrenergic receptor blockade elicits similar alterations in cardiac contractile-protein ATPase activity, adult rats were given twice-daily injections of propranolol 7 days/wk for 2 wk. Effective beta-adrenergic receptor blockade was verified by the lack of hemodynamic responsiveness to isoproterenol infusion. Myofibrils were prepared from left ventricular tissue and analyzed for ATPase activity. Myofibrillar ATPase activity was 295 +/- 8 nmol Pi.mg-1.min-1 in controls. Enzyme activity was not significantly different in propranolol-injected rats. The results demonstrate that chronic propranolol administration does not alter the ATPase activity of cardiac myofibrils. Therefore, it seems likely that the altered contractile-protein enzymatic properties resulting from chronic chemical sympathectomy do not occur as the result of a reducted level of cardiac beta-adrenergic receptor stimulation.
先前的一项研究表明,6-羟基多巴胺注射所致的慢性化学性交感神经切除术会导致心肌收缩功能降低,同时伴有肌原纤维ATP酶活性降低。为了确定慢性β-肾上腺素能受体阻断是否会引起心脏收缩蛋白ATP酶活性的类似改变,成年大鼠每周7天每天注射两次普萘洛尔,持续2周。通过对异丙肾上腺素输注缺乏血流动力学反应来证实有效的β-肾上腺素能受体阻断。从左心室组织制备肌原纤维并分析其ATP酶活性。对照组肌原纤维ATP酶活性为295±8 nmol Pi·mg-1·min-1。注射普萘洛尔的大鼠的酶活性无显著差异。结果表明,长期给予普萘洛尔不会改变心肌肌原纤维的ATP酶活性。因此,慢性化学性交感神经切除术导致的收缩蛋白酶特性改变似乎不是由于心脏β-肾上腺素能受体刺激水平降低所致。