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人体肾上腺素能受体阻断后运动的血流动力学和代谢反应

Hemodynamic and metabolic responses to exercise after adrenoceptor blockade in humans.

作者信息

McLeod A A, Brown J E, Kitchell B B, Sedor F A, Kuhn C, Shand D G, Williams R S

出版信息

J Appl Physiol Respir Environ Exerc Physiol. 1984 Mar;56(3):716-22. doi: 10.1152/jappl.1984.56.3.716.

Abstract

The effects of acute alpha 1-adrenoceptor blockade with prazosin, beta 1-adrenoceptor blockade with atenolol, and nonselective beta-adrenoceptor blockade with propranolol were compared in a placebo-controlled crossover study of the hemodynamic and metabolic responses to acute exercise 2 h after prolonged prior exercise to induce skeletal muscle glycogen depletion, enhancing the dependence on hepatic glucose output and circulating free fatty acids (FFA). Plasma catecholamines were higher during exercise after, as opposed to before, glycogen depletion and were elevated further by all three drugs. Propranolol failed to produce a significant reduction in systolic blood pressure and elevated diastolic blood pressure. Atenolol reduced systolic blood pressure and did not change diastolic blood pressure. Both beta-blockers reduced FFA levels, but only propranolol lowered plasma glucose relative to placebo during exercise after glycogen depletion. In contrast, prazosin reduced systolic and diastolic blood pressures and resulted in elevated FFA and glucose levels. The results indicate important differences in the hemodynamic effects of beta 1-selective vs. nonselective beta-blockade during exercise after skeletal muscle glycogen depletion. Furthermore they confirm the importance of beta 2-mediated hepatic glucose production in maintaining plasma glucose levels during exercise. Acute alpha 1-blockade with prazosin induces reflex elevation of catecholamines, which in the absence of blockade of hepatic beta 2-receptors produces elevation of plasma glucose. The results suggest there is little role for alpha 1-mediated hepatic glucose production during exercise in humans.

摘要

在一项安慰剂对照的交叉研究中,比较了哌唑嗪急性α1肾上腺素能受体阻滞、阿替洛尔β1肾上腺素能受体阻滞以及普萘洛尔非选择性β肾上腺素能受体阻滞对急性运动的血流动力学和代谢反应的影响。该急性运动发生在长时间预先运动导致骨骼肌糖原耗竭2小时后,从而增强了对肝葡萄糖输出和循环游离脂肪酸(FFA)的依赖。与糖原耗竭前相比,运动期间血浆儿茶酚胺在糖原耗竭后更高,且三种药物均使其进一步升高。普萘洛尔未能使收缩压显著降低,反而使舒张压升高。阿替洛尔降低了收缩压,但未改变舒张压。两种β受体阻滞剂均降低了FFA水平,但只有普萘洛尔在糖原耗竭后的运动期间相对于安慰剂降低了血浆葡萄糖水平。相比之下,哌唑嗪降低了收缩压和舒张压,并导致FFA和葡萄糖水平升高。结果表明,在骨骼肌糖原耗竭后的运动中,β1选择性与非选择性β受体阻滞的血流动力学效应存在重要差异。此外,它们证实了β2介导的肝葡萄糖生成在运动期间维持血浆葡萄糖水平中的重要性。哌唑嗪急性α1阻滞诱导儿茶酚胺反射性升高,在未阻滞肝β2受体的情况下导致血浆葡萄糖升高。结果表明,α1介导的肝葡萄糖生成在人类运动期间作用不大。

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