【摘要】 在心得安（1μM）阻断β-受体的情况下,本文通过观察苯肾上腺素（PE）对豚鼠和兔心室乳头肌动作电位及收缩的作用,探讨了心脏α-受体兴奋引起正性变力作用的机制。PE（1—16μM）延长豚鼠心室乳头肌动作电位时程（APD）,增加兔和豚鼠心室乳头肌的收缩幅度（AC）。PE 在兔心室乳头肌上表现出的正性变力作用比在豚鼠心室肌上显著得多。FE（16μM）加强兔和豚鼠心室乳头肌收缩力的作用可被α₁-受体阻断剂哌唑嗪（Prazosin）（0.3—0.5μM）所取消。然而,在豚鼠心室乳头肌上被PE延长的APD,仅APD₃₀在哌唑嗪作用下有所缩短,而APD₉₀则不受其影响。在高钾（22mM）除极的心室乳头肌,PE（50μM）使 9个兔标本中的8个、8个豚鼠标本中的2个分别恢复慢反应动作电位。这些慢反应动作电位可被哌唑嗪（1μM）或钙通道阻断剂Mn⁺⁺（1mM）所取消或抑制。以上的结果提示心脏α-肾上腺素能受体兴奋引起正性变力作用可能是由于慢内向电流（I_si）的增加。更多还原

【Abstract】 When β-adrenoceptor was blocked by propranolol（1μM）, the effects of pheny-lephrine （PE） on the action potential and contraction of the isolated guinea pigand rabbit papillary muscles were studied in order to investigate the mechanism ofthe positive inotropic effect mediated via α-adrenoceptors. PE （1-16μM） prolonged the action potential duration （APD） of the guineapig papillary muscles and increased amplitude of contraction （AC） of the musclesof both guinea pig and rabbit. The positive inotropic effects of PE on rabbit papil-lary muscles were much stronger than those on guinea pig papillary muscles. Theseeffects of PE on amplitude of contraction could be abolished by prazosin （0.3-0.5μM）. However, in the guinea pig papillary muscles a slight shortening of APD wasonly observed at the level APD₃₀, but not at the level APD₉₀.In the papillarymuscles which had been depolarized by 22 mM K⁺, slow action potentials were res-tored by PE （50μM） in 8 out of 9 rabbit preparations and in 2 out of 8 guineapig preparations. These responses were abolished or diminished by prazosin （1μM） or calcium channel blocker Mn₂₊ （1 mM）. The results of the present investigation suggest that the positive inotropiceffect mediated via α-adrenoceptors may be due to an increase in slow inward calciumcurrent （Isi） both in guinea pig and in rabbit papillary muscles.更多还原