Broadley K J, Rothaul A L
Pflugers Arch. 1981 Aug;391(2):147-53. doi: 10.1007/BF00657006.
Guinea-pig isolated hearts were perfused in series, the donor heart perfusate supplying the recipient heart. Isoprenaline increased the rate and force of contraction and oxygen consumption of donor hearts and produced a coronary vasodilatation. This was accompanied by the release of vasodilator metabolite as demonstrated by vasodilatation of the recipient heart, the beta-adrenoceptors of which were antagonized by propranolol. During arrest of donor hearts by either carbachol or application of a fibrillating current, isoprenaline still released vasodilator metabolite and increased oxygen consumption but without changes in rate or tension. This release was prevented by beta-adrenoceptor blockade. It is concluded that the sympathomimetic-induced coronary vasodilatation is mediated via the release of a vasoactive metabolite, the trigger for which is not the concomitant mechanical hyperactivity.
豚鼠离体心脏进行串联灌注，供体心脏的灌注液供应受体心脏。异丙肾上腺素增加了供体心脏的收缩速率、收缩力和耗氧量，并引起冠状动脉扩张。这伴随着血管舒张代谢产物的释放，受体心脏的血管舒张证明了这一点，其β - 肾上腺素能受体被普萘洛尔拮抗。在通过卡巴胆碱或施加颤动电流使供体心脏停搏期间，异丙肾上腺素仍能释放血管舒张代谢产物并增加耗氧量，但心率或张力没有变化。这种释放可被β - 肾上腺素能受体阻断所阻止。结论是拟交感神经药诱导的冠状动脉扩张是通过血管活性代谢产物的释放介导的，其触发因素不是伴随的机械性活动增强。
