Koyama K, Yamashita M, Miyauchi T, Goto K
Institute of Clinical Medicine, University of Tsukuba, Ibaraki, Japan.
Eur J Pharmacol. 1994 Apr 4;270(2-3):151-5. doi: 10.1016/0926-6917(94)90057-4.
Iminoctadine, a fungicide used widely in fruit culture, causes hypotension in human acute oral poisoning. In an attempt to elucidate this mechanism, we investigated the effects of iminoctadine on the cardiovascular system of rats. In anesthetized rats, intravenously administered iminoctadine produced hypotension and tachycardia. In isolated right atria beating spontaneously in Krebs-Ringer's solution, iminoctadine produced an increase in heart rate. It also produced a positive inotropic response in electrically driven left atria. These responses were partially diminished by atenolol, a beta 1-adrenoceptor antagonist, and also partially diminished to a similar degree in atria of reserpinized rats. Therefore, the positive inotropic and chronotropic effects of iminoctadine were partially mediated via the release of norepinephrine from sympathetic nerve terminals. In aortic ring segments, iminoctadine caused a rightward shift of the concentration-contractile response curve for phenylephrine but did not affect those for prostaglandin F2 alpha or KCl. Iminoctadine produced a potent vasodilation in aortic segments precontracted with phenylephrine. Removal of the aortic endothelium produced a rightward shift of the concentration-response curve for iminoctadine. When the aortic ring preparations were precontracted with prostaglandin F2 alpha or KCl, iminoctadine produced only slight vasodilation. Therefore, the vasodilation caused by iminoctadine is due mostly to its alpha 1-adrenoceptor antagonizing action, and partly to endothelium-dependent mechanisms our data suggest that the hypotension induced by iminoctadine is due to its vasodilator effects.
双胍辛胺是一种广泛用于水果种植的杀菌剂，人体急性口服中毒时会导致低血压。为了阐明其作用机制，我们研究了双胍辛胺对大鼠心血管系统的影响。在麻醉的大鼠中，静脉注射双胍辛胺会导致低血压和心动过速。在Krebs-Ringer溶液中自发搏动的离体右心房中，双胍辛胺会使心率增加。它还会在电驱动的左心房中产生正性肌力反应。β1肾上腺素能受体拮抗剂阿替洛尔可部分减弱这些反应，在利血平化大鼠的心房中也会部分减弱至相似程度。因此，双胍辛胺的正性肌力和变时性作用部分是通过交感神经末梢释放去甲肾上腺素介导的。在主动脉环段中，双胍辛胺使去氧肾上腺素的浓度-收缩反应曲线向右移动，但不影响前列腺素F2α或氯化钾的曲线。双胍辛胺在预先用去氧肾上腺素收缩的主动脉段中产生强力血管舒张作用。去除主动脉内皮会使双胍辛胺的浓度-反应曲线向右移动。当主动脉环制剂预先用前列腺素F2α或氯化钾收缩时，双胍辛胺仅产生轻微的血管舒张作用。因此，双胍辛胺引起的血管舒张主要是由于其α1肾上腺素能受体拮抗作用，部分是由于内皮依赖性机制。我们的数据表明，双胍辛胺引起的低血压是由于其血管舒张作用。
