Smith D J, Rushin J M, Urquilla P R, Rhee C W, Yoon H J, Simpson F A, Srichomkuan T, Lee H S, Knapp R B
Anesth Analg. 1979 May-Jun;58(3):189-94.
The cardiovascular effects of benzquinamide were evaluated in anesthetized dogs. Intravenous benzquinamide, 0.5 to 5 mg/kg, caused tachycardia, elevated blood norepinephrine levels, frequent ventricular arrhythmias, and brief hypotension. Ganglionic blockade by hexamethonium prior to administration of benzquinamide prevented the tachycardia and alterations in norepinephrine levels but prolonged the period of hypotension. In isolated mesenteric arterial preparations benzquinamide interfered with contractile force generated by potassium chloride, norepinephrine, and prostaglandin F2 alpha. It is concluded that benzquinamide directly relaxes vascular smooth muscle thereby producing in vivo reduced peripheral vascular resistance and hypotension, which are compensated for by reflex sympathetic activation.
在麻醉犬中评估了苄喹酰胺的心血管效应。静脉注射苄喹酰胺，剂量为0.5至5毫克/千克，可引起心动过速、血液去甲肾上腺素水平升高、频发室性心律失常和短暂低血压。在给予苄喹酰胺之前用六甲铵进行神经节阻断可预防心动过速和去甲肾上腺素水平的改变，但会延长低血压的持续时间。在离体肠系膜动脉制剂中，苄喹酰胺会干扰由氯化钾、去甲肾上腺素和前列腺素F2α产生的收缩力。得出的结论是，苄喹酰胺直接松弛血管平滑肌，从而在体内产生外周血管阻力降低和低血压，这会通过反射性交感神经激活得到代偿。
