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以希氏束电图各间期为指标,观察烟酰胺对在位和离体兔心房室传导的影响。麻醉兔静脉注射烟酰胺(0.6g/kg)A～H间期明显缩短,St-A、H-V间期无明显变化。烟酰胺可对抗戊脉安延长A-H间期的效应,戊脉安剂量增加,烟酰胺作用减弱,甚至消失。在等效剂量异丙肾上腺素失去作用的条件下,烟酰胺仍使心得安所延长的A-H间期明显缩短。低Ca~(++)、高Ca~(++)均致离体灌流心脏A-H间期延长。烟酰胺对抗低Ca~(++)的效应,却加重高Ca~(++)的作用。结果表明,烟酰胺可加速房室结传导,对心房、希-浦氏纤维系统的传导无明显影响;烟酰胺作用机理不同于β受体激动剂,其可能为慢通道促进剂,通过增强缓慢内向电流而发挥作用。
The interval of His sonogram was used as an index to observe the effect of niacinamide on atrioventricular conduction in and out of rabbit. Anesthesia rabbit intravenous injection of nicotinamide (0.6g / kg) A ~ H interval was significantly shortened, St-A, H-V interval was no significant change. Nicotinamide can antagonize the effect of verapamil on the prolongation of A-H interval. The dose of verapamil is increased, and the effect of nicotinamide is weakened or even disappeared. Nicotinamide significantly shortened the prolonged A-H interval when propranolol was deprotected at equivalent doses. Low Ca ~ (++), high Ca ~ (++) induced prolonged A-H interval in isolated perfused heart. Nicotinamide antagonizes the effect of low Ca ~ (++) but aggravates the effect of high Ca ~ (++). The results showed that nicotinamide can accelerate the conduction of atrioventricular node, atrial, Greek - Pui fiber system conduction no significant effect; nicotinamide mechanism of action is different from the beta-agonist, which may be a slow channel enhancer, by increasing the slow Inward current and play a role.