実験的虚血心におけるnicardipine hydrochlorideの血行動態および局所心筋動態に及ぼす影響

Effects of nicardipine hydrochloride on hemodynamics and regional myocardial function in experimental coronary artery occlusion

　急性心筋梗塞における左心不全に対して血管拡張剤療法が行われるが，本法は梗塞心に対する減負荷療法であると共に梗塞部の拡大を防ぐ可能性も期待される。

　Ca拮抗剤は冠血管拡張作用および末梢血管拡張作用を有するため，抗狭心剤および降圧剤として広く用いられているが，最近，血管拡張作用を期待してCa拮抗剤を減負荷療法に用いた報告が散見される^1,2）。

The effects of intravenous nicardipine hydro-chloride (Nic) on left ventricular hemodynamics and regional myocardial function were evaluated in acute myocardial ischemia produced by occlusion of the left anterior descending coronary artery of dog.

Nic decreased mean aortic pressure from 93±4 to 73±3 mmHg, increased cardiac output from 3.22±0.26 to 3.81±0.20 L/m, and increased dP/dt/ CDP from 12.04±1.13 to 16.74±1.51 mmHg/sec per mmHg. Left ventricular end-diastolic pressure was unchanged and T was lengthened.

In the ischemic segment, shortening of the last thirds of systole increased and the grade of the holosystolic bulge was reduced. Shortening of the marginal and the control segments increased significantly.