Iwanaga R, Hori S, Suzuki H, Nakajima S, Saruta T, Kojima S, Fukuda K, Satoh T, Kusuhara M, Handa S
Department of Medicine, School of Medicine, Keio University, Tokyo, Japan.
Life Sci. 1988;42(13):1279-86. doi: 10.1016/0024-3205(88)90221-4.
Cardiovascular actions of synthetic 1-28 human natriuretic peptides (hANP) were examined in dogs anesthetized with halothane. In seven closed-chest dogs a Swan-Ganz catheter was inserted for measurement of cardiac output. Intravenous infusion of increasing doses of hANP (0.1, 0.3, 0.9 microgram/kg/min) lowered mean aortic pressure without affecting heart rate significantly. Cardiac output and pulmonary wedge pressure were markedly decreased while total peripheral resistance was increased significantly. All these parameters returned to control levels after 1 hr of recovery with an 100-150ml of saline infusion to increase pulmonary capillary wedge pressure to the preinfusion value. Intracoronary infusion of hANP (0.05 and 0.1 microgram/kg/min) did not cause any significant changes in coronary flow and regional contraction. These results indicate that the hypotensive action of hANP is due to a decrease in cardiac output mediated by reduced preload but not by negative inotropic action.
在氟烷麻醉的犬中研究了合成的1-28人利钠肽(hANP)的心血管作用。在7只开胸犬中插入Swan-Ganz导管以测量心输出量。静脉输注递增剂量的hANP(0.1、0.3、0.9微克/千克/分钟)可降低平均主动脉压,而对心率无明显影响。心输出量和肺楔压显著降低,而总外周阻力显著增加。在输注100-150毫升生理盐水使肺毛细血管楔压恢复到输注前值后1小时的恢复过程中,所有这些参数均恢复到对照水平。冠状动脉内输注hANP(0.05和0.1微克/千克/分钟)对冠状动脉血流和局部收缩无任何显著影响。这些结果表明,hANP的降压作用是由于前负荷降低介导的心输出量减少,而非负性肌力作用。