Peripheral vascular effects of nitroglycerin in a conscious rat model of heart failure.

The effects of intravenous nitroglycerin (NG; 2, 8, 32 micrograms/kg) on cardiocirculatory dynamics were evaluated in control normal (C) and chronically volume-overloaded [high-output heart failure (aortocaval fistula), HCO] conscious rats. Pressures were recorded in the left ventricle, the caudal artery, and the right atrium. Regional blood flows were determined by radioactive microsphere injection into the left ventricle with reference sampling from the caudal artery. Cardiac output (CO) was 289 ml . min-1 . kg in C and did not change with NG; however, in HCO systemic CO was decreased 31, 23, and 23% by NG from 350 ml . min-1 . kg. In both groups left ventricular end-diastolic pressure was reduced (C, 8.4-5.0; HCO, 19.8-12.7 mmHg); however, central venous pressure was reduced only in C (1.2-0.3 mmHg). During NG primarily at 2 and 8 micrograms/kg, arterial blood flow was lower and vascular resistance was higher in HCO compared with C in the following regions: kidney, ileum, jejunum, skin, heart, spleen, stomach, and testes, whereas no major differences were noted in the cerebellum, cerebrum, liver, or skeletal muscle. Thus acute NG infusion is a more potent regional vasodilator in C than in HCO. It is suggested that this difference is related to a more powerful NG-induced sympathetic reflex activation in the HCO group, which strongly attenuates the direct vasodilator effect of NG that was apparent in C.