Effects of continuous intravenous infusions of nitroglycerin on canine systemic and hind limb microcirculatory hemodynamics

Abstract

Systemic and hind limb hemodynamics were assessed in anesthetized dogs during continuous 30-minute intravenous infusions of nitroglycerin at 1, 5, 10, and 25 ~g/kg/min. Nitroglycerin at I gtg/kg/min redistributed hind limb blood flow; hind limb arteriovenous shunting increased from 5.6% ± 4.0% to 17.8% ± 7.4% after 30 minutes (p < 0.01); absolute hind limb shunt flow increased from 12 ± 10 ml/min to 31 ± 26 ml/min at 10 minutes (p < 0.01); whereas hind limb nutrient blood flow decreased from 184 ± 81 ml/min to 150 ± 55 ml/min and 132 ± 32 ml/min, respectively, at 10 and 30 minutes (p < 0.05). Such hind limb blood flow redistribution was absent during infusion of all other nitroglycerin dosages. Total catecholamines increased at 30 minutes during both 1 and 10 I~g/kg/min nitroglycerin infusions (p < 0.05) with perhaps a slightly greater catecholamine response to 10 ILg/kg/min after 30 minutes (0.05 < p < 0.10). The reninanglotensin response at 3 minutes differed between nitroglycerin infusions of 1 and 10 I~g/kg/min with an initial significant reduction from baseline in plasma renin activity at the lower dose compared with a significant increase from baseline in plasma renin activity at the higher dose. Nitroglycerin did not increase femoral artery flow or cardiac output and did not lower total peripheral vascular resistance at any dose studied. Despite this, arterial pressure and cardiac work were reduced at all nitroglycerin doses tested. Massive volume loading prevented the anticipated blood pressure reduction and blunted the expected cardiac work reduction during nitroglycerin infusions of 10 Itg/kg/min. This study demonstrates that (1) nitroglycerin is not a potent peripheral arteriolar vasodilator, (2) 1 ixg/kg/min nitroglycerin infusions increase hind limb arteriovenous shunting and decrease hind limb nutrient blood flow, and (3) myocardial work and arterial pressure reductions during nitroglycerin infusions appear to be caused by mechanisms other than generalized peripheral arterial dilation.