Pulmonary hypertension has been recognized in critically ill patients with respiratory failure and results from an increase in vascular resistance caused by persistent hypoxia. ATP, in modulating vascular tone in blood vessels, acts mainly at the site of application due to its rapid degradation and therefore might be superior to other vasodilators in controlling pulmonary vascular resistance. The purpose of this study was to investigate the effects of administration of ATP into the pulmonary artery on hemodynamic changes occurring in anesthetized adult dogs subjected to hypoxic pulmonary hypertension. Eight dogs (11.4 ± 1.2 kg) were anesthetized with pentobarbital, intubated, and mechanically ventilated to ensure PaCO2 values in the range of 35-45 mm Hg. Heart rate (HR), systemic (ABP) and pulmonary arterial blood pressure (PAP), central venous pressure (CVP), pulmonary occlusion pressure (POP), cardiac index (CI), stroke volume index (SVI), and systemic (SVRI) and pulmonary vascular resistance index (PVRI) as well as arterial pH and blood gas tension were determined after insertion of arterial, venous, and balloon-tipped pulmonary arterial catheters. The animals were ventilated first under normoxic conditions (21% O2/79% N2) to obtain baseline values and then with hypoxic gases (10% O2/90% N2). Data were analyzed by analysis of variance (ANOVA), followed by posthoc comparisons using a parametric T-test (P < 0.05). Hypoxia caused an increase in mean PAP, CVP, CI, and PVRI by 71%, 102%, 38%, and 56%, respectively from baseline values (P < 0.01). SVRI slightly decreased by 21%. ATP (0.02-1.65 mg/kg/min), when infused under these conditions into the pulmonary artery, concomitantly reduced both ABP (P < 0.01) and PAP (P < 0.05) in a dose-dependent manner. However, maximum decrease in mean ABP was more marked than the maximum decrease in mean PAP - i.e., 52% versus 20% (P < 0.01). SVRI and PVRI also decreased (P < 0.05), whereas POP increased during infusion of ATP (P < 0.05). HR, CVP, CI and SVI were not dose-dependently affected by ATP. These results indicate that pulmonary arterial administration of ATP during hypoxic pulmonary hypertension causes not only significant dilation in the pulmonary vasculature, but is even more effective in the systemic vascular bed. Due to the marked fall in ABP, ATP cannot be recommended for treatment of pulmonary hypertension in adult dogs.
©1998, The American College of Veterinary Anesthesiologists, all rights reserved.
This page is hosted for the American College of Veterinary Anesthesiologists by the Informatics Program of the Virginia-Maryland Regional College of Veterinary Medicine.
. Direct your questions or comments about the web page to our site host.