ABSTRACT
INTRODUCTION: The present study was aimed to investigate the hemodynamic effects of protamine and to determine whether the increases of pulmonary arterial pressure (deltaPAP) after protamine is related to development of systemic hypotension in heparinized dogs. METHODS: Nineteen mongrel dogs were acutely instrumented during 1.5% halothane anesthesia. All dogs then received protamine 3 mg.kg (-1) over a period of 30 s given through right atrium 5 minutes after heparin (300 IU.kg (-1), iv). Animals were retrospectively assigned into two groups, control (deltaPAP<6 mmHg, n=9) and pulmonary hypertensive (PHT, deltaPAP<6 mmHg, n=10) groups. Mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP), left ventricular pressure, heart rate (HR), and cardiac output and left circumflex coronary flow (LCX flow) via Doppler flowmeter were continuously recorded throughout the experiments. Changes in MPAP were related to changes in MAP using standard regression analysis. RESULTS: MPAP (66% in PHT vs 7% in control group) and pulmonary vascular resistance index (5.1- vs 3.0-fold) increased more markedly immediately after protamine administration in PHT group than in control group. However, protamine caused similar reductions of MAP (-40 vs -46%), cardiac index (-60 vs -59%), and left ventricular end- diastolic pressure (-47 vs -53%) in both groups. No correlation was found between deltaPAP and deltaMAP in either group. LCX flow increased significantly but similarly immediately after protamine in both groups (183 vs 238%), indicating rapid release of potent vasodilator. CONCLUSIONS: These results suggest that, in heparinized dogs, protamine produces transient severe hypotension but does not consistently elevate pulmonary arterial pressure and, that acute pulmonary vasoconstriction does not play a major role in protamine-induced hypotension.
Subject(s)
Animals , Dogs , Anesthesia , Arterial Pressure , Blood Pressure , Cardiac Output , Control Groups , Flowmeters , Halothane , Heart Atria , Heart Rate , Hemodynamics , Heparin , Hypertension, Pulmonary , Hypotension , Retrospective Studies , Vascular Resistance , Vasoconstriction , Ventricular PressureABSTRACT
BACKGROUND: The mechanisms of pulmonary hypertension(PHT) are usually quite different in acquired disorders of the left side of the heart from those of congenital heart disease. Accordingly, this study was designed to compare pulmonary hemodynamics immediately after cardiopulmonary bypass(CPB) in patients with undergoing repair of atrial(ASD) or ventricular septal defect(VSD) and mitral valve replacement(MVR). METHODS: 49 patients with PHT defined as a resting systolic pulmonary arterial pressure(SPAP) greater than 35 mmHg were studied and were divided preoperatively into two groups; repair of ASD or VSD(Group I, n=18) and MVR(Group II, n=31). Measurements were made after sternotomy and prior to initiation of CPB and upon stabilization following discontinuation of CPB. RESULTS: In group I, SPAP, DPAP and MPAP decreased by 44%, 22% and 35% respectively and pulmonary vascular resistance index(PVRI) decreased by 47% after CPB. In group II, SPAP, DPAP and MPAP revealed 25%, 32% and 29% reduction respectively and PVRI decrease by 39% after CPB. SPAP decreased more significantly after CPB in group I(44% vs 25%, p<0.05). CI increased significantly in group II while decreased in group I. Intraoperative inotropes and vasodilators were used more in group II than in group I(24/31 vs 6/18). CONCLUSIONS: The successful replacement of the valve and patch repair of defect may reduce both PAP and PVRI moderately in patients with PHT.