Acute effects of nicardipine on the vascular reactivity of oxygen in patients with respiratory insufficiency and pulmonary hypertension

Pulmonary vascular response to the inhalation of various concentrations of oxygen (FIO2) was studied under basal conditions and after nicardipine in 10 patients with pulmonary hypertension secondary to chronic bronchitis. Hemodynamic data and blood gases were measured during inhalation of 3 gas mixtures: hypoxia (FIO2 = 0.15), normoxia (FIO2 = 0.21) and hyperoxia (FIO2 = 0.30). Each gas mixture was administered for 20 minutes, initially during an infusion of placebo and then of nicardipine giving a steady plasma concentration of 29 +/- 4 ng/ml. This was obtained by continuous I.V. infusion of 0.06 mg/kg/hour. Under basal conditions with placebo, the heart rate, cardiac output and pulmonary hypertension increased with decreasing concentrations of inhaled oxygen. The systemic blood pressure was unchanged with hypoxia but decreased during hyperoxia. Nicardipine increased the heart rate and the cardiac output but reduced the blood pressure with every inhaled oxygen mixture. The blood pressure was independent of FIO2 and the reduction observed during hyperoxia with placebo no longer occurred with nicardipine. However, the pulmonary hypertension was unaffected. At the dosage used in this study, nicardipine modified the systemic vascular response to oxygen but not the pulmonary vascular response. The vasodilation induced was much greater in the systemic than in the pulmonary circulation. In relation to the absence of significant pulmonary vasodilation, no changes in blood gases, due to a possible pulmonary shunting effect, were observed. At this dosage, nicardipine is ineffective in reducing pulmonary hypertension. However, its systemic hypotensive action may be used in patients with respiratory failure due to chronic bronchitis without deleterious effects on blood gases.