Abstract
To determine whether the vasodilator effects of prostaglandin E1 (PGE1) differ according to the etiology and pathophysiology of pulmonary hypertension, we studied 30 patients with pulmonary hypertension after mitral valve replacement (MVR) (n = 16) or with the adult respiratory distress syndrome (ARDS) (n = 14). PGE1 was administered to decrease the mean pulmonary artery pressure to below 30 mm Hg in both groups. Cardiac index and oxygen delivery tended to increase, whereas mean systemic artery pressure, mean pulmonary artery pressure, systemic vascular resistance index (SVRI), and pulmonary vascular resistance index (PVRI) significantly decreased in both groups. A vasodilatory index was defined in this study to allow evaluation of vasodilation relative to PGE1 dose: systemic vasodilatory index (VIs) = SVRI change/PGE1 dose; and pulmonary vasodilatory index (VIp) = PVRI change/PGE1 dose. The VIp was similar in both groups, but the VIs was significantly greater in the ARDS group compared with the MVR group (13.3 +/- 7.8 vs 4.8 +/- 5.1, P < 0.01). A good correlation was found between the pretreatment intrapulmonary shunt fraction (Qs/Qt [%]) value and PGE1 extraction rate in the lung (r = 0.60), and between the pretreatment Qs/Qt value and PGE1 concentration in the radial artery (r = 0.65) in an additional 15 patients. We conclude that the vasodilator effects of PGE1 on the pulmonary circulation are similar in the two groups, whereas the vasodilator effects on the systemic circulation are significantly greater in the ARDS group and that significant reduction in VIs in the ARDS group was associated with decreased PGE1 extraction in the lung. Pulmonary hypertension after mitral valve replacement, or with adult respiratory distress syndrome, is a major medical problem. The authors found that administration of prostaglandin E1 significantly dilated the pulmonary circulation with a concomitant decrease in pulmonary artery pressure. Because the systemic vasodilatory effect was greater in the adult respiratory distress syndrome group, the authors concluded that prostaglandin E1 concentrations in the systemic circulation depend on the severity of lung injury.
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