A COMPARATIVE-STUDY OF THE VASODILATOR EFFECTS OF PROSTAGLANDIN E-1 IN PATIENTS WITH PULMONARY-HYPERTENSION AFTER MITRAL-VALVE REPLACEMENT AND WITH ADULT-RESPIRATORY-DISTRESS-SYNDROME

To determine whether the vasodilator effects of prostaglandin E-1 (PGE (1)) differ according to the etiology and pathophysiology of pulmonary hypertension, we studied 30 patients with pulmonary hypertension afte r mitral valve replacement (MVR) (n = 16) or with the adult respirator y distress syndrome (ARDS) (n = 14). PGE(1) was administered to decrea se the mean pulmonary artery pressure to below 30 mm Hg in both groups . Cardiac index and oxygen delivery tended to increase, whereas mean s ystemic artery pressure, mean pulmonary artery pressure, systemic vasc ular resistance index (SVRI), and pulmonary vascular resistance index (PVRI) significantly decreased in both groups. A vasodilatory index wa s defined in this study to allow evaluation of vasodilation relative t o PGE(1) dose: systemic vasodilatory index (VIs) = SVRI change/PGE(1) dose; and pulmonary vasodilatory index (VIp) = PVRI change/ PGE, dose. The VIp was similar in both groups, but the VIs was significantly gre ater 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 pretrea tment intrapulmonary shunt fraction (Qs/Qt [%]) value and PGE, extract ion rate in the lung (r = 0.60), and between the pretreatment Qs/Qt va lue and PGE(1) concentration in the radial artery (r = 0.65) in an add itional 15 patients. We conclude that the vasodilator effects of PGE(1 ) 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 PGE(1) extraction in the lun g. Implications: Pulmonary hypertension after mitral valve replacement , or with adult respiratory distress syndrome, is a major medical prob lem. The authors found that administration of prostaglandin E-1 signif icantly 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 aut hors concluded that prostaglandin E-1 concentrations in the systemic c irculation depend on the severity of lung injury.