Hemodynamic effects of exogenous nitric oxide in ovine transitional pulmonary circulation
Kinsella, J.P.; McQueston, J.A.; Rosenberg, A.A.; Abman, S.H.
American Journal of Physiology 263(3 Pt 2): H875-H880
1992
ISSN/ISBN: 0002-9513 PMID: 1415614 Document Number: 401634
To determine the hemodynamic effects of exogenous nitric oxide (NO) on the immature pulmonary circulation, we studied the response to NO inhalation in 19 mechanically ventilated late-gestation ovine fetuses in three separate protocols. In protocol 1, we examined the relative effects of 1) mechanical ventilation while maintaining fetal arterial O2 tension (Pao2) constant [fractional inspired O2 concentration (FIO2) < 0.10)], 2) NO inhalation [5-20 parts per million (ppm)] at fetal PaO2, and 3) high FIO2 (1.0) (n = 7). NO increased left pulmonary artery blood flow (.ovrhdot.Qlpa) in a dose-dependent fashion, from 254 .+-. 62 (baseline) to 398 .+-. 49 ml/min with 20 ppm NO (P < 0.001). The response of .ovrhdot.Qlpa to a FIO2 equal to 1.00 was not different from NO alone. Systemic arterial pressure was not affected by NO. In protocol 2 we studied the effects of prolonged NO inhalation (2 h, 20 ppm) during mechanical ventilation with low FIO2 (n = 4). NO increased .ovrhdot.Qlpa from 267 .+-. 92 to 468 .+-. 75 ml/min at 10 min of NO inhalation (P < 0.001). The increase in .ovrhdot.Qlpa was sustained during the entire 2-h study period. In protocol 3 we measured left ventricular output (LVO), systemic vascular resistance (SVR), and ductus arteriosus shunting using radiolabeled microspheres (n = 8) during baseline mechanical ventilation and 20 ppm NO inhalation. LVO and SVR were not significantly different in the two study periods; however, the percentage of LVO that reached the lungs (predominantly left-to-right shunting across the ductus arteriosus) increased from 18 .+-. 5 to 43 .+-. 4% during NO inhalation. We conclude that exogenous NO causes potent, sustained, and selective pulmonary vasodilation in the immature lamb.