These experiments were designed to example the hypothesis that inhaled nitric oxide (NO).

These experiments were designed to example the hypothesis that inhaled nitric oxide (NO), an endothelium-derived relaxing factor, causes a decrease in pulmonary arterial press and pulmonary vascular resistance (PVR) in the normal and constricted ovine neonatal pulmonary circulation (N = 7; age = 139 [+ or -] SD 33; mass = 57 [+ or -] SD 08 kg)

Using aseptic surgery catheters were placed in the pulmonary, carotid, and femoral arteries, left atrium, and jugular vein. Additionally, the ductus arteriosus was ligated and a Doppler pour probe positioned around the pulmonary artery. Lambs were allowed a minimum of 5 days retrieval before experimentation. Mean pulmonary arterial crushing systemic arterial pressure (SAP), left atrial influence (LAP), heart rate (HR), and pulmonary arterial be molten (PAF) were monitored constantly using a Gould eight-channel physiograph. The issues of NO inhalation in the normotensive lamb were examined initially. Inhaling gas containing 80 ppm NO ([FIo.sub.2] = 060) caused a slight however significant decrease in PVR (repeated measures ANOVA; p [les than]0.05). No changes occurr in the other hemodynamic variables or vital fluid gases (pH, [PCO.sub.2], [PO.sub.2], total hemoglobin make easy [O.sub.2] saturation, or [O.sub.2] content) Lambs were then infused with the constrictor, U46619 (19 [+ or -] 7 [mu]g/min/kg), and PAP rose from 211 ([+ or -] 48) to 399 ([+ or -] 48) mm Hg) and SAP from 826 ([+ or -] 108) to 981 ([+ or -] 68) mm Hg

To proof the effects of NO inhalation forward lambs with acute pulmonary hypertension, lambs breathed gases containing NO at concentrations of 5 10 20 40 and 80 ppm ([FIO.sub.2] = 060) Lambs breathed hinder gas prior to and following each experimental gas. Significant changes in PAP and PVR occurr (repeated measures ANOVA; p [les than] 005 for each variable). Each gas containing NO, excepting 5 ppm, caused a significant decrease in PVR relative to the preceding rule period; however, NO at any concentration did not recur PVR to normotensive values. No changes occurr in any of the other hemodynamic variables or in house gases. In a third contemplation mild pulmonary hypertension (PAP = 269 [+ or -] 62 mm Hg) resulting from breathing a hypoxic gas mixture ([FIO.sub.2] = 008) was revers (PAP = 203 [+ or -] 56 mm Hg) during inhalation of the hypoxic gas with 80 ppm NO. The following day, lambs were again made hypertensive by way of infusion of U46619 (2.0 [+ or -] 04 [mu]g/min/kg). They then breathed 80 ppm NO for a period of 3 h kindred was sampled every half hour for relations gas analysis. The PAP and PVR replyed to normotensive values throughout the 3-h period. No changes occurr in any of the other hemodynamic variables or in vital fluid gases during the period of infusion of U46619 Following 30 min of NO inhalation, mean methemoglobin (Co-oximeter, Instrumentation Laboratories, Lexington, Mass) increased significantly to 36 percent ([+ or -] 11) from a hinder mean of 1.5 percent ([+ or -] 09) Methemoglobin peaked at 47 percent ([+ or -] 17) in the third hour.

In conclusion, NO inhalation subverts acute pulmonary hypertension in the newborn lamb without causing systemic hypotension. These data are similar to those reported in older lambs. However, unlike the older lambs, methemoglobin evens increase significantly in neonates.

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