CEREBRAL HEMODYNAMICS AND DISTRIBUTION OF LEFT-VENTRICULAR OUTPUT DURING INHALATION OF NITRIC-OXIDE

Objectives: Inhaled nitric oxide is being utilized as a selective pulm onary vasodilator in the treatment of persistent pulmonary hypertensio n of the newborn, However, the effects of inhaled nitric oxide on cere bral hemodynamics and distribution of left ventricular output in newbo rn subjects have not been studied. This study was designed to measure quantitatively the effect of inhaled nitric oxide on the distribution of left ventricular output and on cerebral hemodynamics in a perinatal animal model. Design: Prospective, controlled, experimental study. Se tting: Research laboratory. Subjects: Eight fetal sheep. Interventions : Each animal was exposed to three separate study periods: a) mechanic al ventilation with low FIO2 (maintaining fetal levels of Pao(2)); b) inhalation of nitric oxide (20 parts per million) during mechanical ve ntilation and low FIO2; and c) mechanical ventilation with an FIO2 of 1.0. Measurements and Main Results: Left ventricular output and cerebr al blood flow were measured with radiolabeled microspheres. Cerebral o xygen delivery and consumption variables were calculated using measure ments of arterial and cerebral venous (sagittal sinus) oxygen content. Total left ventricular output did not differ among the three treatmen t groups: 235 +/- 16 mL/min/kg with hypoxic ventilation; 283 +/- 13 mL /min/kg with nitric oxide inhalation; and 242 +/- 17 mL/min/kg with an FIO2 of 1.0, Lung blood flow increased 2.7-fold with inhaled nitric o xide and 1.6-fold during mechanical ventilation with an FIO2 of 1.0. W ith a left ventricle microsphere injection, increased lung blood flow is indicative of increased systemic-to-pulmonary shunt across the duct us arteriosus. Whole brain blood flow did not differ between the three groups: 49.6 +/- 6.7 mL/min/100 g with hypoxic ventilation; 46.4 +/- 7.4 mL/min/100 g with nitric oxide inhalation; and 36.4 +/- 3.8 mL/min /100 g with an FIO2 of 1.0. Cerebral oxygen delivery increased during inhalation of an FIO2 of 1.0 when compared with nitric oxide inhalatio n (p < .007); fractional extraction of oxygen decreased (p < .004 comp ared with hypoxic ventilation, p < .0005 compared with nitric oxide in halation). Cerebral oxygen consumption did not differ between the thre e groups (1.11 +/- 0.12 mu m/min/100 g with hypoxic ventilation, 0.95 +/- 0.12 mu m/min/ 100 g with nitric oxide inhalation, and 0.96 +/- 0. 08 mu m/min/100 g with an FIO2 of 1.0). Conclusion: Acute pulmonary va sodilation caused by inhalation of nitric oxide does not change left v entricular output, cerebral blood flow, or cerebral oxygen consumption , despite an increased systemic-to-pulmonary shunt across the ductus a rteriosus.