Rosenberg A A, Kinsella J P, Abman S H
Department of Pediatrics, University of Colorado School of Medicine, Denver, USA.
Crit Care Med. 1995 Aug;23(8):1391-7. doi: 10.1097/00003246-199508000-00013.
Inhaled nitric oxide is being utilized as a selective pulmonary vasodilator in the treatment of persistent pulmonary hypertension of the newborn. However, the effects of inhaled nitric oxide on cerebral hemodynamics and distribution of left ventricular output in newborn 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.
Prospective, controlled, experimental study.
Research laboratory.
Eight fetal sheep.
Each animal was exposed to three separate study periods: a) mechanical ventilation with low FIO2 (maintaining fetal levels of PaO2); b) inhalation of nitric oxide (20 parts per million) during mechanical ventilation and low FIO2; and c) mechanical ventilation with an FIO2 of 1.0.
Left ventricular output and cerebral blood flow were measured with radiolabeled microspheres. Cerebral oxygen delivery and consumption variables were calculated using measurements of arterial and cerebral venous (sagittal sinus) oxygen content. Total left ventricular output did not differ among the three treatment 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 oxide and 1.6-fold during mechanical ventilation with an FIO2 of 1.0. With a left ventricle microsphere injection, increased lung blood flow is indicative of increased systemic-to-pulmonary shunt across the ductus 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 inhalation (p < .007); fractional extraction of oxygen decreased (p < .004 compared with hypoxic ventilation, p < .0005 compared with nitric oxide inhalation). Cerebral oxygen consumption did not differ between the three groups (1.11 +/- 0.12 microns/min/100 g with hypoxic ventilation, 0.95 +/- 0.12 microns/min/100 g with nitric oxide inhalation, and 0.96 +/- 0.08 microns/min/100 g with an FIO2 of 1.0).
Acute pulmonary vasodilation caused by inhalation of nitric oxide does not change left ventricular output, cerebral blood flow, or cerebral oxygen consumption, despite an increased systemic-to-pulmonary shunt across the ductus arteriosus.
吸入一氧化氮正被用作一种选择性肺血管扩张剂来治疗新生儿持续性肺动脉高压。然而，吸入一氧化氮对新生儿脑血流动力学及左心室输出量分布的影响尚未得到研究。本研究旨在定量测定吸入一氧化氮对围产期动物模型左心室输出量分布及脑血流动力学的影响。
前瞻性、对照、实验性研究。
研究实验室。
8只胎羊。
每只动物经历三个独立的研究阶段：a）低FiO₂机械通气（维持胎儿水平的PaO₂）；b）在低FiO₂机械通气期间吸入一氧化氮（百万分之20）；c）FiO₂为1.0的机械通气。
用放射性微球测量左心室输出量和脑血流量。通过测量动脉血和脑静脉（矢状窦）氧含量来计算脑氧输送和消耗变量。三个治疗组的总左心室输出量无差异：低氧通气时为235±16 mL/min/kg；吸入一氧化氮时为283±13 mL/min/kg；FiO₂为1.0时为242±17 mL/min/kg。吸入一氧化氮时肺血流量增加2.7倍，FiO₂为1.0的机械通气期间增加1.6倍。通过左心室微球注射，肺血流量增加表明动脉导管处体肺分流增加。三组间全脑血流量无差异：低氧通气时为49.6±6.7 mL/min/100g；吸入一氧化氮时为46.4±7.4 mL/min/100g；FiO₂为1.0时为36.4±3.8 mL/min/100g。与吸入一氧化氮相比，FiO₂为1.0时吸入期间脑氧输送增加（p<.007）；氧分数提取降低（与低氧通气相比p<.004，与吸入一氧化氮相比p<.0005）。三组间脑氧消耗无差异（低氧通气时为1.11±0.12微摩尔/min/100g，吸入一氧化氮时为0.95±0.12微摩尔/min/100g，FiO₂为1.0时为0.96±0.08微摩尔/min/100g）。
尽管动脉导管处体肺分流增加，但吸入一氧化氮引起的急性肺血管扩张并未改变左心室输出量、脑血流量或脑氧消耗。
