Effect of inhaled nitric oxide during group B streptococcal sepsis in piglets.
Effect of inhaled nitric oxide during group B streptococcal sepsis in piglets.
复制标题
吸入一氧化氮对仔猪 B 族链球菌败血症的影响。
DOI：
10.1164/ajrccm/147.5.1080
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Truog,WE
中科院分区：
文献类型：
--
作者：
Berger,JI;Gibson,RL;Redding,GJ;Standaert,TA;Clarke,WR;Truog,WE
B族链球菌（GBS）是一种常见的革兰氏阳性病原体，在新生人类和动物中引起相似的病理生理变化。将GBS输注到新生动物中在早期（1小时）和晚期（2至6小时）反应中产生肺动脉高压和通气/灌注（VA/a）失配。与早期相反，晚期会导致肺血管损伤。一氧化氮（NO）是一种吸入性血管扩张剂，其对GBS脓毒症早期和晚期肺动脉高压和VA/a匹配的影响尚不清楚。我们假设吸入NO（150 ppm）将：（1）逆转GBS诱导的早期肺动脉高压;（2）由于血管损伤，在逆转GBS诱导的晚期肺动脉高压方面表现出较低的有效性;（3）改善GBS诱导的晚期VA/a失配。麻醉的机械通气仔猪（n= 10; 14±4日龄）接受240分钟GBS输注（1.5 x 109 CFU/kg/h）。仔猪在GBS输注30和210分钟时接受30分钟的NO（研究）或N2（对照）。我们发现，吸入NO选择性逆转GBS诱导的肺动脉高压的早期和晚期，并且NO在每个阶段的有效性相同。吸入NO不能逆转GBS晚期VA/a的不匹配。我们的结论是，4小时的GBS脓毒症不足以损害新生儿肺血管平滑肌，以损害其对吸入NO的反应。原发性肺动脉高压和继发性肺动脉高压是重要的原因或影响心肺疾病在所有年龄组，包括新生儿。新生儿肺动脉高压可能与严重低氧血症和通气/灌注（lA/a）不匹配有关（1-4）。静脉注射血管扩张剂治疗新生儿肺动脉高压在选择性降低肺血管阻力（PVR）而不降低全身血管阻力（SVR）方面并不总是有效的。静脉注射血管扩张剂可加重无心内分流的既存肺动脉高压患者的VA/a不匹配和低氧血症（5，6）。
Group B streptococcus (GBS), a common gram-positive pathogen, causes similar pathophysiologic changes in newborn humans and animals. Infusion of GBS into neonatal animals produces pulmonary hypertension and ventilation/perfusion (VA/a) mismatch in both early-phase «1 h) and late-phase (2 to 6 h) responses. Contrary to early phase, late phase causes pulmonary vascular injury. Nitric oxide (NO) is an inhaled vasodilator whose effect on pulmonary hypertension and VA/a matching during early and late phases of GBS sepsis is unclear. We hypothesized that inhaled NO (150ppm) would:(1) reverse early-phase GBS-induced pulmonary hypertension;(2) demonstrate less effectiveness in reversing late-phase GBS-induced pulmonary hypertension because of vascular injury;(3) improve late-phase GBS-induced VA/a mismatching. Anesthetized, mechanically ventilated piglets (n= 10; 14±4 days of age) received a 240-min infusion of GBS (1.5 x 109 CFU/kg/h). Piglets received 30 min of NO (Study) or N2 (Control) at 30 and 210 min of GBS infusion. We found that inhaled NO selectively reversed early-and late-phase GBS-induced pulmonary hypertension and that NO was equally as effective in each phase. Inhaled NO did not reverse VA/a mismatching during late-phase GBS. We conclude that 4 h of GBS sepsis does not injure neonatal pulmonary vascular smooth muscle sufficiently to impair its response to inhaled NO.Primary pulmonary hypertension and secondary pulmonary hypertension are important causes or effects of cardiopulmonary disease in all age groups, including neonates. Neonatal pulmonary hypertension can be associated with severe hypoxemia and ventilation/perfusion (lA/a) mismatching (1-4). Treatment of neonatal pulmonary hypertension with intravenously administered vasodilators is not always effective in selectively reducing pulmonary vascular resistance (PVR) without also reducing systemic vascular resistance (SVR). The use of intravenously administered vasodilators can exacerbate VA/a mismatching and hypoxemia in preexisting pulmonary hypertension without intracardiac shunts (5, 6).