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目的:研究犬败血症急性呼吸窘迫综合征时吸入一氧化氮(NO)的药效和药代动力学特点.方法:12只成年犬静脉注射内毒素导致败血症性急性呼吸窘迫综合征,表现为pao_2/F_((io)_2)基线水平(62.5±2.8)kPa下降为(26±4)kPa,kPa,动态顺应性(Cdyn)由(14.8±0.7)下降为(8.6±0.6)mL·kPa~(-1)·kg~(-1).气道死腔由(0.14±0.06)增加到(0.58±0.05),肺内分流由4.7％±1.7％增加到39％±7％,肺血管阻力指数由(16±4)增加至(51±8)kPa·s·L~(-1)·m~(-2)(P<0.05),并伴随大量白细胞肺内集聚和外周循环白细胞减少.动物随机分组给予单纯机械通气或机械通气加吸入NO 0.4-3.2μmol·L~(-1)(10-80 ppm)自疗10 h.结果:NO治疗组比时照组生存率高(4/6比0/6,P<0.05).吸入NO迅速提高血氧分压,降低肺血管阻力,以0.8μmol·L~(-1)(20 ppm)为理想浓度.吸入NO可降低细胞促炎症介质(TNF_(α),IL-8,CD11b)基因表达,且不对肺表面活性物质和肺液吸收产生不良影响.结论:吸入NO对于犬感染性急性肺损伤具有调节肺血管张力和抑制细胞炎症介质表达的双重作用,吸入高浓度NO可导致高铁血红蛋白血症.
Objective: To study the pharmacodynamic and pharmacokinetic characteristics of inhaled nitric oxide (NO) during acute respiratory distress syndrome (SARS) in canine septicemia.Methods: Twelve adult dogs received intravenous injection of endotoxin, causing sepsis-induced acute respiratory distress syndrome The baseline (62.5 ± 2.8) kPa decreased to (26 ± 4) kPa, kPa, and the dynamic compliance decreased from (14.8 ± 0.7) to (8.6 ± 0.6) mL · kPa ~ (-1) · kg -1 .The dead space of the airway increased from (0.14 ± 0.06) to (0.58 ± 0.05), the pulmonary shunt increased from 4.7% ± 1.7% to 39% ± 7%, and pulmonary vascular resistance The index increased from (16 ± 4) to (51 ± 8) kPa · s · L -1 · m -2 (P <0.05), accompanied by massive leukocyte accumulation and peripheral leukopenia. The animals were randomized to receive mechanical ventilation alone or mechanical ventilation for 10 h after inhalation of NO 0.4-3.2 μmol·L -1 (10-80 ppm) for 10 h.Results: The NO treatment group had a higher survival rate than the control group (4 / 6, 0/6, P <0.05). NO inhaled rapidly increased partial pressure of oxygen and reduced pulmonary vascular resistance, and the optimal concentration was 0.8 μmol·L -1 (20 ppm) Media (TNF alpha (α), IL-8, CD11b) gene expression, and does not adversely affect lung surfactant and pulmonary fluid absorption. CONCLUSION: Inhaled NO plays a dual role in regulating pulmonary vascular tone and inhibiting the expression of inflammatory mediators in dogs with acute infectious lung injury. High levels of NO inhaled lead to methemoglobinemia.