摘要
目的 :对风湿性心脏病 (风心病 )二尖瓣狭窄合并肺动脉高压患者 ,观察术前和术后吸入 40 ppm一氧化氮 (NO)其血液动力学效应 ,以及体外循环对其效应的影响。 方法 :选择 15例风心病合并肺动脉高压行择期瓣膜置换术的患者 ,在体外循环前、后吸入 40 ppm NO气体。 结果 :术前肺血管阻力 (PVR)为 2 0~ 135 k Pa·s/ L,肺动脉压为 2 8/ 17~ 87/ 45 mm Hg(1mm Hg=0 .133k Pa)。吸入 40 ppm NO后肺动脉收缩压、肺动脉舒张压、肺动脉平均压及 PVR在体外循环前、后均明显降低 (P均 <0 .0 0 1)。在体外循环前、后肺血管阻力差值 (△ PVR) / PVR分别为 (5 3.2± 18.5 ) % (P<0 .0 0 1)和 (2 2 .7± 2 2 .2 ) % (P<0 .0 1) ,体外循环前、后两者差异极显著 (P<0 .0 0 1)。吸入 NO治疗前、后肺毛细血管楔压均无明显改变 (P>0 .0 5 ) ,而心排血量均明显增加 (P<0 .0 1)。 结论 :风心病合并肺动脉高压患者吸入 40 ppm NO,可选择性地扩张肺动脉 ,体外循环可明显减弱其效应。
Objective:To investigate the pulmonary vasodilatation resulting from 40 ppm inhaled NO and how it is affected by cardiopulmonary bypass(CPB). Method:We chose 15 cases of valvular heart disease mitral stenosis with pulmonary hypertension undergoing mitral valvular replacement.These patients were ventilated with 40 ppm NO for 10 min before and after CPB,respectively. Results:Before CPB the baseline of pulmonary vascular resistance (PVR) were 20~135 kPa·s/L,and pulmonary pressure were 28/17~87/45 mmHg(1mmHg=0.133 kPa).Before and after CPB,pulmonary artery systole pressure(PAPS),pulmonary artery diastole pressure(PAPD),pulmonary artery mean pressure(PAPM),and PVR decreased significantly on inhaling NO(all p <0.01).Before and after CPB the PVR decreased by(53.0±18.5)%and(22.7±22.2)%respectively( p <0.01).PCWP did not change on inhaling NO( p >0.05),but NO increased significantly( p <0.01). Conclusion:This study demonstrates that 40 ppm nitric oxide is a selective pulmonary vasodilator in valvular heart disease and it's effect is attenuated by CPB.Furthermore,inhalation of 40 ppm NO can improve cardiac function in patients with valvular heart disease with pulmonary hypertension before CPB.
出处
《中国循环杂志》
CSCD
北大核心
1999年第6期365-367,共3页
Chinese Circulation Journal
关键词
风湿性心脏病
肺动脉高压
一氧化氮
体外循环
Valvular heart disease
Pulmonary hypertension
Nitric oxide
Cardiopulmonary Bypass