吸入一氧化氮对吸入性损伤患者心功能的影响

目的观察吸入一氧化氮(NO)对吸入性损伤患者心功能的疗效,初步探讨其作用机制. 方法选择12例烧伤伴中度以上吸入性损伤的成年患者,随机分为2组.对照组(C组)6例,按常规治疗;治疗组(T组)6例,行常规治疗+吸入体积分数1×10-6 的NO.两组患者均留置各种导管.于治疗前及治疗后6、12、24、48和72 h观察两组患者各项心功能指标和血浆内皮素(ET)及NO含量的变化,对T组患者ET、NO的变化进行相关性分析. 结果 T组心排出量(CO)和心搏出量(SV)在24 h后显著高于治疗前,其变化早于C组 (P﹤0.05～0.01).T组左室每搏功指数(LVSWI)和右室每搏功指数(RVSWI)与C组相比均改善较早,且两组RVSWI比较差异有显著性意义(P<0.05).与C组比较,T组ET水平明显降低(P﹤0.05～0.01),而血浆NO水平明显升高(P<0.01),此两项指标呈负相关(r＝-0.98,P<0.01). 结论吸入体积分数1×10-6的NO可以改善吸入性损伤患者的心功能,其机制可能是NO对肺血管平滑肌张力具有调节作用.

The effects of NO inhalation on cardice function in the burn patients with inhalation injury

Objective To observe the effects of nitric oxide (NO) inhalation on the cardiac function of the burn patients with inhalation injury. Methods Twelve burn patients with moderate degree of inhalation injury were enrolled in the study and randomly divided into control group(C, six cases with conventional therapy) and treatment group(T, six cases with conventional therapy and NO inhalation of 10 ppm). Swan-Ganz catheters were placed in all of the patients. The changes in the indices of the cardiac function and plasma contents of endothelin (ET) and NO in the patients in both groups were measured before treatment time and 6, 12, 24, 48 and 72 hours after treatment (HAT).The changes in the plasma contents of ET and NO in the T group were analyzed correlatively. Results Both the cardiac output(CO) and stroke volume(SV) in the T group were significantly higher than the normal values at 24 HAT (P<0.05, P<0.01), and the ineredse occurred earlier than those in control group (P<0.05). The improvement in LVSWI and RVSWI in T group was observed earlier than those in C group. There was evident difference of RVSWI between T and C groups(P<0.01).The plasma content of ET decreased significantly, while the NO content increased dramatically in T group compared with those in C group(P<0.01). Conclusion The cardiac function of the patients with inhalation injury could be improved by NO inhalation of 10ppm , which might be related to the regulation of the tension of the pulmonary vascular smooth muscle by NO.