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心脏病患者一氧化氮基础生成量减少。

Decreased basal production of nitric oxide in patients with heart disease.

作者信息

Sumino H, Sato K, Sakamaki T, Masuda H, Nakamura T, Kanda T, Nagai R

机构信息

Second Department of Internal Medicine, Gunma University School of Medicine, Maebashi, Japan.

出版信息

Chest. 1998 Feb;113(2):317-22. doi: 10.1378/chest.113.2.317.

DOI:10.1378/chest.113.2.317
PMID:9498945
Abstract

STUDY OBJECTIVES

The pathophysiologic role of nitric oxide (NO) released in the lung is not well understood. To determine whether the production of endogenous NO is correlated with any hemodynamic parameters, we measured the amount of NO released from the lung tissue of patients with heart disease.

METHODS

Twenty patients (14 with ischemic heart disease, 4 with dilated cardiomyopathy, and 2 with mitral stenosis) and 16 normal control subjects were enrolled in the study. We measured exhaled air samples by using a method developed in our laboratory. The NO release rate from the lungs was calculated from the amount of exhaled NO and the duration of the exhalation.

RESULTS

The rate of NO release was significantly lower in the patients with moderate-to-severe heart failure (New York Heart Association [NYHA] II or III) than in those with mild heart failure (NYHA I) or in normal control subjects. The rate of NO release was positively correlated with the cardiac index (r=0.50, p<0.05), and was negatively correlated with either the systemic (r= -0.58, p<0.01) or pulmonary vascular resistance (r=-0.45, p<0.05). In the patients with moderate-to-severe heart failure, the amount of NO released and the oxygen tension in the pulmonary artery were significantly lower compared with those parameters in patients with mild heart failure.

CONCLUSIONS

Results suggest that the basal production of endogenous NO in the lung tissue of patients with heart failure is impaired, perhaps leading to the elevated pulmonary vascular tone seen in patients with moderate-to-severe heart failure.

摘要

研究目的

肺中释放的一氧化氮(NO)的病理生理作用尚未完全明确。为了确定内源性NO的产生是否与任何血流动力学参数相关,我们测量了心脏病患者肺组织中释放的NO量。

方法

本研究纳入了20例患者(14例缺血性心脏病患者、4例扩张型心肌病患者和2例二尖瓣狭窄患者)以及16名正常对照者。我们使用本实验室开发的方法测量呼出的空气样本。根据呼出的NO量和呼气持续时间计算肺的NO释放率。

结果

中重度心力衰竭患者(纽约心脏协会[NYHA] II级或III级)的NO释放率显著低于轻度心力衰竭患者(NYHA I级)或正常对照者。NO释放率与心脏指数呈正相关(r = 0.50,p < 0.05),与全身血管阻力(r = -0.58,p < 0.01)或肺血管阻力(r = -0.45,p < 0.05)呈负相关。在中重度心力衰竭患者中,与轻度心力衰竭患者相比,释放的NO量和肺动脉中的氧分压显著降低。

结论

结果表明,心力衰竭患者肺组织中内源性NO的基础产生受损,这可能导致中重度心力衰竭患者肺血管张力升高。

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