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目的探讨高原肺水肿(high altitude pulmonary edema,HAPE)患者肺血管活性因子变化及其与肺动脉高压(pulmonary artery hypertension,PAH)的关系。方法采用放射免疫分析方法检测22例HAPE患者治疗前及治愈后血浆中介素(inter medin,IMD)、肾上腺髓质素(adrenomedulin,ADM)、内皮素-1(endo-thelin-1,ET-1)含量及动脉血氧分压(PaO2),用彩色多普勒超声心动仪测定肺动脉血流频谱,计算平均肺动脉压(mPAP),并与30例当地健康人比较。结果治疗前,HAPE患者血浆IMD、ADM、ET-1及mPAP[分别为(174.23±17.44)pg/mL、(77.45±6.87)pg/mL、(93.6±10.2)ng/L、(46.51±7.20)mmHg]较对照组[分别为(62.76±10.60)pg/mL、(22.04±3.15)pg/mL、(35.52±4.52)ng/L、(20.14±3.34)mm Hg]显著升高,PaO2[(33.82±5.66)mm Hg]较对照组[(69.27±3.35)mm Hg]显著降低(均P<0.01)。HAPE患者血浆IMD、ADM、ET-1水平与mPAP均呈显著正相关(分别r=0.752、0.733、0.812,均P<0.01),PaO2与IMD、ADM、ET-1、mPAP呈显著负相关(分别r=-0.689、-0.710、-0.741、-0.744,均P<0.01)。HAPE组治愈后血浆IMD、ADM、ET-1及mPAP[分别为(65.33±9.88)pg/mL、(23.56±3.53)pg/mL、(36.73±3.90)ng/L、(21.22±3.63)mm Hg]较治疗前显著降低,PaO2[(69.01±3.62)mm Hg]显著升高(均P<0.01),并与对照组比较差异无显著性(均P>0.05)。结论 IMD、ADM、ET-1参与了HAPE患者PAH形成的病理生理过程,其比例失衡可能是导致低氧性肺动脉高压发生发展的重要因素之一。
Objective To investigate the changes of pulmonary vasoactive factors and its relationship with pulmonary artery hypertension (PAH) in patients with high altitude pulmonary edema (HAPE). Methods Radioimmunoassay was used to detect the plasma levels of inter-medulin (IMD), adrenomedulin (ADM), endo-the-1 (ET- 1) and arterial oxygen tension (PaO2). Pulmonary arterial blood flow spectrum was measured by color Doppler echocardiography, mean pulmonary arterial pressure (mPAP) was calculated and compared with 30 healthy local people. Results Before treatment, the plasma levels of IMD, ADM, ET-1 and mPAP in HAPE patients were (174.23 ± 17.44) pg / mL, 77.45 ± 6.87 pg / mL, 93.6 ± 10.2 and 46.51 ± 7.20 ) mmHg] was significantly higher than that of the control group [(62.76 ± 10.60) pg / mL, (22.04 ± 3.15) pg / mL, (35.52 ± 4.52) ng / L, (33.82 ± 5.66) mm Hg] compared with the control group [(69.27 ± 3.35) mm Hg] (all P <0.01). The plasma levels of IMD, ADM and ET-1 in patients with HAPE were significantly and positively correlated with mPAP (r = 0.752,0.733,0.812, P <0.01, respectively). PaO2 was negatively correlated with IMD, ADM, ET- Respectively r = -0.689, -0.710, -0.741, -0.744, all P <0.01). The plasma levels of IMD, ADM, ET-1 and mPAP after treatment in HAPE group were (65.33 ± 9.88) pg / mL, (23.56 ± 3.53) pg / mL and (36.73 ± 3.90) ng / L and (21.22 ± 3.63) mm Hg] was significantly lower than that before treatment. PaO2 [(69.01 ± 3.62) mm Hg] were significantly increased (all P <0.01), and there was no significant difference with the control group (all P> 0.05). Conclusion IMD, ADM and ET-1 are involved in the pathophysiological process of PAH formation in patients with HAPE. The imbalanced ratio may be one of the important factors leading to the development of hypoxic pulmonary hypertension.