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目的研究超短波对慢性肺源性心脏病患者肺动脉高压的影响,并探讨其作用机制。方法将87例急性发作期慢性肺源性心脏病患者随机分为超短波治疗组45例和对照组42例。对照组给予常规治疗,超短波治疗组在常规治疗的基础上给予超短波治疗。2组患者均于治疗前、后测定血浆中血管内皮生长因子(VEGF)和内皮素-1(ET-1)含量,动脉血氧分压(PaO2)和平均肺动脉压(mPAP)水平以及肺通气功能中第1秒用力呼气量(FEV1.0)。结果与对照组比较,超短波治疗组治疗后FEV1.0%pred和PaO2水平显著升高(P<0.01),VEGF、ET-1含量和mPAP水平明显降低(P<0.01);VEGF、ET-1与PaO2呈负相关(P<0.01),与mPAP呈正相关(P<0.01)。结论超短波治疗可降低慢性肺源性心脏病患者的肺动脉高压,其作用机制可能与VEGF、ET-1的合成和释放有关。
Objective To investigate the effect of ultrashort wave on pulmonary hypertension in patients with chronic cor pulmonale and to explore its mechanism. Methods 87 cases of acute exacerbation of chronic cor pulmonale were randomly divided into 45 cases of ultrashort wave treatment group and 42 cases of control group. Control group given conventional treatment, ultrashort wave treatment group in the conventional treatment based on the treatment of ultrashort wave. The plasma levels of vascular endothelial growth factor (VEGF) and endothelin-1 (ET-1), PaO2 and mPAP were measured in both groups before and after treatment, and pulmonary ventilation Function 1 second forced expiratory volume (FEV1.0). Results Compared with the control group, FEV1.0% pred and PaO2 levels were significantly increased (P <0.01), VEGF, ET-1 levels and mPAP levels were significantly decreased (P <0.01) Negatively correlated with PaO2 (P <0.01), and positively correlated with mPAP (P <0.01). Conclusion Ultrashort wave therapy can reduce pulmonary hypertension in patients with chronic cor pulmonale. Its mechanism may be related to the synthesis and release of VEGF and ET-1.