COPD患者伴肺性缺氧与肝功能损害的相关性研究

目的探讨慢阻肺患者伴肺性缺氧与肝功能损害的相关性研究。方法测定患者周围白细胞计数、肝功能及动脉血气分析,各参数值的组间采用t检验,动脉血气值与肝功能检测结果间作相关性直线回归分析。结果COPD患者治疗后周围血白细胞、中性粒细胞计数和肝功能各参数值均有明显改善(P<0.01);患者治疗后PaO2比治疗前明显升高,PaCO2比治疗前明显下降(P<0.01);pH值、PaO2与ALT、AST结果显著负相关;PaCO2与ALT、AST结果显著正相关(P均<0.01)。结论COPD患者肺性缺氧或伴有二氧化碳潴留时合并酸中毒对肝脏功能损害明显加重;COPD患者给予抗感染、保肝、支持疗法等治疗后肺性缺氧控制,肝功能可恢复正常。

老年慢性阻塞性肺疾病患者伴肺性缺氧与肝功能损害的相关性研究

目的探讨老年慢性阻塞性肺疾病(COPD)患者伴肺性缺氧、二氧化碳潴留与肝功能损害的相关性研究。方法测定患者治疗前后外周白细胞计数、肝功能及动脉血气分析,各参数值的组间采用t检验,动脉血气值与肝功能检测结果间作相关性直线回归分析。结果老年COPD患者治疗后动脉血氧分压(PaO2)、外周血白细胞、中性粒细胞计数和肝功能各参数值均有明显改善(P<0.01);患者治疗后PaO2比治疗前明显升高,动脉血二氧化碳分压(PaCO2)比治疗前明显下降(P<0.01);pH值、PaO2与谷氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)结果呈显著负相关;PaCO2与ALT、AST结果呈显著正相关(P均<0.01)。结论老年COPD患者伴肺性缺氧或伴有二氧化碳潴留时合并酸中毒对肝脏功能损害明显加重;给予抗感染、保肝、支持疗法等治疗后肺性缺氧控制,肝功能可恢复正常。

RELAXANT EFFECTS OF VASOACTIVE INTESTINAL PEPTIDE ON PULMONARY ARTERY IN CHRONICALLY HYPOXIC RATS

The object of this study is to investigate the effect of VIP on pulmonary artery of chronically hypoxic rats. It was shown that chronic hypoxia depressed significantly pulmonary artery relaxation induced by VIP as compared with those of control (P<0. 001). The vascular relaxation of both groups was correlated with concentration of VIP. In addition, the relaxant effect of VIP on pulmonary arteries in rats was endothelium─independent, and was not prevented by indomethacin or nordihydroguaiaretic acid, but was abolished completely by methylene blue. These results suggest that the lower relaxation of pulmonary artery in rats might not be due to the endothelial injury caused by chronic hypoxia, and chronic hypoxia may inhibit directly the soluble guanylate cyclase in vascular smooth muscle cells invloved in synthesis of cGMP and thus reduced the sensitivity and reactivity of pulmonary artery to VIP.

Hypoxia-inducible factor 1 alpha upregulates the expression of inducible nitric oxide synthase gene in pulmonary arteries of hypoxic rat

Objective To investigate the expression of hypoxia inducible factor 1 alpha (HIF 1α) and inducible nitric oxide synthase (iNOS) genes in rats’ pulmonary arteries in different phases of hypoxia induced pulmonary hypertension development Methods Models of chronic hypoxic pulmonary hypertension rat were duplicated by intermittent hypoxia Mean pulmonary arterial pressure (mPAP) was measured by right heart catheterization HIF 1α and iNOS messenger ribonucleic acid (mRNA) were detected by in situ hybridization HIF 1α and iNOS protein were measured by immunohistochemical analysis Results Expression of HIF 1α protein was upregulated in pulmonary arterial tunica intimae of all hypoxic rats In pulmonary arterial tunica media, the level of HIF 1α protein was markedly upregulated at days 3 and 7 of hypoxia ( P 【0 01), then tended to restore at 14 days and 21 days HIF 1α mRNA levels in pulmonary arteries of rats began to increase significantly at day 14 of hypoxia ( P 【0 01) Expression of iNOS mRNA and protein in pulmonary arteries of rats were upregulated by hypoxia for 3 days ( P 【0 01), then reached its peak and maitained the same level while the extension of hypoxia Linear correlation analysis showed that iNOS protein was associated with both mean pulmonary arterial pressure ( r =0 74, P 【0 01) and hypoxic pulmonary vascular remodeling ( r =0 78, P 【0 01), whereas the inverse was associated with HIF 1α protein ( r =-0 52, P 【0 01) Conclusions HIF 1α and iNOS are both involved in the pathogenesis of hypoxia induced pulmonary hypertension in rat HIF 1α protein may upregulate the expression of iNOS gene by transcriptional activation; in addition, iNOS protein may inhibit the expression of HIF 1α protein

Protection of carbon monoxide-releasing molecule against lung injury induced by limb ischemia-reperfusion

Objective： To observe the role and mechanism of CO- releasing molecule （CORM）-2 in lung injury induced by ischemia-reperfusion （IR） of hind limbs in rats. Methods： Arat model of lung injury induced by IR of hind limbs was established. A total of 40 Sprague Dawley （SD） rats were randomly divided into 5 groups （n = 8）： sham, sham ＋ CORM-2, IR, IR ＋ CORM-2 and IR ＋ dimethyl sulfoxide （DMSO）. Rats in the IR group received hind limb ischemia for 2 hours and reperfusion for 2 hours, rats in the sham group underwent sham surgery without infrarenal aorta occlusion, rats in the IR＋CORM-2 group and in the sham ＋ CORM-2 group were given CORM-2 （10 μmol/kg intravenous bolus） 5 minutes before reperfusion or at the corresponding time points, while rats in the IR ＋ DMSO group was treated with the same dose of vehicle （DMSO） at the same time. The lung tissue structure, polymorphonuclear neutrophil （PMN） count, wet-to-dry weight ratio （W/D）, malondialdehyde （MDA） content, myeloperoxidase （MPO） activity, intercellular adhesion molecule- 1 （ICAM- 1）expression, I κBα degradation and nuclear factor （NF）-κB activity in the lungs were assessed. Results： As compared with the sham group, lung PMNs number, W/D, MDA content, MPO activity, ICAM-1 expression and NF- κB activity significantly increased in the IR group, but the level of I κBα decresed （P〈0.01）. Compared with the IR group, lung PMNs number, W/D, MDA content, MPO activity and ICAM- 1 expression significantly decreased in the IR＋COMR-2 group （P〈0.01）, while the level of IκBα increased. Conclusions： These data demonstrate that CORM-2 attenuates limb IR-induced lung injury through inhibiting ICAM-1 protein expression, NF-κB pathway and the leu- kocytes sequestration in the lungs following limb IR in rats, suggesting that CORM-2 may be used as a therapeutic agent against lung injury induced by limb IR.