本文選題：缺氧　切入點(diǎn)：高碳酸血癥　出處：《中國病理生理雜志》2017年08期

【摘要】：目的:通過研究缺氧和/或高碳酸血癥時(shí)賴氨酰氧化酶(LOX)以及細(xì)胞外基質(zhì)膠原蛋白的交聯(lián)變化,探討高碳酸血癥對(duì)缺氧性肺動(dòng)脈高壓的影響機(jī)制。方法:SD大鼠隨機(jī)均分為4組,分別為常氧對(duì)照組、缺氧組、高碳酸血癥組以及缺氧+高碳酸血癥組。比色法測(cè)定膠原蛋白含量,熒光光譜法分析LOX酶活性,免疫組織化學(xué)和Western blot法檢測(cè)肺動(dòng)脈LOX蛋白含量,實(shí)時(shí)熒光定量PCR檢測(cè)肺動(dòng)脈LOX的mRNA水平。結(jié)果:缺氧組大鼠平均肺動(dòng)脈壓(m PAP)、右心室/(左心室+室間隔)重量比值[RV/(LV+S)]及血管壁面積(WA)/血管總面積(TA)均明顯高于常氧對(duì)照組;高碳酸血癥組與常氧對(duì)照組的m PAP、RV/(LV+S)差異無統(tǒng)計(jì)學(xué)顯著性;缺氧+高碳酸血癥組大鼠的m PAP及RV/(LV+S)顯著低于單純?nèi)毖踅M。缺氧組大鼠肺組織的膠原交聯(lián)程度則明顯高于常氧組及高碳酸血癥組;高碳酸血癥組大鼠肺組織的膠原交聯(lián)程度與常氧組比較無顯著差異;缺氧+高碳酸血癥組大鼠肺組織的膠原交聯(lián)程度顯著低于缺氧組。缺氧組大鼠肺動(dòng)脈LOX的mRNA、蛋白表達(dá)量及其酶活性均高于常氧組(P0.01);缺氧+高碳酸血癥組大鼠肺動(dòng)脈LOX mRNA、蛋白表達(dá)以及酶活性均明顯低于缺氧組(P0.01)。結(jié)論:缺氧能誘導(dǎo)肺動(dòng)脈LOX高表達(dá),通過促進(jìn)膠原合成及交聯(lián),參與肺動(dòng)脈高壓的形成。高碳酸血癥通過抑制缺氧誘導(dǎo)的LOX表達(dá)和膠原交聯(lián),延緩缺氧性肺動(dòng)脈高壓的進(jìn)展。
[Abstract]:Objective: to investigate the effects of hypercapnia on hypoxic pulmonary hypertension by studying the changes of lysyl oxidase LOX) and collagen in extracellular matrix during hypoxia and / or hypercapnia. Methods: the rats were randomly divided into 4 groups. The content of collagen was measured by colorimetric method, the activity of LOX enzyme was analyzed by fluorescence spectrometry, the content of LOX protein in pulmonary artery was detected by immunohistochemistry and Western blot. Results: the mean pulmonary artery pressure (MPP), the ratio of right ventricular / left ventricular septal weight [RV/(LV S] and the wall area of pulmonary artery in hypoxic group were significantly higher than those in normoxic control group. There was no significant difference between hypercapnia group and normoxic control group. The m PAP and RV/(LV S of hypoxic hypercapnia group were significantly lower than those of pure hypoxia group, while the degree of collagen cross-linking in hypoxic group was significantly higher than that in normoxic group and hypercapnia group. There was no significant difference in the degree of collagen cross-linking between hypercapnia group and normoxic group. The degree of collagen crosslinking in hypoxic hypercapnia group was significantly lower than that in hypoxia group, and the expression of LOX, protein expression and enzyme activity of pulmonary artery in hypoxia group were higher than those in normoxic hypercapnia group, and pulmonary motility in hypoxic hypercapnia group was higher than that in hypoxia hypercapnia group. The expression of LOX mRNAs, protein and enzyme activity were significantly lower than those in hypoxia group (P 0.01). Conclusion: hypoxia can induce high expression of LOX in pulmonary artery. Hypercapnia delays the development of hypoxic pulmonary hypertension by inhibiting hypoxia-induced LOX expression and collagen crosslinking.
【作者單位】： 溫州醫(yī)科大學(xué)附屬第二醫(yī)院育英兒童醫(yī)院呼吸內(nèi)科;山東大學(xué)齊魯醫(yī)院呼吸內(nèi)科;
【基金】：浙江省自然科學(xué)基金資助項(xiàng)目(No.LY12H01002) 溫州市科技計(jì)劃資助項(xiàng)目(No.2017Y0182)
【分類號(hào)】：R544.1

【參考文獻(xiàn)】

相關(guān)期刊論文 前1條

1 夏曉東;楊雷;徐正坸;戴元榮;吳淑珍;張洪勤;;肺動(dòng)脈高壓大鼠一氧化氮及過氧化氫依賴的可溶性鳥苷酸環(huán)化酶通路的變化[J];中國病理生理雜志;2006年04期

【共引文獻(xiàn)】

相關(guān)期刊論文 前6條

1 江穎娟;蔣作鋒;吳小蘭;黃s，

本文編號(hào)：1670502