本文選題：缺氧預(yù)處理 + 心臟挫傷�。� 參考：《山西醫(yī)科大學(xué)》2006年碩士論文

【摘要】：目的：探討缺氧預(yù)處理對(duì)大鼠鈍性心臟挫傷的保護(hù)作用及其機(jī)制。 方法：建立大鼠鈍性心臟挫傷模型，健康成年wistar大鼠60只，隨機(jī)分為缺氧預(yù)處理組、單純挫傷組(每組各24只)和正常對(duì)照組(12只)，并將每組大鼠分為2h、4h、6h、12h四個(gè)時(shí)間段。挫傷前以O(shè)_2(10％)和N_2(90％)_2的混合氣體進(jìn)行全身缺氧3h，，常氧正常飼養(yǎng)24h復(fù)制缺氧預(yù)處理模型。HE染色觀察大鼠心肌組織學(xué)改變，免疫組化法檢測(cè)心肌組織中cTnT及bcl-2蛋白含量并用圖像分析儀對(duì)其進(jìn)行定量分析。 結(jié)果：免疫組織化學(xué)染色(1)心臟挫傷2h可見大鼠心肌cTnT明顯脫失，隨著時(shí)間延長(zhǎng)挫傷組cTnT脫失逐漸加重，與單純挫傷組相比缺氧預(yù)處理組cTnT的脫失顯著減輕(p＜0.05)，對(duì)照組心肌未見明顯脫失；(2)對(duì)照組有少量bcl-2表達(dá)，挫傷2h組bcl-2表達(dá)減少，隨時(shí)間延長(zhǎng)挫傷組bcl-2表達(dá)逐漸增多，與假手術(shù)組和挫傷組相比HPC組bcl-2表達(dá)明顯增強(qiáng)(p＜0.05)。 結(jié)論：bcl-2的表達(dá)說明其參與了心臟挫傷后心肌損傷的形成。缺氧預(yù)處理對(duì)大鼠鈍性心肌挫傷有保護(hù)作用，表現(xiàn)為HPC能減輕心肌細(xì)胞cTnT的脫失及促進(jìn)bcl-2的表達(dá)。缺氧預(yù)處理的心肌保護(hù)作用很可能是通過上調(diào)bcl-2的表達(dá)來實(shí)現(xiàn)的，但其具體機(jī)制有待進(jìn)一步研究。
[Abstract]:Objective: to investigate the protective effect and mechanism of anoxic preconditioning on blunt cardiac contusion in rats. Methods: a blunt cardiac contusion model was established in rats. 60 healthy adult wistar rats were randomly divided into hypoxia preconditioning group, simple contusion group (24 rats in each group) and normal control group (12 rats). Before contusion, the mixture of O _ 2 (10%) and N _ 2 (90%) was used for 3 h of systemic hypoxia. The hypoxic preconditioning model was induced by normoxic feeding for 24 h. The histological changes of myocardium were observed by HE staining. The contents of cTnT and bcl-2 protein in myocardial tissue were detected by immunohistochemical method and quantitatively analyzed by image analyzer. Results: immunohistochemical staining (1) the myocardial cTnT loss was observed at 2h after cardiac contusion in rats, and increased gradually with time prolonging in the contusion group. Compared with the simple contusion group, the loss of cTnT in hypoxia preconditioning group was significantly reduced (p < 0. 05), but no significant loss of cTnT was found in the control group. (2) there was a small amount of bcl-2 expression in the control group, while the bcl-2 expression decreased in the contusion group for 2 hours, and the bcl-2 expression in the contusion group gradually increased with the extension of time. The expression of bcl-2 in HPC group was significantly higher than that in sham operation group and contusion group (p < 0. 05). Conclusion the expression of BCL 2 suggests that it is involved in the formation of myocardial injury after cardiac contusion. Hypoxia preconditioning has protective effect on blunt myocardial contusion in rats, which shows that HPC can attenuate the loss of cTnT and promote the expression of bcl-2 in cardiac myocytes. The myocardial protective effect of hypoxia preconditioning may be achieved by upregulating the expression of bcl-2, but its mechanism needs further study.
【學(xué)位授予單位】：山西醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2006
【分類號(hào)】：D919

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