首页> 外文期刊>Journal of International Medical Research >Increased Heme Oxygenase-1 Gene Expression in the Livers of Patients with Portal Hypertension Due to Severe Hepatic Cirrhosis
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Increased Heme Oxygenase-1 Gene Expression in the Livers of Patients with Portal Hypertension Due to Severe Hepatic Cirrhosis

机译:严重肝硬化导致门静脉高压症患者肝脏血红素加氧酶-1基因表达增加

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Surgical bleeding associated with splanchnic hyperaemia due to portal hypertension complicates the anaesthetic management of hepatic transplantation. Although the mechanism(s) of portal hypertension are not fully understood, carbon monoxide, a product of the heme oxygenase (HO) reaction, is thought to be one of the endogenous vasodilators in the liver. In this study, the expression of mRNA encoding inducible HO isozyme (HO-1) in the livers of patients with portal hypertension undergoing hepatic transplantation was determined in comparison with those without portal hypertension. HO-1 mRNA levels were significantly greater in the portal hypertension group than in the group without portal hypertension. In contrast with HO-1, the gene expression of non-specific δ-aminolevulinate synthase (ALAS-N), which is down-regulated by heme in the liver, was the same in both groups. These results suggest that HO-1 is up-regulated through heme-independent stimuli according to the development of portal hypertension, and that induced HO-1 plays a pathophysiological role in portal hypertension through carbon monoxide production.
机译:门静脉高压引起的与内脏充血相关的手术出血使肝移植的麻醉处理变得复杂。尽管尚未完全理解门静脉高压的机制,但一氧化碳是血红素加氧酶(HO)反应的产物,被认为是肝脏中的内源性血管扩张剂之一。在这项研究中,与没有门静脉高压症的患者相比,确定了门静脉高压症患者接受肝移植的患者肝脏中编码诱导型HO同工酶(HO-1)的mRNA的表达。门脉高压组的HO-1 mRNA水平明显高于无门脉高压组。与HO-1相比,两组中非特异性δ-氨基乙酰丙酸合酶(ALAS-N)的基因表达均受肝脏血红素下调。这些结果表明,HO-1通过不依赖血红素的刺激而随门静脉高压的发展而上调,并且诱导的HO-1通过一氧化碳的产生在门静脉高压中发挥病理生理作用。

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