Nitric oxide synthase and heme oxygenase expressions in human liver cirrhosis

瞄准：门静脉高血压是肝肝硬化的普通复杂并发症。肝内压力能以几个方法被提高。从内脏的内脏影响脉管系统， vasoconstrictors 的增加和增加的循环进门静脉系统的反常建筑学都可以作出贡献。因而内长的血管扩张药也许能减轻高血压。我们因此试图调查内长的血管扩张药的层次，氮的氧化物(没有) 并且通过氮的氧化物 synthase (NOS ) 的表示的一氧化碳(公司) 并且他我氧合酶(惊讶) 。方法：肝脏硬化症(n=20 ) 并且非肝脏硬化症(n=20 ) 肝从经历了外科的病人被获得。NOS 的各种各样的 isoforms 的 mRNA 和蛋白质表情并且惊讶用竞争 PCR，西方的污点和免疫组织化学被检验。结果：当内皮 NOS (eNOS ) 在硬变肝是起来调整的时，在可诱导的 NOS (i NOS ) 或神经元 NOS (nNOS ) 表情没有重要变化。附随地， caveolin-1， eNOS 的一个确定的下面管理者，是起来调整的。可诱导的 HO-1 和组成的 HO-2 被发现在不同本地化在硬变肝虽然显示出增加的表示。结论：NOS 表示力量的差别由于他们在在肝硬化的病理维持肝动态平衡或参与的不同角色。在高血压的肝以内的纯粹的应力可以导致 eNOS 的增加的表示。接着， caveolin-1 也被增加。这是否对进一步的肝硬化用作一个防御机理或是肝硬化的后果，是还未知的。HO-1 和 HO-2 的提高的表示建议公司可以微弱地作为血管扩张药虽然在它的角色补偿。它是可能的那个公司并且不在肝以内有平行或协调的功能并且可以在门静脉高血压的病理生理学反对地工作。

AIM： Portal hypertension is a common complication of liver cirrhosis. Intrahepatic pressure can be elevated in several ways. Abnormal architecture affecting the vasculature, an increase in vasoconstrictors and increased circulation from the splanchnic viscera into the portal system may all contribute. It follows that endogenous vasodilators may be able to alleviate the hypertension. We therefore aimed to investigate the levels of endogenous vasodilators, nitric oxide （NO） and carbon monoxide （CO） through the expression of nitric oxide synthase （NOS） and heme oxygenase （HO）. METHOD： Cirrhotic （n = 20） and non-cirrhotic （n = 20） livers were obtained from patients who had undergone surgery. The mRNA and protein expressions of the various isoforms of NOS and HO were examined using competitive PCR, Western Blot and immunohistochemistry. RESULTS： There was no significant change in either inducible NOS （iNOS） or neuronal NOS （nNOS） expressions while endothelial NOS （eNOS） was up- regulated in cirrhotic livers. Concomitantly, caveolin-1, an established down-regulator of eNOS, was upregulated. Inducible HO-1 and constitutive HO-2 were found to show increased expression in cirrhotic livers albeit in different Iocalizations. CONCLUSION： The differences of NOS expression might be due to their differing roles in maintaining liver homeostasis and/or involvement in the pathology of cirrhosis. Sheer stress within the hypertensive liver may induce increased expression of eNOS. In turn, caveolin-1 is also increased. Whether this serves as a defense mechanism against further cirrhosis or is a consequence of cirrhosis, is yet unknown. The elevated expression of HO-1 and HO-2 suggest that CO may compensate in its role as a vasodilator albeit weakly. It is possible that CO and NO have parallel or coordinated functions within the liver and may work antagonistically in the pathophysiology of portal hypertension.