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首页> 外文期刊>Life sciences >Differential regulation of hepatic arterial and portal venous vascular resistance by nitric oxide and carbon monoxide in rats.
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Differential regulation of hepatic arterial and portal venous vascular resistance by nitric oxide and carbon monoxide in rats.

机译：一氧化氮和一氧化碳对大鼠肝动脉和门静脉血管阻力的差异调节。

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Nitric oxide (NO), a gaseous mediator that accounts for the biological activity of endothelium-derived relaxing factor, has been shown to play an important role in the reduction of basal vascular tone in multiple vascular beds, including the hepatic circulation. On the other hand, recent studies have provided first evidence that endogenously generated carbon monoxide (CO) may exert vasodilatory effects in the hepatic portal vein and within sinusoids. Thus, we defined the differential role of NO and CO in the regulation of vascular resistance in the two inflows to the liver in the normal rat in vivo. Male Sprague-Dawley rats were anesthetized with pentobarbital sodium and surgically instrumented in order to study the change in hepatic arterial (Rha) and portal venous vascular resistance (Rpv) in response to intravenous bolus administration of either the NO-synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) (1 mg/kg; n = 7 animals) or of tin protoporphyrin-IX (SnPP-IX) (50 micromol/kg), a specific inhibitor of the CO-generating enzyme heme oxygenase (n = 8 animals). While L-NAME caused a substantial increase in Rha, Rpv increased only slightly under these conditions. In sharp contrast, SnPP-IX did not affect Rha, but caused a profound increase in Rpv. In conclusion, Rha and Rpv are differentially regulated by NO and CO in the normal rat liver in vivo, i.e., NO serves as a potent vasodilator in the hepatic arterial circulation, but exerts only a minor vasodilatory effect in the portal venous vascular bed. In contrast, while there is no intrinsic CO-mediated vasodilation in the hepatic artery, CO acts to maintain portal venous vascular tone in a relaxed state.
机译：一氧化氮（NO）是一种气体介体，可解释内皮源性舒张因子的生物活性，已被证明在降低包括肝循环在内的多个血管床的基础血管张力方面起着重要作用。另一方面，最近的研究提供了第一个证据，即内源性生成的一氧化碳（CO）可能在肝门静脉和正弦曲线内产生血管舒张作用。因此，我们定义了正常大鼠体内两次流入肝脏的NO和CO在调节血管阻力中的不同作用。为了研究雄性Sprague-Dawley大鼠的戊巴比妥钠浓度，并对其进行手术操作，以研究其对静脉内推注NO合酶抑制剂N（omega）后肝动脉（Rha）和门静脉血管阻力（Rpv）的变化。 -硝基-L-精氨酸甲酯（L-NAME）（1 mg / kg; n = 7动物）或原卟啉-IX锡（SnPP-IX）（50 micromol / kg），一种产生CO的特异性抑制剂血红素加氧酶（n = 8只动物）。虽然L-NAME导致Rha大幅增加，但在这些条件下Rpv只是略有增加。与之形成鲜明对比的是，SnPP-IX并未影响Rha，但导致Rpv大幅增加。总之，Rha和Rpv在体内正常大鼠肝脏中受到NO和CO的差异调节，即NO在肝动脉循环中起有效的血管舒张作用，但在门静脉血管床中仅发挥较小的血管舒张作用。相反，尽管在肝动脉中没有内在的CO介导的血管舒张，但CO的作用是使门静脉血管张力保持松弛状态。

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