Lemberg A, Rubio M, Bengochea L, Romay S, Eizayaga F, Diez A, Perazzo J C
Catedra de Fisiopatologia, Facultad de Farmacia y Bioquimica, Universidad de Buenos Aires, Argentina.
Hepatogastroenterology. 1998 Mar-Apr;45(20):547-50.
BACKGROUND/AIMS: Portal hypertension in patients and rat models are characterized by splanchnic and systemic hemodynamic alterations. Both the central and autonomic nervous systems are implicated in its pathophysiology. The aim of our research was to study the tyrosine hydroxylase activity and the rate limiting step in the biosynthesis of catecholamines in partial ligated portal hypertensive and in control rat brains.
The following seven discrete brain regions were investigated: Subfornical Organ, Organum Vasculosum Lamina Terminalis, Median Eminence, Periventricular Nucleus, Area Postrema, Locus Coeruleus and Nucleus Tractus Solitarius.
The enzyme activity showed a significant increment in six nuclei and a decrease in Area Postrema Nucleus when portal hypertensive rats were compared to controls.
These results suggest the participation of some discrete brain regions in the mechanism of hepatic portal hypertension under the present rat model.
背景/目的：患者和大鼠模型中的门静脉高压症表现为内脏和全身血流动力学改变。中枢神经系统和自主神经系统均参与其病理生理过程。我们研究的目的是研究部分结扎门静脉高压大鼠和对照大鼠脑内酪氨酸羟化酶活性以及儿茶酚胺生物合成中的限速步骤。
研究了以下七个离散的脑区：穹窿下器官、终板血管器、正中隆起、室周核、最后区、蓝斑和孤束核。
与对照组相比，门静脉高压大鼠的六个核内酶活性显著增加，最后区核内酶活性降低。
这些结果表明，在当前大鼠模型下，一些离散的脑区参与了肝门静脉高压的机制。
