Abstract
ABSTRACTBackground: The role of autonomic nervous system in the development and maintenance of portal hypertension is not fully elucidated. It is known that the gene expression of norepinephrine in the superior mesenteric artery varies with time, and it may contribute for splanchnic vasodilation and its consequent hemodynamic repercussions. It is still not known exactly how the adrenergic expression behaves at the heart level in the initial stages of this process. Aim: To evaluate the immunohistochemical expression of the enzyme tyrosine hydroxylase (tyrosine 3-monooxygenase), involved in the synthesis of norepinephrine, in the myocardium of rats submitted to partial ligation of the portal vein. Methods: Twenty-four Wistar rats were divided into two groups: Sham Operated and Portal Hypertension. The partial ligation was performed in the Portal Hypertension group, and after 1/6/24 h and 3/5/14 days the animals were euthanized. Immunohistochemical analysis was performed to quantify the expression of the stained enzyme using the ImageJ program. Results:The Portal Hypertension group expressed percentages between 4.6-6% of the marked area, while the Sham Operated group varied between 4-5%. Although there was no statistical significance, the percentage stained in the Portal Hypertension group followed an increasing pattern in the first 6 h and a decreasing pattern after 24 h, which was not observed in the Sham Operated group. Conclusion: The expression of noradrenaline in rat myocardium during the first two weeks after partial ligation of the portal vein, with tyrosine hydroxylase as marker, did not show differences between groups over time.
Highlights
The portal vein is formed by the union of superior mesenteric and splenic veins, and its tributaries include gastric and pancreatoduodenal veins
Portal hypertension (PH) is the clinical syndrome usually secondary to intrahepatic or extrahepatic obstruction of the portal flow, in which the increased portal blood flow resistance is the primary factor in the pathophysiology of portal hypertension[12]
The animals were treated daily with filtered water and appropriate ration administered freely. They were divided into two groups: Sham Operated, group submitted to the simulation of the operation, without the portal vein partial ligation model (PVPL); and PVPL
Summary
The portal vein is formed by the union of superior mesenteric and splenic veins, and its tributaries include gastric and pancreatoduodenal veins. It extends to the hepatic hilum, and it is divided into right and left hepatic veins. The liver receives a total blood flow about 1,200 ml/min, which represents approximately 25% of the cardiac output. It receives a dual blood supply: 25% of the volume comes from the hepatic artery, and 75% from the portal vein[3]. Portal hypertension (PH) is the clinical syndrome usually secondary to intrahepatic or extrahepatic obstruction of the portal flow, in which the increased portal blood flow resistance is the primary factor in the pathophysiology of portal hypertension[12]
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