| Portal hypertensive gastropathy (PHG) is now recognized to be a unique entity, and distinct from other forms of gastritis present in non-portal hypertensive patients. In the presence of portal hypertension (PHT), due to the high portal venous pressure, the result that blood flow is an abnormality and gastric microvessels circulation become disorder can be observed. Experiment demonstrated a striking increase of gastric submucosal arteriovenous communication with deduction of effective mucosal blood flow in PHG. Morphology studies had shown PHG to be a pronounced dilation of mucosal and submucosal blood vessels along with the absence of inflammation. So abnormalities of gastric mucosal microvessels circulation are recognized an important cause in PHG.Recently, angiogenesis has been noticed as a key factor for clarifying the pathophysiology of the microvessels of various diseases (such as malignant tumor and cardiovascular circulation). Many studies showed some cytokines and growth factors had been to be modulator of angiogenesis. Among the growth factors known to accelerate angiogenesis,vascular endothelial growth factor (VEGF) is a potent angiogentic factor and has been found to play a pivotal role in vascular formation and permeability. Clinical studies and animal experiments suggested an abnormality of angiogenesis had been observed in PHG. We postulate VEGF can be associated with a marked dilation of the mucosal and submucosal vessels in PHG.The mechanisms underlying the gastric circulation disorders in PHG are not fully understood. Nowadays, it has been suggested that an overproduction of endogeneous vasodilators, such as glucagons, prostaglandin, and nitric oxide (NO) could be involved. CO is, like NO, also a new endogenous vasodilator that mediates various physiological functions, such as relaxing the vessel, increasing blood flow and reducing vascular resistance. Recent studies suggested that CO was associated with the regulation of local and systemic vascular tone. Heme oxygenase(HO) is the rate-controlling enzyme for heme degradation in mammals and metabolizes heme into biliverdin and releases free iron, CO and bilirubin . Two isoforms of HO have been identified: the inducible HO-1 and constitutive HO-2. The main function of HO-1 is the protection of cells against oxidative stress and its consequences. Besides PHT and some endogenous vasodilators, it is to be known whether other factors are involved in the mechanisms of PHG, especially, whether CO and VEGF contributed to mechanisms of PHGneed us to study further. Hence, we set about our research from the gastric microvessels circulation disorders. By animal experiment, we investigated the expression of VEGF and HO-1 and explored the possible role in PHG .The experiment contained two parts as below:Part one: Immunohistochemical localization of VEGF in portal hypertensive gastropathy ratsObjectives: To investigate the changes of gastric mucosal blood flow dynamics in PHG rat and whether VEGF appears more strongly in PHG than in normal gastric mucosa and, if so, what is the exact role of the VEGF in PHG.Methods: PHG was induced by partial portal vein ligation. The Sprague Dawley rats were randomly divided into two groups, ie, sham operation and model group (PHG). Fourteen days after a portal ligation or sham operation, the portal venous pressure was measured with physiology recorder, and the gastric mucosal blood flow volume was measured with the neutral red clearance method. Histopathological changes were evaluated by hematoxylin and eosin staining, the expression of VEGF in gastric mucosal specimens was immunohistochemically assessedResults: ①Fourteen days after the surgery, morphology studies showed a number of mucosal capillaries and submucosal veins were dilated markedly without anyinflammation. Vessels were full with lots of red blood cells, accompanied with erythrocytes outside the vessels. ②The portal pressure (2.13±0.37) kPa in the PHG rats was significantly greater than that in the contro...
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