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- W2034302754 abstract "Considerable number of arteriovenous anastomoses (AVA) have been shown to exist in the ears and skin and to play an important role in blood flow regulation, while most studies concerning the gastric microcirculation have denied the existence of AVA. Aim: The present study was undertaken to clarify the alteration of the microcirculatory architecture during the healing of acetic acid-induced gastric ulcer, effect of basic fibroblast growth factor (bFGF) and changes of the autonomic nerve distribution. Methods: Wistar strain male rats, weighing 200 to 250 g, were used. Acetic acid-induced ulcers were induced by the direct application of 100% acetic acid on the serosal surface of the glandular stomach for 30 sec. Three, seven, and fourteen days after the treatment, a polyethylene catheter was inserted into either abdominal aorta or inferior vena cava and 4% aqueous solution of agar mixed with FITC-dextran was infused orthodromically or retrogradely, and fixed with Zamboni' s solution. 20J.L cryostat sections were made and observed by confocal laser microscopy (Zeiss LSM41O), which made it possible to reconstruct the microcirculatory system. In addition, some rats were treated with oral administration of CS23, acidstable human recombinant bFGF (IJ.LgllOOg b.w.) every twelve hours after the ulcer formation. To clarify the localization of cholinergic, adrenergic and neuronal nitric oxide synthase (nNOS)-positive nerve fibers, indirect fluorescent immunohistochemical studies were performed using anti-choline acetyltransferase, dopamine f3-hydroxylase and nNOS monoclonal antibodies. Results: In the control rat stomach, the gastric mucosal microvascular network consisted of arterioles, venules in the basal portion and true capillaries but no AVA were found. Fourteen days after ulcer formation, direct communication of arterioles and venules, i.e. AVA, was observed in the basal portion of the fundic mucosa in three out of five rats, while no AVA was found in the bFGF-treated rats. nNOS immunoreactive nerve fibers were densely distributed surrounding the AVA. The addition of NO donor, nitroprusside (40J.Lgl l OOg b.w.) brought about the marked opening of this AVA. Conclusions: From these observations, it was concluded that AVA was often recognized in the healing process of acetic acid-induced ulcer, while bFGF administration inhibited the AVA formation. This new blood channel was innervated by nNOS-positive nerve fibers and could be regulated by NO." @default.
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- W2034302754 date "2000-04-01" @default.
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- W2034302754 title "Formation of arteriovenous anastomosis during healing of acetic acid-induced ulcer: Inhibitory effect of bFGF and regulation by nNOS-positive nerve fibers" @default.
- W2034302754 doi "https://doi.org/10.1016/s0016-5085(00)83029-2" @default.
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