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The purpose of this work was to compare the organisation of the gastric mucosal venous system in larger animals, exemplified by rabbits, with that of the rat and the hamster which we have described previously. Rabbits were given atropine and hexamethonium followed by intravital ligation of all veins draining the stomach, causing strong hyperaemia. The distribution of vessels was studied in the non-mounted mucosa, in mounts of mucosa cleared in light mineral oil and in paraffin or semi-thin plastic sections. We found that blood from rabbit gastric mucosa is drained by collecting venules, running from the subepithelial layer towards the muscularis mucosae. The collecting venules join the paramuscular vessels parallel and adjacent to the muscularis mucosae. Neighbouring venules form numerous arcade-like connections and gradually enlarge. Two venules and an arteriole form triplets initially situated at the luminal face of the muscularis mucosae and gradually passing onto its abluminal surface. In rats vascular triplets were absent and the collecting venules drained into paramuscular vessels joining submucosal veins. In hamsters both connections between paramuscular vessels and submucosal veins and the passing of vascular triplets across muscularis mucosae were observed. Contraction/relaxation of the muscularis mucosae may regulate the amount of blood in the venous system of the mucosa and change the intramucosal pressure, affecting movement of the tissue fluid and, indirectly, the function of the gastric cells.
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Histamine H3 receptors modulate reactive hyperemia in rat gut

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Reactive hyperemia (RH) is an abrupt blood flow increase following release from mechanical occlusion of an artery, with restoration of intra-arterial pressure. The mechanism of this postocclusion increase in blood flow in the gut is multifactorial. Relaxation of intestinal resistance vessels, observed during RH, may involve myogenic, metabolic, hormonal and neurogenic factors. Evidence exists that histamine is an important endogenous mediator of various functions of the gut, including blood flow. The vascular effects of histamine in the intestinal circulation are due its agonistic action on histamine H1, H2 and H3 receptors. In the present study the hypothesis was tested that peripheral histamine H3 receptors are involved in the mediation of RH in the intestinal circulation. In anesthetized rats, anterior mesenteric artery blood flow (MBF) was determined with ultrasonic Doppler flowmeter, and arterial pressure (AP) was determined with a transducer. The increase in the volume of blood accumulating during RH (RH-volume), the peak increase of arterial blood flow (RH-peak response) and the duration of the hyperemia (RH-duration) were used to quantify RH after occluding the anterior mesenteric artery for 30, 60 and 120 s. Hyperemia parameters were determined before and after administration of the selective histamine H3 receptor antagonist clobenpropit. Pretreatment with clobenpropit was without any effect on control MBF and AP but significantly reduced most of RH responses. These findings support the hypothesis that histamine H3 receptors do not play any role in the control of intestinal vasculature at basal conditions but these receptors participate in the intestinal hyperemic reaction in response to complete temporal intestinal ischemia.
Blood from the glandular part of hamster gastric mucosa is drained by collecting venules, running from the subepithelial layer towards lamina muscularis mucosae. To visualise vessels involved in the venous outflow, hamsters were exposed to atropine and subjected to intravital ligation of portal vein, causing strong hyperaemia. Distribution of vessels and their connections were studied a) in translucent, flat preparations of the glandular stomach, b) in thick sections of glandular mucosa cleared in the mineral oil, and c) in semi-thin plastic or paraffin sections. Collecting venules were drained by single vessels running parallel to the lamina muscularis mucosae (paramuscular venules), which, in turn, joined submucosal veins through openings in muscularis mucosae. Moreover, some collecting and paramuscular venules discharged into venules belonging to vascular triples composed of two venules and arteriole. The triplets were also parallel to muscularis mucosae. Triplets did not form connections with submucosal veins but passed on the abluminal surface of muscularis mucosae. Thus, some structural elements involved in venous outflow from glandular gastric mucosa differ from those in rats, in which vascular triplets were absent and all collecting venules drained into single paramuscular vessels. Contraction/relaxation of muscularis mucosae may regulate the amount of blood present in the venous system of the mucosa and the diameter of venules. Rhythmical changes of the latter could cause changes in intramucosal pressure, affecting movement of tissue fluid in the mucosa and thus the function of gastric cells.
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