Related Experiment Video
Updated: May 5, 2026

An Acute Retinal Model for Evaluating Blood Retinal Barrier Breach and Potential Drugs for Treatment
Published on: September 13, 2016
Histamine is involved in ethanol-induced jejunal microvascular injury in rabbits
P K Dinda1, D J Leddin, I T Beck
1Department of Medicine Queen's University, Hotel Dieu Hospital, Kingston, Ontario, Canada.
Abstract:
To examine for the possible involvement of histamine in the jejunal microvascular effects of ethanol, we investigated the effects of (a) intraluminal ethanol on histamine release by the jejunum and (b) simultaneous inhibition of both histamine1 and histamine2 receptors (using promethazine and cimetidine, respectively) on ethanol-induced intestinal plasma protein loss in rabbits. Ethanol increased histamine release by the jejunum both in vivo (p less than 0.01) and in vitro (p less than 0.05). To investigate the effect of antihistamines on ethanol-induced plasma protein loss, we determined the dose of blockers that would completely inhibit the histamine1 and histamine2 receptors. In the absence of antihistamines, ethanol caused a 10-fold increase in jejunal protein loss over the controls (p less than 0.001). Simultaneous inhibition of histamine1 and histamine2 receptors attenuated (p less than 0.025), but did not abolish, the ethanol-induced protein loss. These data are discussed in relation to the literature, and it is concluded that histamine may play a role in the jejunal microvascular effects of ethanol. As the ethanol-induced protein loss was not completely inhibited, other mediators or mechanisms were probably involved.
Related Concept Videos
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Gastritis II: Pathophysiology

