Verapamil alters eicosanoid synthesis and accelerates healing during experimental colitis in rats
Gastroenterology, ISSN: 0016-5085, Vol: 102, Issue: 4, Page: 1229-1235
1992
- 21Citations
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations21
- Citation Indexes21
- CrossRef21
Article Description
In inflammatory bowel disease, prostaglandins are mucosal protective whereas leukotrienes are proinflammatory. Recent evidence suggests that the formation and action of leukotrienes are calcium-dependent, whereas the formation and action of prostaglandins are not. To examine the possibility that, because of differential regulation of arachidonic acid metabolism, calcium channel blockade might alter mucosal eicosanoid synthesis and accelerate healing during inflammatory bowel disease, we treated a 4% acetic acid-induced colitis model with verapamil and/or misoprostol and determined the effects on colonic macroscopic injury, mucosal inflammation as measured by myeloper-oxidase activity, in vivo intestinal fluid absorption, and mucosal prostaglandin E 2 and leukotriene B 4 (LTB 4 ) levels as measured by in vivo rectal dialysis. In colitic animals, verapamil treatment significantly improved colonic fluid absorption and macroscopic ulceration. This mucosal-protective effect of verapamil occurred in the presence of a twofold reduction in mucosal LTB 4 synthesis. In noncolitic animals, verapamil alone had no effect on in vivo fluid absorption, macroscopic ulceration, or myeloperoxidase activity but did induce a threefold reduction in LTB 4 synthesis in addition to shifting arachidonic acid metabolism towards a sixfold stimulation of prostaglandin E 2 synthesis. Our results show that, when administered before the experimental induction of colitis, the calcium channel blocker, verapamil, has a mucosal-protective effect that occurs as a consequence of reduced mucosal leukotriene synthesis and increased prostaglandin synthesis. This differential regulation of arachidonic acid metabolism may play an important role in the development of novel therapeutic agents for inflammatory bowel disease.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/001650859290760V; http://dx.doi.org/10.1016/0016-5085(92)90760-v; http://linkinghub.elsevier.com/retrieve/pii/001650859290760V; http://api.elsevier.com/content/article/PII:001650859290760V?httpAccept=text/xml; http://api.elsevier.com/content/article/PII:001650859290760V?httpAccept=text/plain; https://linkinghub.elsevier.com/retrieve/pii/001650859290760V; http://dx.doi.org/10.1016/0016-5085%2892%2990760-v; https://dx.doi.org/10.1016/0016-5085%2892%2990760-v
Elsevier BV
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