Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Superior mesenteric artery occlusion leads to mesenteric ischemia, activation of arachidonic acid metabolism and release of endotoxins into the systemic circulation. The effect of leukotriene and prostaglandin antagonists on hemodynamic response and survival of rats after superior mesenteric artery (SMA) occlusion was investigated. The animals were divided into five groups: in group 1 (n = 105) the SMA was clamped for 2 h and mortality assessed after 24 h. Group 2 animals (n = 20) were pretreated with 5 mg/kg indomethacin and the SMA clamped similarly to group 1, group 3 animals (n = 15) were pretreated with 5 mg/kg Voltaren, group 4 animals (n = 20) received 20 mg/kg BW 755C before mesenteric artery occlusion, and group 5 animals (n = 50) were pretreated with 100 mg diethylcarbamazine. The blood pressure and pulse response as well as histologic appearance of the bowel 1 h after declamping was similar in all five groups. The mortality rate after 24 h was 34% in the control group, 36% with indomethacin treatment, 36% with voltaren, 47% with BW 755C and 40% with diethylcarbamazine. The mortality rate in all the treated groups was not significantly different from the control group. Plasma thromboxane B2 levels were inhibited significantly by indomethacin and Voltaren and to a lesser extent by BW 755C. There was a paradoxical rise in thromboxane B2 following diethylcarbamazine treatment. It is concluded that inhibition of the cyclooxygenase and/or the lipoxygenase pathways of arachidonic acid did not alter the hemodynamic response and mortality following 2 h of acute superior mesenteric artery occlusion.
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PMID:Effect of prostaglandin and leukotriene antagonists in acute mesenteric artery occlusion. 314 80

Recent evidence suggests that enhanced cell apoptosis is responsible for germ cell loss following testicular ischemia-reperfusion (IR) injury. A nonsteroidal anti-inflammatory drug diclofenac sodium (Voltaren) is a prostaglandin-synthesis inhibitor, which is widely used in many testicular disorders. The purpose of the present study was to examine the effect of diclofenac (DIC) on germ cell apoptosis in the ischemic and contralateral testes following testicular IR in a rat. Forty rats were divided randomly into four experimental groups of ten rats each: group A (Sham)-Sham operated animals; group B (Sham-DIC)-Sham operated rats that were treated with DIC given subcutaneously at a dose of 10 mg/kg, once daily, 24, 48 and 72 h following operation; group C (IR) underwent 90 min of unilateral testicular IR; group D (IR-DIC)-rats underwent 90 min of unilateral testicular IR and were treated with DIC similarly to group B. Ninety-six hours following operation, the rats were sacrificed and testes were harvested. Johnsen's criteria and the number of germinal cell layers were used to categorize the spermatogenesis. TUNEL assay was used to determine germ cell apoptosis in both the ischemic and contralateral testes. Statistical analysis was performed using the non-parametric Kruskal-Wallis ANOVA test, with P less than 0.05 considered statistically significant. Testicular ischemia in rats led to histological damage in the ipsilateral testis. In the contralateral testis, minimal damage was observed. Germ cell apoptosis in both the ischemic and the contralateral testes increased significantly after IR. Treatment with DIC did not change histologic parameters of spermatogenesis in both the ischemic and contralateral testes, but decreased germ cell apoptosis in both testes following testicular IR. We conclude that testicular ischemia causes an increase in germ cell apoptosis in the contralateral testis. Diclofenac may be beneficial for spermatogenesis following testicular IR by decreasing germ cell apoptosis.
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PMID:Effect of diclofenac on germ cell apoptosis following testicular ischemia-reperfusion injury in a rat. 1628 37