![]() ![]() Sumatriptan (0.3 mg/kg) decreased lipid peroxidation, CK-MB and lactate dehydrogenase levels tumor necrosis factor concentration and Nf-ҡB’ protein production. Post-infarct treatment with sumatriptan increased left ventricular function, which was damaged in I/R animal’s heart. Animals were randomly divided into five groups: (1) Sham (2) I/R (3) I/R treated with sumatriptan (0.3 mg/kg i.p.) 20 min after induction of I/R rats, (4) GR127935 (a selective antagonist of 5-HT1B/D serotonin receptors 0.3 mg/kg) 20 min after induction of I/R, and (5) GR127935 (0.3 mg/kg) 15 min before administration of sumatriptan. Male Wistar rats were subjected to 30-min ligation of left anterior descending coronary artery and 120-min reperfusion. In this study, we aimed to assess the possible cardioprotective effect of sumatriptan in a rat model of I/R injury. Sumatriptan, which is mainly used to relieve migraine headache, has recently been shown to exert anti-inflammatory properties. Myocardial ischaemia and reperfusion (I/R)-induced tissue injury is associated with alteration in activity of inflammatory system and nitric oxide pathway. Ischemic heart disease is a leading cause of death on a global scale, placing major socio-economic burdens on health systems worldwide. These studies offer new insights into the development of strategies that may improve therapy of visceral pain conditions using already available medications. Actions at 5HT1(B) receptors within the RVM offer an additional potential site of action for the modulation of visceral pain by triptans. Our findings suggest that sumatriptan suppresses either inflammatory or noninflammatory visceral pain, most likely through peripheral 5HT1(B)/(D) receptors. Microinjection of 5HT1(B) or 5HT1(D) antagonists into the RVM did not block the effects of systemic sumatriptan. This was blocked by local microinjection of the 5HT1(B) antagonist but not the 5HT1(D) antagonist. Sumatriptan administered into the RVM similarly produced dose- and time-related blockade of referred hypersensitivity in both visceral pain models. Systemic sumatriptan elicited a dose- and time-related blockade of referred hypersensitivity in both models that was blocked by systemic administration of either 5HT1(B) or 5HT1(D) antagonists. Effects of sumatriptan within the rostral ventromedial medulla (RVM), a site of descending modulation of visceral pain, was determined by (1) testing the effects of RVM administration of 5HT1(B/D) antagonists on systemic sumatriptan action and (2) determining whether RVM application of sumatriptan reproduced the actions of systemic drug administration. The effects of systemic sumatriptan on referred hypersensitivity were tested in both models. Noninflammatory irritable bowel syndrome was induced by intracolonic instillation of sodium butyrate. Pancreatic inflammation was induced by intravenous injection of dibutyltin dichloride. The possible efficacy of sumatriptan was investigated in 2 models of visceral pain. Sumatriptan is used specifically to relieve headache pain.
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