Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelets are a source of vasoactive mediators that regulate vascular tone. Platelets also play a role in intravascular thrombus formation and dynamic coronary constriction that result in myocardial ischemia. However, effects of platelets on myocardial function after ischemia and reperfusion are unknown. In this study, we examined the effects of platelets on myocardial dysfunction caused by ischemia/reperfusion. Buffer-perfused isolated rat hearts, after global ischemia (15 minutes) and reperfusion (10 minutes), developed marked myocardial dysfunction, indicated by a 65 +/- 4% decrease in the force of cardiac contraction (FCC) and a 26 +/- 7% increase in coronary perfusion pressure (CPP). Ischemia/reperfusion was also associated with release of creatine kinase (CK) and ATP metabolites in the coronary effluents. Perfusion of hearts with buffer containing washed rat platelets (3-8 x 10(7) cells/ml) protected hearts against dysfunction from ischemia/reperfusion, indicated by minimal changes in CPP (-1 +/- 1%) and FCC (-1 +/- 3%). Release of CK in the coronary effluent was also reduced, as was the release of ATP metabolites in the platelet-perfused hearts. Perfusion of hearts with serotonin receptor antagonist LY53,857 (10(-6) M), thromboxane A2 receptor antagonist SQ29,548 (10(-6) M), adenine nucleotide scavenger apyrase (0.4 units/ml), or nitric oxide synthetase inhibitor NG-monomethyl-L-arginine (2 x 10(-4) M) attenuated (p < 0.05) the platelet-mediated cardioprotective effects. Perfusion of the hearts with L-arginine (2 x 10(-4) M) instead of platelets also showed modest protective effects on FCC (-4.3 +/- 13%), CPP (+18 +/- 7%), and CK release. Prolongation of the ischemic period to 30 minutes and reperfusion to 20 minutes also demonstrated marked cardiac dysfunction (FCC, -58 +/- 10%; CPP, +36 +/- 8%) in buffer-perfused hearts. Perfusion of hearts with platelets in this setting of prolonged ischemia/reperfusion also exhibited protective effects on FCC (-24 +/- 10%), CPP (+12 +/- 6%), and CK release. Thus, platelets protect myocardium from ischemia/reperfusion-induced injury, and these protective effects of platelets are evident regardless of the duration of ischemia/reperfusion. Furthermore, these cardioprotective effects of platelets seem to be related to the release of serotonin, thromboxane A2, and adenine nucleotides. These substances most likely elicit release of endothelium-derived relaxing factor, with its attendant tissue-protective effects, from the microvascular endothelium of hearts.
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PMID:Platelets protect against myocardial dysfunction and injury induced by ischemia and reperfusion in isolated rat hearts. 849 48

Ondansetron is a serotonin receptor antagonist used widely in the prophylaxis and treatment of postoperative nausea and vomiting (PONV) and vomiting associated with cancer chemotherapy. The common side effects of ondansetron are fever, malaise, diarrhoea, constipation, and allergic reactions. Extra-pyramidal reactions are rare and cardiovascular side effects are even rarer. Even though its clinical safety has been established in a large number of studies, its adverse effects have been reported and these include cardiovascular events like acute myocardial ischemia and arrhythmias in adults.([1]) Studies of its adverse effects in children are few. We report a rare adverse effect of ondansetron in a 14-year-old girl, presenting as ventricular tachycardia.
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PMID:Ondansetron induced fatal ventricular tachycardia. 2004 Sep 55

Personality traits of the patient with ischemic heart disease (IHD) are thought to determine disease course. Their level depends on clinical presentations of IHD including the presence of cardiac pain. The aim of the study was to identify the modifying effect of genes coding for serotonin transporter (5-HTTLPR), serotonin receptor type 2A (A-1438G) and 2C (Cys23Ser) as well as brain-derived neurotrophic factor (Val66Met) on personality traits in pain and painless forms of IHD. We found interaction between pain and personality factors mediated by genetic variant. Pain syndrome was associated with higher neuroticism scores in carriers of allele S (5-HTTLPR), allele Ser (5-HTR2C), and the genotype ValVal (BDNF) and with higher hostility levels in patients with allele Ser. The results may be used for purposes of personalized examination of IHD patients directed to prevention of unfavorable course of the disease.
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PMID:[Interaction Between Personality, Pain, and Genes in Ischemic Heart Disease]. 2829 Sep 2