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)

Atherosclerosis was induced in New Zealand White rabbits by feeding them a 0.5% cholesterol-enriched rabbit chow for 10-12 wk. Half of the cholesterol-fed rabbits were given BM 13505, a specific thromboxane A2/endoperoxide (TxA2/PGH2) receptor antagonist, and the other half were given its vehicle (i.e., 2% Na2CO3). At the end of 10-12 wk, the rabbits underwent experimental myocardial ischemia or an identical sham operation, except that the coronary artery was not occluded. BM 13505 was shown to protect the ischemic rabbit myocardium by three different methods: 1) maintenance of myocardial tissue creatine kinase (CK) activity in the ischemic myocardium; 2) reduced loss of free amino nitrogen-containing compounds from the myocardium; and 3) blunting the rise of plasma CK activity. Part of the mechanism for these effects may be due to inhibition of platelet aggregation and blockade of the vasoconstrictor effect of TxA2. However, these protective effects were not due to differences in myocardial oxygen demand among the groups. Finally, BM 13505 exhibited an antiatherogenic effect by reducing the deposition of cholesterol in the aortic wall and by retarding plaque formation in coronary arteries. However, it does not achieve this antiatherogenic effect by lowering plasma cholesterol concentrations or by scavenging superoxide free radicals. Thus blockade of TxA2 receptors exerts a variety of beneficial effects that reduce the severity of ischemic damage resulting from myocardial ischemia.
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PMID:Cardioprotective actions of thromboxane receptor antagonism in ischemic atherosclerotic rabbits. 297 Feb 33

Thromboxane A2 (TxA2), leukotriene C4 (LTC4), leukotriene D4 (LTD4), and platelet-activating factor (PAF) are novel lipids which exert a variety of biological actions. TxA2, LTC4 and LTD4 have been shown to induce direct vasoconstriction in several species, while PAF contracts isolated guinea pig ileum and lung parenchyma. We studied the direct vasoconstricting activities of these lipid mediators in isolated cat renal, superior mesenteric and coronary arteries. The TxA2 analog 9,11-methanoepoxy PGH2 (U-46619) constricted both perfused and helical strips, with the renal and mesenteric arteries being 4 times more responsive than the coronary arteries. LTC4 and LTD4 constricted coronary arteries to a significantly greater extent than renal and superior mesenteric arteries in both perfused arteries and helical strips. Furthermore, PAF failed to contract any of the perfused arteries or helical strips at concentrations from 1 ng to 20 micrograms. TxA2 was a potent vasoconstrictor in all the vessels studied, suggesting a role for this substance as a vasoactive mediator in ischemia and shock. The coronary arteries were more responsive to the leukotrienes than the mesenteric and renal arteries, suggesting that the leukotrienes may play an important role in myocardial ischemia. Moreover, both thromboxane and leukotriene effects were blocked in all preparations by specific receptor antagonists. While the biological effects of PAF are still poorly understood, PAF does not directly vasoconstrict large arteries of the feline renal, superior mesenteric or coronary vasculatures.
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PMID:Heterogeneity of vascular smooth muscle responsiveness to lipid vasoactive mediators. 356 63

Myocardial ischaemia may occur during spasm or thrombosis of the coronary arteries. The vascular endothelium plays an essential role in the lesions observed during ischaemia and myocardial reperfusion by the intermediary of the numerous endothelium-derived vasoactive factors. These include the "endothelium-derived relaxing factors" (EDRFs) nitrous oxide, prostacyclin, which are vasodilators and platelet antiaggregants ant the "endothelium-derived contracting factors" (EDCFs), endothelin, PGH2, oxygen-free radicals which are vasoconstrictive. The endothelial cells also produce the platelet activating factor and factors essential for coagulation. The metabolism and biological properties of these different mediators are reviewed. During the phenomena of myocardial ischemia-reperfusion, endothelial regulation is activated by tissue hypoxia and reduction of coronary flow and perfusion pressure. This regulation also depends on the functional state of the arteries (macroscopically normal or pathological). These vasomotor phenomena are associated with the effects of platelet aggregation and myocardial accumulation of neutrophil polynuclear blood cells. During the second phase of reperfusion cellular lesions are produced by the generation of cytotoxic oxygen-free radicals. Assays of mediators present a clinical interest when the modalities of sampling have been fixed (systemic blood samples or during cardiac catheterisation, sites of sampling, choice of timing of sampling with respect to the biological half lives of the mediators). Determining a correlation between the in vitro biological effects on those in isolated organs and clinical data has become possible with the improvement in techniques of sampling and the increasing collaboration between biologists and clinicians.
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PMID:[Mediators of the vascular endothelium as markers of myocardial ischemia and reperfusion]. 830 14

Nowadays, the prevention of severe myocardium injury resulting from myocardial ischemia/reperfusion injury (I/R) has been recognized as an important subject in the field of ischemic heart disease. In this study, H9c2 cardiomyocytes were exposed to cycles of hypoxia/reoxygenation (H/R) to mimic myocardial I/R injury. Western blot analysis and qRT-PCR were performed to detect the expression of Cox-2, Akt and p-Akt. Cell viability, LDH release and activity of Caspase-3 were assessed to determine the protective effect of propofol. The results proved that the protective effect of propofol for H/R challenged cardiomyocytes was associated with Akt phosphorylation. We also revealed that treatment of propofol suppressed the expression of Cox-2 in cardiomyocytes which was up-regulated after H/R treatment. Conversely, the over-expression of Cox-2 inhibited Akt phosphorylation while enhancing cardiomyocytes apoptosis. Interestingly, Akt activator exhibited similar protective effect with propofol and could diminish the influences brought by over-expression of Cox-2. Thus, it could be concluded that Cox-2 negatively affects the protective effect of propofol against hypoxia/reoxygenation induced cardiomyocyte apoptosis by suppressing Akt phosphorylation.
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PMID:Cox-2 Negatively Affects the Protective Role of Propofol against Hypoxia/Reoxygenation Induced Cardiomyocytes Apoptosis through Suppressing Akt Signaling. 3138 Apr 37