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)

For more than 25 years the chemistry and the function of the protein-hormonal complexes (produced by magnocellular nuclei of human and same animals) have been studied. The methods of radioimmunological analyses (RIA) for the detection of new neuropecific cardioactive protein-hormone "K" (RHK) in rat organism with myocardial ischemia has been developed. Concentration of PHK in various regions of the brain by RIA a four days after the occlusion of the carotid artery has a sharp decrease. Particularly concentration of PHK decreases 100-fold in the cerebral cortex. At the same time the level of PHK content in the blood increased from 13 +/- 0.85 to 630 +/- 3.9 ng/ml. The maximum concentration of PHK shows a sharp rise in the spleen 200-fold of their original level. This distribution pattern implies that PHK may be of importance for peripheral tissues and to the scarring in heart neurosis zone.
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PMID:[Distribution of neurospecific cardioactive protein-hormone complex in the rat body during experimental myocardial ischemia]. 233 46

Ischemic preconditioning (IPC) refers to the ability of short periods of ischemia to make the myocardium more resistant to a subsequent ischemic insult. It is the most powerful form of endogenous protection against myocardial infarction and has been demonstrated in all species evaluated to date. However, the cellular mechanisms that drive IPC remain poorly understood. This hypothesis describes an important role for alpha(1)-adrenoreceptors in mediating IPC and discusses the underlying mechanisms by which this is likely achieved. alpha(1)-Adrenoreceptors are present in the myocardium of all mammalian species, and several lines of evidence suggest that they play an important role in mediating IPC. During periods of myocardial hypoxia/ischemia, cardiomyocytes have to rely solely on anaerobic glycolysis for energy production; for this, the cells have to depend on increased glucose entry inside the cell as well as increased glycolysis. Stimulation of alpha(1)-adrenoreceptors increases glucose transport inside the cardiomyocytes by translocating glucose transporter (GLUT)-1 and GLUT-4 from the cytoplasm to the plasma membrane, enhances glycogenolysis by activating phosphorylase kinase, increases the rate of glycolysis by activating the enzyme phosphofructokinase, reduces intracellular acidity produced during excessive glycolysis by activating the Na(+)/H(+) exchanger, and inhibits apoptosis by increasing the levels of the antiapoptotic protein Bcl-2. Myocardial ischemia produces an increase in the expression of alpha(1)-adrenoreceptors in cardiomyocytes, as well as increases the levels of its agonist norepinephrine by several fold. During ischemic states, upregulation of alpha(1)-adrenoreceptors and increase in norepinephrine release could be a powerful adaptive mechanism that drives IPC. An understanding into the role of alpha(1)-adrenoreceptors in mediating IPC could not only point to newer treatments for limiting myocardial damage during myocardial infarction or heart surgery, but could also help in avoiding the use of alpha(1)-antagonists in patients with ischemic heart disease.
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PMID:Protecting the myocardium from ischemic injury: a critical role for alpha(1)-adrenoreceptors? 1129 92