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)

The etiology of sudden-death ischemic heart disease (SDIHD) remains an enigma. Data will be presented which suggest that SDIHD may be due to hypomagnesemia in and around the coronary arterial and arteriolar vessels. We have found that blood vessels (especially arteries and arterioles) deficient with respect to Mg can undergo constriction and spasm; the greater the reduction in Mg2+, the greater the magnitude of the spontaneous contractile responses. The higher the Ca2+:Mg2+ ratio, the greater are the magnitudes of these contractile responses. A severe deficit in surface membrane Mg2+, in particular, results in intense vasospasm. Using direct in situ high resolution microscopy (3000 x), we have found that a lowering of Mg2+ around perfused arterioles (15--20 microns i.d.) will also result in spontaneous vasoconstriction and, in addition, increased arteriolar resistance, tissue ischemia and reduced venous outflow. We have also found that the constrictor actions of certain circulating vasoconstrictor hormones (i.e., angiotensin, serotonin, acetylcholine) are enhanced when [Mg2+] is lowered below the levels normally found in plasma. Other direct studies, from our laboratory, indicate that [Mg2+]o regulates calcium exchange and content of vascular smooth muscle. In summary, the concept to be presented suggests that a deficiency in dietary Mg2+ is a key factor in the high incidence of mortality noted in SDIHD in nations of the Western world. The hypomagnesemia produces progressive vasoconstriction, vasospasm and ischemia, which, given time, will lead to SDIHD.
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PMID:Sudden-death ischemic heart disease and dietary magnesium intake: is the target site coronary vascular smooth muscle? 39 Mar 30

Several workers have used histochemical, enzymatic, and fluorescent methods to diagnose early myocardial ischemia, but the problem of unequivocal detection of early ischemia still remains an enigma to pathologists. In the present study, the left coronary artery was ligated in an animal model, rat, in order to produce myocardial ischemia at different time intervals, from five minutes to six hours. Fluorescent techniques and tetrazolium staining of myocardial succinic dehydrogenases have been used to detect onset of ischemia with the purpose of identifying a sensitive technique for use in routine pathologic specimens. Nitroso-blue tetrazolium and triphenyl tetrazolium chloride staining of myocardium showed loss of dehydrogenases within five to twenty minutes of ligation of the coronary artery. This loss was consistent and progressively increased at longer time intervals, the mean ischemic area mapped being 25.74 mm2 and 66.87 mm2 at five to twenty minutes and six hours respectively. Such comparison of ischemic area of myocardium at different time intervals has not been reported earlier. Autofluorescence in formalin-fixed, hematoxylin and eosin-stained sections showed positive fluorescence only after fifty to seventy-five minutes of ischemia and was patchy in distribution in the left ventricular wall even up to six hours of ligation. Examination of myocardium under fluorescent light after acridine orange staining proved to be more sensitive than autofluorescence for detecting ischemia. At five to twenty minutes, the mean ischemic area was 18.67 mm2 and by six hours it increased to 27.48 mm2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Histochemical and fluorescent techniques for detection of early myocardial ischemia following experimental coronary artery occlusion: a comparative and quantitative study. 245 Apr 89

Angiotensin II (Ang II) plays important roles in the development of cardiovascular diseases including hypertension, renal diseases, cardiac hypertrophy, congestive heart failure, and ischemic heart disease. Angiotensin II exerts classic hemodynamic and renal effects, but it is also a local biologically active mediator with direct effects on endothelial and smooth muscle cells. Two subtypes of Ang II receptors, type 1 (AT(1)) and type 2 (AT(2)), have been identified. Their roles have been investigated in depth in vivo and in vitro, although few data are available concerning the role of the AT(2) receptors in the adult circulation in humans. The two receptors, both of which belong to the superfamily of G-protein-coupled receptors, have different signaling pathways and different functions. The AT(1) receptor subtype is expressed ubiquitously and is involved in most of the well-known biological functions of Ang II. The AT(1) receptor transactivates growth pathways and mediates major Ang II effects such as vasoconstriction, increased cardiac contractility, renal tubular sodium reabsorption, cell proliferation, vascular and cardiac hypertrophy, inflammatory responses, and oxidative stress. In contrast to AT(1), the physiologic role of AT(2) receptors has long remained an enigma. The AT(2) receptors are highly expressed in fetal tissues, although their expression dramatically decreases after birth, being restricted to a few organs, including the cardiovascular system. The AT(2) receptor is re-expressed in the adult animal after cardiac and vascular injury and during wound healing, suggesting a role for this receptor in tissue remodeling, growth, or development. Recent and concordant data suggested that overstimulation of AT(2) receptors might be implied in cardiac and vascular hypertrophic processes. Both Ang II receptors are involved in hypoxia-induced neovascularization. A large set of experimental evidence suggests that activation of the AT(1) receptor results in proangiogenic effects, whereas AT(2) receptors mediate apoptosis and thus antiangiogenic effects. Furthermore, bradykinin through its B(1) or B(2) receptors is a potent activator of experimental hypoxia-induced neovascularization. Thus, pharmacologic blockade of the AT(1) receptor and resulting overactivation of AT(2) receptors could impair or delay neovascularization in ischemic tissues in patients receiving chronic treatment with angiotensin receptor blockers. In contrast, increased tissue bradykinin resulting from inhibition of converting enzyme could help to restore functional vascularization in ischemic tissues. These basic concepts deserve a second reading and reevaluation to discuss differences in vascular protection in large clinical trials with different classes of drugs acting on the renin-angiotensin system.
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PMID:How to explain the differences between renin angiotensin system modulators. 1612 50

Myocardial ischemia-reperfusion (MIR) injury is a major contributor to the morbidity and mortality associated with coronary artery disease, which accounts for approximately 450,000 deaths a year in the United States alone. Chinese herbal medicine, especially combined herbal formulations, has been widely used in traditional Chinese medicine for the treatment of myocardial infarction for hundreds of years. While the efficacy of Chinese herbal medicine is well documented, the underlying molecular mechanisms remain elusive. In this review, we highlight recent studies which are focused on elucidating the cellular and molecular mechanisms using extracted compounds, single herbs, or herbal formulations in experimental settings. These studies represent recent efforts to bridge the gap between the enigma of ancient Chinese herbal medicine and the concepts of modern cell and molecular biology in the treatment of myocardial infarction.
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PMID:Effects and mechanisms of chinese herbal medicine in ameliorating myocardial ischemia-reperfusion injury. 2428 71