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Selected Publication:
Gasser, RN; Klein, W.
Contractile failure in early myocardial ischemia: models and mechanisms.
CARDIOVASC DRUG THERAPY. 1994; 8(6): 813-822.
Doi: 10.1007/BF00877399
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- Leading authors Med Uni Graz
- Gasser Robert
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- Abstract:
- In early myocardial ischemia we find a number of salient electrical and ionic alterations. This article reviews action potential shortening, K accumulation, and contractile failure. Enhanced K efflux during early myocardial ischemia has been attributed to a number of mechanisms, including: the inhibition of active K uptake, osmotic changes, efflux of K ions linked to anion extrusion, cation exchange, altered cellular energy levels, in particular, the opening of ATP-dependent K channels, the involvement of other ion channels, a H/K-ion exchanger, and a catecholamine-dependent pathway. The different mechanisms are discussed. Action potential shortening was described as a salient characteristic of myocardial ischemia in 1954 by Trautwein and Dudel, and was attributed to enhanced outward current. Recently it has been shown by several authors that ATP-dependent potassium channels play a key role in this context. Contractile failure in early myocardial ischemia has been explained by shortening of the action potential duration, reduced cytoplasmic free calcium levels, intracellular acidification, and a rise in inorganic phosphate and Mg. In summary, it is concluded that ATP-dependent K channels may be involved in each of these three phenomena.
- Find related publications in this database (using NLM MeSH Indexing)
- Animals -
- Disease Models, Animal -
- Humans -
- Myocardial Contraction - physiology
- Myocardial Ischemia - physiopathology
- Find related publications in this database (Keywords)
- Potassium
- Myocardium
- Ischemia
- K-ATP Channel
- Contractile Failure