Rna. Gasser et W. Klein, CONTRACTILE FAILURE IN EARLY MYOCARDIAL-ISCHEMIA - MODELS AND MECHANISMS, Cardiovascular drugs and therapy, 8(6), 1994, pp. 813-822
Citations number
98
Categorie Soggetti
Pharmacology & Pharmacy","Cardiac & Cardiovascular System
In early myocardial ischemia we find a number of salient electrical an
d ionic alterations. This article reviews action potential shortening,
K accumulation, and contractile failure. Enhanced K efflux during ear
ly 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 ca
techolamine-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 attrib
uted to enhanced outward current. Recently it has been shown by severa
l authors that ATP-dependent potassium channels play a key role in thi
s context. Contractile failure in early myocardial ischemia has been e
xplained by shortening of the action potential duration, reduced cytop
lasmic free calcium levels, intracellular acidification, and a rise in
inorganic phosphate and Rig. In summary, it is concluded that ATP-dep
endent K channels may be involved in each of these three phenomena.