2003, Number 4
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Arch Cardiol Mex 2003; 73 (4)
Considerations on the myocardial damage due to ischemia and reperfusion
de Micheli A, Chávez E
Language: Spanish
References: 39
Page: 284-290
PDF size: 114.08 Kb.
ABSTRACT
In this article, we present some considerations on the myocardial damage due
to a deficit of oxygen supply. In fact, this damage properly constitutes a partial
diastolic depolarization or injury, i. e., a moderate reduction of the rest
transmembrane potential. This phenomenon is characteristic of the acute phase
of the myocardial infarction syndrome and is responsible for the main electrical
manifestations appearing in this phase: disorders of rhythm and conduction,
as well as a reduced contractility of the involved myocardial fibers. All the
mentioned phenomena are due to a defect of the myocardial energetic mechanisms,
owing to the mitochondrial alterations in myocytes: early reduction of the nicotinamide
adenine nucleotides, accumulation of calcium (“calcium overload”)
into mitochondria, and a drop in oxidative phosphorylation. These changes can
present again, more exaggerated, in a following phase of evolution of the myocardial
infarction due to myocardial reperfusion. Its severity is related to the duration
of the initial ischemia period. Moreover, consequences of the oxidative stress
can add producing cellular damage by liberation of reactive oxygen species.
Oxidant stress causes also alterations in the mitochondrial DNA, i. e., mutations
due to oxidation of nitrogenous bases. During the initial ischemia phase, as
well as during reperfusion, metabolic therapy can be very useful as, for example,
glucose-insulin-potassium solutions (G-I-K). These could act as scavengers of
the free radicals derived from oxygen and avoid or reduce the myocardial damage
due to reperfused myocytes. Metabolic drugs, as for example trimetazidine, antioxidants,
etc, can also be used in the myocardial reperfusion phase.
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