Abstract
The damaging action of ischemia in the myocardium leads to profound dystrophic changes at the myocyte organelle level [5, ii]. these changes also involve the myocardial contractile protein system, leading not only to irreversible loss of contractility of the myofilaments [I], but also to deformation and partial disappearance of actin and myosin filaments [4]. The writers showed previously [2] that treatment of animals with experimental myocardial ischemia (EMI) with various antianginal agents has a positive action on contractility of the contractile apparatus of the ischemic myocardium. The complexity of the search for and evaluation of antianginal agents has to be taken into account [7].
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