The energy allowance and calcium homeostasis of the cardiomyocytes in the early stages of myocardial ischemia

: Morphofunctional equivalents are described of adaptive and abnormal reconstitution of CMC in acute coronary failure, using methods of light-transmission optics in combination with those of electron microscopy. It has been established that the contractile myocardium cell compensatory hyperfunction is provided by mobilization of a maximum number of the CMC organelles. Documented for the first time cytochemically is a direct interrelation between the metabolic activity of oxidoreductases, ability of mitochondria to accumulate Ca2+, and the status of their membranes. Exhaustion of the CMC adaptive potential was found to be associated with inconsistencies between metabolic and Ca(2+)-binding capacity of mitochondria, sarcoplasmic reticulum (CPR), and sarcolemma, these causing desynchronization of myofibrils restricting the CMC contractile apparatus function. The above changes develop prior to the destruction of the organelle membranes, resolved with the routine electron microscopy. It has been shown that inhibition of ion-exchange functions of the basal and plasmic membranes involves redistribution of Ca2+ on these and is accompanied by a progressive impairment of the barrier properties of sarcolemmas.