Prevention of myocardial Ca overload and necrotization by Mg and K salts or acidosis.
The crucial point in the pathogenesis of isoproterenol-induced myocardial necrotization is an abundant intracellular Ca accumulation leading to high energy phosphate exhaustion. Accordingly, in the early stage of the isoproterenol-induced necrotization process, the onset of ATP and creatine phosphate breakdown strictly parallels the acute Ca gain. In this type of necrosis, the Mg losses from the myocardium appear as a concomitant phenomenon. The hearts can be protected against the deleterious Ca overload and necrotization by increasing the plasma concentration of Mg, K, or H ions in order to counterbalance Ca according to the ration (see article). On the other hand, if Mg, K, or H ion concentrations are too low, isoproterenol-induced Ca uptake and myocardial lesions are potentiated.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000037:antagonists & inhibitors* / Q000378:metabolism; D009202:Cardiomyopathies / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D004305:Dose-Response Relationship, Drug; D006863:Hydrogen-Ion Concentration; D007545:Isoproterenol / Q000037:antagonists & inhibitors; D008274:Magnesium / Q000494:pharmacology / Q000627:therapeutic use*; D009206:Myocardium / Q000378:metabolism; D009336:Necrosis; D010725:Phosphocreatine / Q000378:metabolism; D011188:Potassium / Q000494:pharmacology / Q000627:therapeutic use*; D051381:Rats
D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D008274:Magnesium; D007545:Isoproterenol; D011188:Potassium; D002118:Calcium