A Novel Mechanism for Myocardial Stunning Involving Impaired Ca 2+ Handling

Publisher Website
Google Scholar
Abstract
The mechanism of myocardial stunning has been studied extensively in rodents and is thought to involve a decrease in Ca2+ responsiveness of the myofilaments, degradation of Troponin I (TnI), and no change in Ca2+ handling. We studied the mechanism of stunning in isolated myocytes from chronically instrumented pigs. Myocytes were isolated from the ischemic (stunned) and nonischemic (normal) regions after 90-minute coronary stenosis followed by 60-minute reperfusion. Baseline myocyte contraction was reduced, PP2+ transients (stunned, 0.33±0.04 versus normal, 0.49±0.05, P2+-current density (stunned, −4.8±0.4 versus normal, −6.6±0.4 pA/pF, P2+ ATPase (SERCA2a), and phospholamban protein quantities. However, the fraction of phosphorylated phospholamban monomer was reduced in stunned myocardium. In rats, stunned myocytes demonstrated reduced systolic contraction but actually accelerated relaxation and no change in Ca2+ transients. Thus, mechanisms of stunning in the pig are radically different from the widely held concepts derived from studies in rodents and involve impaired Ca2+ handling and dephosphorylation of phospholamban, but not TnI degradation.

This publication has 23 references indexed in Scilit: