AI Article Synopsis
- The study examined how the loss of dystrophin in heart cells affects their vulnerability to mechanical stress during reperfusion after ischemia.
- Dystrophin normally resides in the cell membrane of heart cells, but during ischemia it relocates to myofibrils and is lost upon reperfusion, leading to increased membrane fragility.
- The accumulation of Evans blue dye in cells lacking dystrophin indicates injury, but using a contractile blocker prevented this accumulation, suggesting that the loss of dystrophin plays a role in reperfusion injuries related to contractile force.
Article Abstract
Because the absence of sarcolemmal dystrophin renders cardiomyocytes vulnerable to mechanical force, the present study investigated whether sarcolemmal membrane fragility upon reperfusion is associated with the loss of membrane dystrophin. Dystrophin was distributed exclusively in the sarcolemmal membrane of buffer-perfused rat cardiomyocytes, but was translocated to the myofibrils during 30 min of ischemia and then lost during reperfusion. Upon reperfusion, the membrane impermeable dye, Evans blue (EB), accumulated in cardiomyocytes depleted of dystrophin. Reperfusion with the contractile blocker 2,3-butanedione monoxime (BDM) resulted in no accumulation of EB in cardiomyocytes despite the loss of dystrophin. Upon withdrawal of BDM, however, EB accumulated in dystrophin-depleted cardiomyocytes. Loss of sarcolemmal dystrophin may be involved in the mechanism of contractile force-induced reperfusion injury.
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| http://dx.doi.org/10.1253/circj.67.725 | DOI Listing |
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