Loss of intracellular dystrophin: a potential mechanism for myocardial reperfusion injury.

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.

• Authors: Shiori Kyoi, Hajime Otani, Tomohiko Sumida, Takayuki Okada, Motohiko Osako, Hiroji Imamura, Hiroshi Kamihata, Hiroaki Matsubara, Toshiji Iwasaka
• Journal: Circulation journal : official journal of the Japanese Circulation Society (Circ J) Vol. 67 Issue 8 Pg. 725-7 (Aug 2003) ISSN: 1346-9843 [Print] Japan
• PMID: 12890920 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Coloring Agents
• Dystrophin
• diacetylmonoxime
• Evans Blue
• Diacetyl

Topics

• Animals
• Biological Transport
• Coloring Agents (pharmacokinetics)
• Diacetyl (analogs & derivatives, pharmacology)
• Dystrophin (deficiency)
• Evans Blue (pharmacokinetics)
• Fluorescent Antibody Technique
• Immunoblotting
• Male
• Myocardial Contraction (drug effects)
• Myocardial Ischemia (metabolism)
• Myocardial Reperfusion Injury (etiology)
• Myocardium (metabolism)
• Myocytes, Cardiac (metabolism)
• Myofibrils (metabolism)
• Rats
• Rats, Sprague-Dawley
• Sarcolemma (metabolism)