Alterations to subplasmalemmal leptomeres in adult canine myocytes during total in vitro ischemia.
Published evidence suggests that ischemia-induced cell swelling renders myocytes vulnerable to plasmalemmal disruption and consequent cell death. Alterations to the myocyte cytoskeleton may be involved in the pathogenesis of this plasmalemmal injury. One putative cytoskeletal structure in cardiac muscle that has received little consideration is the subplasmalemmal network of periodic densities with linking microfilaments termed leptomeres or leptofibrils. We demonstrate these structures in dog heart papillary muscle and describe the improvement in their definition brought about by tissue fixation at 37 degrees C in 2% glutaraldehyde with addition of 0.05 M lysine-HCl, followed by brief postfixation with osmium tetroxide. Alterations to leptomeres during ischemic injury were examined in myocardium subjected to total in vitro ischemia for 30-180 min at 37 degrees C. Leptomeres showed little morphological alteration during the first 90-120 min, after which leptomere periodic densities (striae) increased in size, from 10-20 to 50-80 nm, and were more densely stained. The leptomeres eventually (150-180 minutes) lose definition. The course of these alterations coincided with the appearance of ultrastructural evidence of irreversible ischemic injury to the myocytes.
Sage
M D
MD
Department of Pathology, Duke University Medical Center, Durham, North Carolina.
Jennings
R B
RB
D000818:Animals; D003326:Coronary Circulation; D003599:Cytoskeleton / Q000473:pathology*; D004285:Dogs; D005260:Female; D005404:Fixatives; D066298:In Vitro Techniques; D008297:Male; D008854:Microscopy, Electron; D009206:Myocardium / Q000473:pathology* / Q000648:ultrastructure; D009210:Myofibrils / Q000473:pathology*; D012518:Sarcomeres / Q000473:pathology*; D013696:Temperature
D005404:Fixatives