TY - JOUR
T1 - Surface ultrastructural features of isolated perfused rat hearts during calcium paradox
AU - Ashraf, M.
AU - Onda, M.
AU - Benedict, J.
AU - Hirohata, Y.
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 1981
Y1 - 1981
N2 - Cellular damage caused by calcium (Ca++) paradox is of significant importance under both experimental and clinical conditions. Electron microscopy was used to study the surface changes of the isolated rat hearts perfused with normal Krebs-Henseleit (KH) medium, Ca++ -free KH medium, Ca++- free KH medium followed by normal KH medium. The hearts perfused with Ca++ -free medium and normal KH medium showed elongated parallel myofibrils with transverse ridges spaced at regular intervals. The major change in Ca++ -free hearts consisted of wide cellular separation. For the Ca++ -paradox hearts, the myofibrils were twisted and narrowed at several locations. The myocardial fiber surfaces were bulged out, frequently with sarcolemmal ruptures and holes. Supercontraction of cells caused breaks in the sarcolemma and aggregation of mitochondria at the cell periphery. These results suggest that Ca++ -depletion primarily affects the myocardial cell junctions which, following reintroduction of Ca++, accelerate the entry of Ca++ into the cells, supercontraction of cells and stretching of sarcolemma.
AB - Cellular damage caused by calcium (Ca++) paradox is of significant importance under both experimental and clinical conditions. Electron microscopy was used to study the surface changes of the isolated rat hearts perfused with normal Krebs-Henseleit (KH) medium, Ca++ -free KH medium, Ca++- free KH medium followed by normal KH medium. The hearts perfused with Ca++ -free medium and normal KH medium showed elongated parallel myofibrils with transverse ridges spaced at regular intervals. The major change in Ca++ -free hearts consisted of wide cellular separation. For the Ca++ -paradox hearts, the myofibrils were twisted and narrowed at several locations. The myocardial fiber surfaces were bulged out, frequently with sarcolemmal ruptures and holes. Supercontraction of cells caused breaks in the sarcolemma and aggregation of mitochondria at the cell periphery. These results suggest that Ca++ -depletion primarily affects the myocardial cell junctions which, following reintroduction of Ca++, accelerate the entry of Ca++ into the cells, supercontraction of cells and stretching of sarcolemma.
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M3 - Article
C2 - 7330571
AN - SCOPUS:0019393429
SN - 0586-5581
VL - 1981
SP - 109
EP - 114
JO - Scanning Electron Microscopy
JF - Scanning Electron Microscopy
IS - 3
ER -