The case of missing skin: Congenital Volkmann ischemic contracture

2020 ◽  
Vol 37 (4) ◽  
pp. 762-763
Author(s):  
Kathleen M. Coerdt ◽  
Emily L. Guo ◽  
Karl M. Saardi ◽  
Kaiane A. Habeshian
Keyword(s):  
Ischemic Contracture

VOLKMANN’S ISCHEMIC CONTRACTURE OF THE UPPER EXTREMITY

Hand Clinics ◽  
1998 ◽  
Vol 14 (3) ◽  
pp. 483-497
Author(s):  
Michael J. Botte ◽  
Mary Ann E. Keenan ◽  
Richard H. Gelberman
Keyword(s):  
Upper Extremity ◽  
Ischemic Contracture

Ischemic Contracture

1979 ◽  
pp. 232-235
Author(s):  
H. R. Mittelbach
Keyword(s):  
Ischemic Contracture

Flexor Sliding Operation for Established Volkmann's Ischemic Contracture

1993 ◽  
Vol 28 (3) ◽  
pp. 1199
Author(s):  
Ik Kong Kim ◽  
Poong Taek Kim ◽  
Byung Chul Park ◽  
Suck Han
Keyword(s):  
Ischemic Contracture

scholarly journals Correlation of mitochondrial function and ischemic contracture

1980 ◽  
Vol 79 (4) ◽  
pp. 570-578 ◽  
Author(s):  
James D. Sink ◽  
William D. Currie ◽  
Gary L. Pellom ◽  
Ronald C. Hill ◽  
W. Randolph Chitwood ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Ischemic Contracture

Mechanism of ischemic contracture in ferret hearts: relative roles of [Ca2+]i elevation and ATP depletion

1990 ◽  
Vol 258 (1) ◽  
pp. H9-H16 ◽  
Author(s):  
Y. Koretsune ◽  
E. Marban
Keyword(s):  
Atp Depletion ◽  
Free Calcium ◽  
Coronary Perfusion ◽  
Ischemic Contracture ◽  
Steady Level ◽  
Intracellular Free Calcium Concentration ◽  
Free Calcium Concentration ◽  
Cross Bridges ◽  
Time Required ◽  
Mean Time

When coronary perfusion is interrupted, the diastolic force generated by the myocardium first falls but eventually increases. The delayed rise in force, ischemic contracture, has been attributed either to ATP depletion or to elevation of the intracellular free calcium concentration ([Ca2+]i). To distinguish between these possibilities, we measured [Ca2+]i and ATP concentration [( ATP]) in ferret hearts using nuclear magnetic resonance (NMR) spectroscopy. Mean time-average [Ca2+]i and [ATP] equaled 0.25 microM and 2.7 mumol/g wet wt, respectively, under control perfusion conditions. [Ca2+]i increased and [ATP] fell during total global ischemia. Although [Ca2+]i exceeded the usual systolic levels of 1.7 microM within 20-25 min of ischemia and reached a steady level between 2 and 3 microM by 30-35 min, force only began to rise after 40 min. In contrast, the time required for [ATP] to fall to less than 10% of control levels coincided closely with the onset of contracture. Ischemia in the presence of iodoacetate, an inhibitor of glycolysis, led to a precipitous fall in [ATP] and a concomitant rise in force, both of which preceded any elevation of [Ca2+]i. Thus changes in [Ca2+]i are neither sufficient nor necessary for the initiation of ischemic contracture. We conclude that ATP depletion is primary and that the rise in resting force reflects the formation of rigor cross bridges.

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