reversible injury

reversible injury

Pathology Ischemic changes–eg, of the myocardium, that can be reversed with timely return of normal circulation to the tissue of interest
McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.
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The objective is to produce a reversible injury, however, its shortcomings are the recurrence of pain and the necessity to repeat the ablative procedure.
The use of the tourniquet entails reversible injury triggered by ischemic conditions during determined periods of time [1-3].
Then, the recovery of the muscle tissue underwent to reversible injury should lead to a proper rearrangement spontaneously.
The observation that myocardial dysfunction found during sepsis is reversible also supports the idea of troponin release associated with reversible injury (Parker et al., 1984).
The erroneous application of the Batson process itself does not constitute a reversible injury.
This speculation has been supported by cardiac troponin release kinetics in certain clinical situations, which has led to the argument that perhaps cardiac troponin is released after reversible injury. The argument goes as follows: An early-releasable cytosolic pool of cardiac troponin (although whether this pool resides exclusively in the cytosol is not clear) appears to be responsible for the early release of cardiac troponin.
For preload increases, the cells die because of apoptosis; therefore, that does not appear to be a circumstance in which reversible injury occurs.
But it may also be speculated that late reabsorption of prilocain if it was injected within the myelin sheath or immediate healing of a small reversible injury of the neuronal fibers might have been the reasons.
Amiodarone, while a highly effective antidysrhythmic, has the potential to cause severe pulmonary toxicity, ranging from mild, reversible injury to pulmonary fibrosis.
Second, increases in cardiac troponin likely reflect irreversible rather than reversible injury, although there is continuing debate on this issue.
In contrast, plasma concentrations of neither mitochondrial nor cytosolic CK were increased in animals with 15 min or less of coronary occlusion despite extensive EKG and morphological evidence of ischemic reversible injury. Two animals that had only 15 min of coronary occlusion demonstrated minute areas of infarction and their plasma total CK was slightly but significantly increased (P = 0.01) over that in the sham-operated controls.
[17], studying the isolated guinea pig heart, showed that after 20 min of ischemia the heart exhibited good hemodynamic recovery despite enzyme release; they concluded that enzyme release reflects reversible injury. However, mechanical recovery does not exclude the presence of subendocardial infarction, which could account for the enzyme release.

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