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Ischemia‐reperfusion injury in rat skeletal muscle assessed with T 2 ‐weighted and dynamic contrast‐enhanced MRI
Author(s) -
Loerakker S.,
Oomens C. W. J.,
Manders E.,
Schakel T.,
Bader D. L.,
Baaijens F. P. T.,
Nicolay K.,
Strijkers G. J.
Publication year - 2011
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/mrm.22801
Subject(s) - ischemia , perfusion , hindlimb , skeletal muscle , medicine , reperfusion injury , contrast (vision) , magnetic resonance imaging , soft tissue , cardiology , anatomy , pathology , nuclear medicine , radiology , artificial intelligence , computer science
Pressure ulcers are localized areas of soft tissue breakdown due to mechanical loading. Susceptible individuals are subjected to pressure relief strategies to prevent long loading periods. Therefore, ischemia‐reperfusion injury may play an important role in the etiology of pressure ulcers. To investigate the inter‐relation between postischemic perfusion and changes in skeletal muscle integrity, the hindlimbs of Brown Norway rats were subjected to 4‐h ischemia followed by 2‐h reperfusion. Dynamic contrast‐enhanced MRI was used to examine perfusion, and changes in skeletal muscle integrity were monitored with T 2 ‐weighted MRI. The dynamic contrast‐enhanced MRI data showed a heterogeneous postischemic profile in the hindlimb, consisting of areas with increased contrast enhancement (14–76% of the hindlimb) and regions with no‐reflow (5–77%). For T 2 , a gradual increase in the complete leg was observed during the 4‐h ischemic period (from 34 to 41 msec). During the reperfusion phase, a heterogeneous distribution of T 2 was observed. Areas with increased contrast enhancement were associated with a decrease in T 2 (to 38 msec) toward preischemic levels, whereas no‐reflow areas exhibited a further increase in T 2 (to 42 msec). These results show that reperfusion after prolonged ischemia may not be complete, thereby continuing the ischemic condition and aggravating tissue damage. Magn Reson Med, 2011. © 2011 Wiley‐Liss, Inc.