title: Morphological, histochemical, and interstitial pressure changes in the tibialis anterior muscle before and after aortofemoral bypass in patients with peripheral arterial occlusive disease.
abstract: BACKGROUND
  Morphological and electrophysiological studies of ischemic muscles in peripheral arterial disease disclosed evidence of denervation and fibre atrophy. The purpose of the present study is to describe morphological changes in ischemic muscles before and after reperfusion surgery in patients with peripheral occlusive arterial disease, and to provide an insight into the effect of reperfusion on the histochemistry of the reperfused muscle.
  
  
  METHODS
  Muscle biopsies were obtained from the tibialis anterior of 9 patients with chronic peripheral arterial occlusive disease of the lower extremities, before and after aortofemoral bypass, in order to evaluate the extent and type of muscle fibre changes during ischemia and after revascularization. Fibre type content and muscle fibre areas were quantified using standard histological and histochemical methods and morphometric analysis. Each patient underwent concentric needle electromyography, nerve conduction velocity studies, and interstitial pressure measurements.
  
  
  RESULTS
  Preoperatively all patients showed muscle fibre atrophy of both types, type II fibre area being more affected. The mean fibre cross sectional area of type I was 3,745 microm2 and of type II 4,654 microm2. Fibre-type grouping, great variation in fibre size and angular fibres were indicative of chronic dennervation-reinnervation, in the absence of any clinical evidence of a neuropathic process. Seven days after the reperfusion the areas of both fibre types were even more reduced, being 3,086 microm2 for type I and 4,009 microm2 for type II, the proportion of type I fibres, and the interstitial pressure of tibialis anterior were increased.
  
  
  CONCLUSIONS
  The findings suggest that chronic ischemia of the leg muscles causes compensatory histochemical changes in muscle fibres resulting from muscle hypoxia, and chronic dennervation-reinnervation changes, resulting possibly from ischemic neuropathy. Reperfusion seems to bring the oxidative capacity of the previously ischemic muscle closer to normal.
authors.affiliation: Department of Physiology, Medical School, Aristotle University of Thessaloniki, Thessaloniki 54006, Greece. albani@med.auth.gr
authors.forename: Maria
authors.initials: M
authors.lastname: Albani
authors.forename: Angelos
authors.initials: A
authors.lastname: Megalopoulos
authors.forename: Dimitris
authors.initials: D
authors.lastname: Kiskinis
authors.forename: Sotirios A
authors.initials: SA
authors.lastname: Parashos
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Grigoriadis
authors.forename: Olympia
authors.initials: O
authors.lastname: Guiba-Tziampiri