Neutrophils accumulate and contribute to skeletal muscle dysfunction after ischemia-reperfusion

Am J Physiol. 1990 Dec;259(6 Pt 2):H1809-12. doi: 10.1152/ajpheart.1990.259.6.H1809.

Abstract

Skeletal muscles subjected to ischemia and then reperfusion develop contractile dysfunction for reasons that are unclear. We found that rats pretreated with vinblastine 4 days before study had decreased numbers of blood neutrophils and increased gastrocnemius muscle function after ischemia (3h) and reperfusion (4 h) compared with untreated rats or rats treated 4 days before study with saline. By comparison, rats pretreated with vinblastine or saline 1 day before study had increased blood neutrophils and decreased gastrocnemius muscle contractile function after ischemia-reperfusion compared with untreated rats. In addition, numbers of neutrophils in gastrocnemius muscles paralleled numbers of blood neutrophils and correlated with gastrocnemius muscle edema and contractile function after ischemia and reperfusion. The results indicate that neutrophils accumulate and may play an important role in the genesis of skeletal muscle contractile dysfunction after ischemia-reperfusion.

MeSH terms

  • Animals
  • Edema / etiology
  • Ischemia / complications
  • Ischemia / pathology
  • Ischemia / physiopathology*
  • Leukocyte Count / drug effects
  • Male
  • Muscle Contraction / drug effects
  • Muscles / blood supply*
  • Muscles / physiopathology
  • Neutrophils / pathology
  • Neutrophils / physiology*
  • Rats
  • Rats, Inbred Strains
  • Reperfusion*
  • Sodium Chloride / pharmacology
  • Vinblastine / pharmacology

Substances

  • Sodium Chloride
  • Vinblastine