Verapamil improves survival of rat hyperemic island skin flaps.
Inability to maintain cellular calcium homeostasis is a critical factor in the pathogenesis of cellular ischemic injury and may mediate oxygen radical release in the reperfusion period. We assessed the effect of the selective calcium channel blocker verapamil on the performance of rat hyperemic island skin flaps. Pretreatment with verapamil markedly improved survival of skin flaps after 6 hours of venous cross-clamping compared with animals receiving placebo only (99% vs 53.3%; p less than 0.01). Verapamil also prevented the formation of lipid peroxidation products and the depletion of the endogenous antioxidant glutathione, suggesting that the beneficial effect of verapamil is the result of protection against oxygen radical injury. After 12 hours of venous cross-clamping, verapamil did not improve survival of skin flaps despite protection against lipid peroxidation. Oxygen radical release is therefore a crucial event in the pathogenesis of skin flap necrosis after short-term ischemia but is of less significance in long-term ischemia.
Stein
H J
HJ
Department of Surgery, University of the Witwatersrand, Johannesburg, South Africa.
Fayman
M S
MS
Oosthuizen
M M
MM
Hinder
R A
RA
D000818:Animals; D003250:Constriction; D005609:Free Radicals; D005978:Glutathione / Q000378:metabolism; D006085:Graft Survival / Q000187:drug effects*; D006940:Hyperemia / Q000378:metabolism; D007511:Ischemia / Q000378:metabolism; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012867:Skin / Q000098:blood supply* / Q000378:metabolism; D013524:Surgical Flaps; D014700:Verapamil / Q000494:pharmacology*
D005609:Free Radicals; D008315:Malondialdehyde; D014700:Verapamil; D005978:Glutathione