Effect of sustained limb ischemia on norepinephrine release from skeletal muscle sympathetic nerve endings

Neurochemistry International
Yosuke KurokoHidezo Mori

Abstract

Acute ischemia has been reported to impair sympathetic outflow distal to the ischemic area in various organs, whereas relatively little is known about this phenomenon in skeletal muscle. We examined how acute ischemia affects norepinephrine (NE) release at skeletal muscle sympathetic nerve endings. We implanted a dialysis probe into the adductor muscle in anesthetized rabbits and measured dialysate NE levels as an index of skeletal muscle interstitial NE levels. Regional ischemia was introduced by microsphere injection and ligation of the common iliac artery. The time courses of dialysate NE levels were examined during prolonged ischemia. Ischemia induced a decrease in the dialysate NE level (from 19+/-4 to 2.0+/-0 pg/ml, mean+/-S.E.), and then a progressive increase in the dialysate NE level. The increment in the dialysate NE level was examined with local administration of desipramine (DMI, a membrane NE transport inhibitor), omega-conotoxin GVIA (CTX, an N-type Ca(2+) channel blocker), or TMB-8 (an intracellular Ca(2+) antagonist). At 4h ischemia, the increment in the dialysate NE level (vehicle group, 143+/-30 pg/ml) was suppressed by TMB-8 (25+/-5 pg/ml) but not by DMI (128+/-10 pg/ml) or CTX (122+/-18 pg/ml). At 6h ischemi...Continue Reading

References

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Jun 25, 2003·Neurochemistry International·Noriyuki TokunagaHidezo Mori
Dec 4, 2003·European Journal of Pharmacology·Toshihide FujiiYasuo Matsumura

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Citations

Mar 31, 2007·Forensic Science International : Synergy·Bao-Li ZhuHitoshi Maeda
Apr 15, 2014·World Journal of Urology·Masataka SunagawaLori A Birder

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