J Reconstr Microsurg 2000; Volume 16(Number 8): 0621-0628
DOI: 10.1055/s-2000-9380
Copyright © 2000 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel. +1(212)584-4662.

Initiation of Microvascular Protection by Nitric Oxide in Late Preconditioning

Wei Z. Wang, Gary L. Anderson, Shang Z. Guo, Tsu-Min Tsai, Frederick N. Miller
  • Division of Plastic Surgery, Department of Surgery, University of Nevada School of Medicine; Department of Physiology and Biophysics, University of Louisville School of Medicine; Center for Applied Microcirculatory Research, University of Louisville; and Christine M. Kleinert Institute for Hand and Micro Surgery, Louisville, Kentucky
Further Information

Publication History

Publication Date:
31 December 2000 (online)

ABSTRACT

-The authors hypothesized that nitric oxide is induced by a brief period of ischemia/reperfusion (ischemic preconditioning, IPC) on postoperative day (POD) 1, and that this released nitric oxide is responsible for initiating a delayed microvascular protection against a prolonged period of ischemia in skeletal muscle on POD day 2. The cremaster muscle of male Sprague-Dawley rats underwent 4 hr of ischemia, and then 60 min of reperfusion. IPC consisted of 45 min of ischemia but was done 24 hr before the prolonged ischemia. Local intraarterial infusion of sodium nitroprusside (SNP, a donor of nitric oxide) or Nw-nitro-L-arginine (L-NA, a nonselective nitric oxide synthase antagonist) were also given 24 hr before prolonged ischemia. Arteriole diameters and capillary perfusion were measured using intravital microscopy. Four groups were compared: 1) control; 2) IPC; 3) SNP + sham IPC; and 4) L-NA + IPC. Four hours of ischemia followed by reperfusion created a significant vasoconstriction and capillary no-reflow in the microcirculation of cremaster muscles. These alterations were largely prevented by IPC. Local intraarterial infusion of SNP without IPC created a similar microvascular protection to that induced by IPC alone. In contrast, intraarterial infusion of L-NA prior to IPC eliminated the IPC-induced microvascular protection. In conclusion, in late preconditioning, nitric oxide contributes to the initiation of a delayed microvascular protection against prolonged ischemia in skeletal muscle.