{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,21]],"date-time":"2025-09-21T17:54:39Z","timestamp":1758477279797},"reference-count":18,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2002,10,9]],"date-time":"2002-10-09T00:00:00Z","timestamp":1034121600000},"content-version":"vor","delay-in-days":281,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Microsurgery"],"published-print":{"date-parts":[[2002,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The purpose of this study was to determine whether nitric oxide (NO) plays a role in the mechanism of acute \u201cclassic\u201d as well as acute remote ischemic preconditioning (IP). Thirty\u2010two male Wistar rats were divided into five experimental groups. The rat cremaster flap in vivo microscopy model was used for assessment of ischemia\/reperfusion injury. In the control group (CG, n = 8), a 2\u2010hr flap ischemia was induced after preparation of the cremaster muscle. The animals of group NO (n = 6) received 500 nmol\/kg of the NO\u2010donor spermine\/nitric oxide complex (Sper\/NO) intravenously 30 min prior to ischemia. The group LN + P (L\u2010NAME + preclamping, n = 6) received 10 mg\/kg N\u03c9\u2010nitro\u2010L\u2010arginine methyl ester (L\u2010NAME) intravenously before preclamping of the flap pedicle (10\u2010min cycle length, 30\u2010min reperfusion). L\u2010NAME (10 mg\/kg) was administered in group LN + T (L\u2010NAME + tourniquet, n = 6) before ischemia of the right hindlimb was induced, using a tourniquet for 10 min after flap elevation. The limb was then reperfused for 30 min. Thereafter, flap ischemia was induced in each group as in group CG. In vivo microscopy was performed after 1 hr of flap reperfusion in each animal. Group NO demonstrated a significantly higher red blood cell velocity (RBV) in the first\u2010order arterioles and capillaries, a higher capillary flow, and a decreased number of leukocytes adhering to the endothelium (stickers) of the postcapillary venules by comparison to all other groups (<jats:italic>P<\/jats:italic> &lt; 0.05). The average capillary RBV and capillary flow were still higher in the CG than in the groups receiving L\u2010NAME (<jats:italic>P<\/jats:italic> &lt; 0.05). The data show that NO plays an important role in the mechanism of both acute \u201cclassic\u201d as well as acute remote IP, since the administration of a NO\u2010donor previous to ischemia simulates the effect of IP, whereas the nonspecific blocking of NO synthesis by L\u2010NAME abolishes the protective effect of flap preconditioning. \u00a9 2002 Wiley\u2010Liss, Inc. 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