The effects of the nitric oxide donor SIN-1 on ischemia-reperfused cutaneous and myocutaneous flaps

被引:28
作者
Khiabani, KT
Kerrigan, CL
机构
[1] Dartmouth Hitchcock Med Ctr, Lebanon, NH 03766 USA
[2] Univ Nevada, Sch Med, Div Plast Surg, Las Vegas, NV 89154 USA
[3] McGill Univ, Royal Victoria Hosp, Microsurg Res Labs, Montreal, PQ H3A 1A1, Canada
关键词
D O I
10.1097/00006534-200207000-00028
中图分类号
R61 [外科手术学];
学科分类号
摘要
Ischemia-reperfusion injure, causes tissue damage that leads to a decrease in bioavailability of nitric oxide. The authors hypothesized that an exogenous supply of nitric oxide will have beneficial effects on survival of skin and skeletal muscle subjected to ischemia-reperfusion injury. By using the nitric oxide donor SIN-1 (3-morpholino-sydnonimine) the effects of direct intraarterial infusion of an exogenous source of nitric oxide in reperfused flags was studied. Bilateral island buttock skin flaps and latis-simus dorsi myocutaneous flaps were elevated in eight pigs, for a total of 32 flaps. Flaps were subjected to 6 hours of ischemia followed by 18 hours of reperfusion. Flaps on one side of each animal were randomized to be treated with the nitric oxide donor (treatment group). The contralateral side was treated with an equivalent volume of saline vehicle (infusion control) SIN-1, or saline was administered as a continuous direct intraarterial infusion at the onset of reperfusion and continued during the observation period. Outcomes measured were tissue neutrophil accumulation by using myeloperoxidase assay and tissue survival (intravenous fluorescein and nitroblue tetrazolium for skin and muscle, respectively). In both skin and myocutaneous flaps, SIN-1 treatment caused a significant improvement in survival and a decrease in neutrophil accumulation. Nitric oxide may play an important role in the pathophysiologic process of ischemia-induced reperfusion injury in skin and skeletal muscle. Nitric oxide donors may be a promising family of therapeutic agents for the prevention of ischemia-induced reperfusion injury in cutaneous and myocutaneous flaps.
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页码:169 / 176
页数:8
相关论文
共 48 条
[1]   PROTECTION AGAINST GASTRIC ISCHEMIA-REPERFUSION INJURY BY NITRIC-OXIDE GENERATORS [J].
ANDREWS, FJ ;
MALCONTENTIWILSON, C ;
OBRIEN, PE .
DIGESTIVE DISEASES AND SCIENCES, 1994, 39 (02) :366-373
[2]   MEASUREMENT OF CUTANEOUS INFLAMMATION - ESTIMATION OF NEUTROPHIL CONTENT WITH AN ENZYME MARKER [J].
BRADLEY, PP ;
PRIEBAT, DA ;
CHRISTENSEN, RD ;
ROTHSTEIN, G .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1982, 78 (03) :206-209
[3]   Use of a nitric oxide precursor to protect pig myocutaneous flaps from ischemia-reperfusion injury [J].
Cordeiro, PG ;
Santamaria, E ;
Hu, QY .
PLASTIC AND RECONSTRUCTIVE SURGERY, 1998, 102 (06) :2040-2048
[4]   DIFFERENTIAL SENSITIVITY OF PROXIMAL AND DISTAL CORONARY-ARTERIES TO A NITRIC-OXIDE DONOR FOLLOWING REPERFUSION INJURY OR INHIBITION OF NITRIC-OXIDE SYNTHESIS [J].
COUGHLAN, MG ;
KENNY, D ;
KAMPINE, JP ;
BOSNJAK, ZJ ;
WARLTIER, DC .
CARDIOVASCULAR RESEARCH, 1993, 27 (08) :1444-1448
[5]   INHIBITION OF ENDOTHELIAL-DERIVED NITRIC-OXIDE PROMOTES P-SELECTIN EXPRESSION AND ACTIONS IN THE RAT MICROCIRCULATION [J].
DAVENPECK, KL ;
GAUTHIER, TW ;
LEFER, AM .
GASTROENTEROLOGY, 1994, 107 (04) :1050-1058
[6]   CONSTITUTIVE NITRIC-OXIDE RELEASE IS IMPAIRED AFTER ISCHEMIA AND REPERFUSION [J].
ENGELMAN, DT ;
WATANABE, M ;
ENGELMAN, RM ;
ROUSOU, JA ;
FLACK, JE ;
DEATON, DW ;
DAS, DK .
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, 1995, 110 (04) :1047-1053
[7]  
FUJINO K, 1991, J PHARMACOL EXP THER, V256, P371
[8]   THE OPPOSING EFFECTS OF AN INHIBITOR OF NITRIC-OXIDE SYNTHESIS AND OF A DONOR OF NITRIC-OXIDE IN RABBITS UNDERGOING MYOCARDIAL-ISCHEMIA REPERFUSION [J].
FUNG, KP ;
WU, TW ;
ZENG, LH ;
WU, J .
LIFE SCIENCES, 1994, 54 (26) :PL491-PL496
[9]   ENDOTHELIUM-DERIVED RELAXING AND CONTRACTING FACTORS [J].
FURCHGOTT, RF ;
VANHOUTTE, PM .
FASEB JOURNAL, 1989, 3 (09) :2007-2018
[10]   NITRIC-OXIDE ATTENUATES LEUKOCYTE-ENDOTHELIAL INTERACTION VIA P-SELECTIN IN SPLANCHNIC ISCHEMIA-REPERFUSION [J].
GAUTHIER, TW ;
DAVENPECK, KL ;
LEFER, AM .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 1994, 267 (04) :G562-G568