1 We have examined the role of nitric oxide (NO) in a model of functional angiogenesis in which survival of a skin¯ap depends entirely on angiogenesis to provide an arterial blood supply to maintain tissue viability. 2 The dierent eects of nitric oxide synthase (NOS) inhibitors on rat skin¯ap survival appeared to be explained on the basis of their NOS isoform selectivity. Skin¯ap survival was decreased by iNOS-selective (inducible NOS) inhibitors, S-methyl-isothiourea, aminoguanidine and aminoethylthiorea; unaected by the non-selective inhibitor nitro-imino-L-ornithine; and enhanced by the cNOS (constitutive NOS, that is endothelial NOS (eNOS) and neuronal NOS (nNOS)) inhibitor, nitro-L-arginine methyl ester. 3 Skin¯ap survival was reduced in mice with targeted disruption of the iNOS gene (iNOS knockout mice), and the administration of nitro-L-arginine methyl ester signi®cantly increased¯ap survival in iNOS knockout mice (P50.05). 4 iNOS immunoreactivity was identi®ed in mast cells in the angiogenic region. Immunoreactive vascular endothelial growth factor (VEGF) and basic ®broblast growth factor were also localized to mast cells. 5 The combination of interferon-g and tumour necrosis factor-a induced NO production and increased VEGF levels in mast cells cultured from bone marrow of wild-type, but not iNOS KO mice. 6 The increased tissue survival associated with the capacity for iNOS expression may be related to iNOS-dependent enhancement of VEGF levels and an ensuing angiogenic response. Our results provide both pharmacological and genetic evidence that iNOS activity promotes survival of ischaemic tissue.

We used the rat medial gastrocnemius free flap, based on a pedicle of the femoral artery and vein, in order to test the tolerance of skeletal muscle to cold ischemia‐reperfusion (IR) injury, and to determine whether tolerance can be enhanced by pre‐ischemic perfusion with tissue/organ preservation solutions. Muscle flaps (n = 6 per group) were subjected to variable periods of cold storage (0, 1, 2, 3, or 4 days) and 24‐h normothermic reperfusion. Muscle viability, as determined by nitroblue tetrazolium (NBT) histochemical staining of viable mitochondria and supported by histological examination, was 100%, 26%, 11%, 4%, and 1%, respectively. Using 24‐h cold storage/24‐h reperfusion as the experimental conditions, groups of muscle flaps (n = 5 per group) were perfused immediately before cold storage with either modified, colloid‐free University of Wisconsin (UW) solution, a solution described by Kohout et al. (Br J Plast Surg 1995;48:132–144) or normal saline. Perfusion with modified UW solution or Kohout's solution increased survival to 33% (P < 0.05) and 28% (not statistically significant), respectively, compared with the 19% viability of separate groups of nonperfused or saline‐perfused controls. These findings indicate that cold‐stored skeletal muscle is highly susceptible to cold IR injury and that the viability can be increased by prior perfusion with a tissue preservation solution such as modified UW solution. © 2000 Wiley‐Liss, Inc. MICROSURGERY 20:343–349 2000

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