| Summary of Background DataIn the past 30 years, because of rapid development of microsurgery, free flap transplantation by anastomosing smaller vessel had been a new important technology in plastic surgery for tissue transplantation, replantation, reconstruction and organ restoration. There still was 10 percent flap necrosis because of ischemia-reperfusion injury, despite every step of perisurgery of free flap transplantation was well done'1'. The pathophysiologic mechanism of flap ischemia-reperfusion injury mainly included: increased neutrophil infiltration in flap tissue, oxygen free radical injury, intracellular calcium overload, short of energy-rich phosphate and no reflow. Documents reported some medicines or methods for attenuating ischemia-reperfusion injury, including anti-adhesion-molecule monoclone antibody, free radical scavenger, immunosuppressant and energy-rich phosphate , hyperbaric oxygen, ischemic preconditioning et al. Nitric oxide was a free radical with extensive biological effect. It could maintain the tonicity of vascular smooth muscle; suppress plateletaggregation and adhesion; and regulate proliferation of vascular smooth muscle cell in cardio-vascular system. It participated in message delivery and coordination between nerves and vessels, and regulated viscera function in nervous system. As a pathophysiologic messenger, Nitric oxide got involved in inflammation and immunoreaction. There were many studies on the effect of NO on flap ischemia-reperfusion. But conclusions were very contradictive. Majority considered that NO protected flap from ischemia-reperfusion injury (2-7). Osei et al observed the change of transgenic sickle cell mice and normal mice after hypoxia and ischemia. There was no cNOS expression, and increased inducible iNOS expression in ischemic region and its round in transgenic sickle cell mice. There was no increased iNOS expression in normal mice. Moreover, the distribution of iNOS expression was disorder. Histological examination demonstrated there was less tissue injury in ischemic region of transgenic mice than that of normal mice. It indicated that iNOS protected mice from hypoxic and ischemic injury. Others considered that NO deteriorated ischemia-reperfusion injury[8-12),Turnage et al discovered that using specific inhibitor of iNOS before reperfusion could attenuated IR-induced pulmonary microvascular dysfunction in a rat intestinal IR model, but there was no attenuation using NOS inhibitor before reperfusion. Therefore, there were different results when using different models or NOS inhibitors.ObjectivesTo study whether L-Arginine (a precursor of NO) can protect flap from ischemia-reperfusion injury or deteriorate flap ischemia-reperfusion injury.Materials and methods1 .Animal model and experimental models25 female SD rats weighing 180-300 gm were used. An axial pattern flap of 6cm X 3cm was designed in right abdomen(Fig. 1,2). Rats were divided into 3 groups at random.ODSham group, 5 rats. There was no ischemia-reperfusion process.(2)Control group, 10 rats. A microvascular clamp was placed on the femoral artery proximal to the flap pedicle at the onset of ischemia. Blood flow of femoral artery and pedicle artery were confirmed to be fully blocked. After 10 hours ischemia,the clamp was removed, 1 ml normal saline was injected intraperitoneally 30 minutes before reperfusion.(3)L-Arg group, 10 rats.5% L-Arg solution (300mg/kg) was injected intraperitoneally 30 minutes before reperfusion.2.HistoIogicaI examinationA full thick biopsy was taken from center of flap after 22 hours operation in Sham group, and other full thick biopsies were taken from center of flap after 12 hours after reperfusion in control and L-Arg groups. Samples were placed in 40% formalin, and processed by paraffin embedding, and sectioned; then stained with hematoxylin and eosin. Sections were evaluated at 400 fold magnification under light microscope. Because PMN infiltration was mainly in subdartrous layer, we selected 10 random and nonoverlapping high-powe...
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