Ischemia-reperfusion injury occurs when tissue is reperfused following a prolonged period of ischemia. It is a subject of interest to plastic surgeons involved in replantation, free tissue transfer, and composite tissue allotransplantation, as it can have a significant impact on the overall success of these procedures. The purpose of this article is to review the recent progress in the investigation of ischemia-reperfusion injury in skeletal muscle and skin and to highlight the potential clinical implications of therapeutic interventions aimed at reducing ischemia-reperfusion injury.

The level of evidence in The Journal has improved significantly over the last thirty years.

Tissue grafts and flaps are used to reconstruct wounds from trauma, chronic disease, tumor extirpation, burns, and infection. Despite careful surgical planning and execution, reconstructive failure can occur due to poor wound beds, radiation, random flap necrosis, vascular insufficiency, or ischemia-reperfusion (IR). Traumatic avulsions and amputated composite tissues-compromised tissue-may fail from crush injury and excessively large sizes. While never intended, these complications result in tissue loss, additional surgery, accrued costs, and negative psychosocial patient effects. Hyperbaric oxygen (HBO) has demonstrated utility in the salvage of compromised grafts/flaps. It can increase the likelihood and effective size of composite graft survival, improve skin graft outcomes, and enhance flap survival. Mechanisms underlying these beneficial effects include increased oxygenation, improved fibroblast function, neovascularization, and amelioration of IR injury. Common strategies for the compromised graft or flap include local wound care, surgical debridement, and repeated reconstruction. These modalities are associated with added costs, time, need for reoperation, morbidity, and psychosocial effects. Preservation of the amputated/avulsed tissues minimizes morbidity and maximizes the reconstructive outcome by salvaging the compromised tissue and obviating additional surgery. HBO is often overlooked as a potential tool that can limit these issues. Animal studies demonstrate a benefit of HBO in the treatment of compromised tissues. Clinical studies support these findings, but are limited to case reports and series. Further research is needed to provide multicenter prospective clinical studies and cost analyses comparing HBO to other adjunctive therapies in the treatment of compromised grafts/flaps.

The purpose of this study was to determine microcirculatory effects and response of nitric oxide synthase (NOS) to melatonin in skeletal muscle after prolonged ischemia. A vascular pedicle isolated rat cremaster muscle model was used. Each muscle underwent 4 hr of zero-flow warm ischemia followed by 2 hr of reperfusion. Melatonin (10 mg/kg) or saline as a vehicle was given by intraperitoneal injection at 30 min prior to reperfusion and the same dose was given immediately after reperfusion. After reperfusion, microcirculation measurements including arteriole diameter, capillary perfusion and endothelial-dependent and -independent vasodilatation were performed. The cremaster muscle was then harvested to measure endothelial NOS (eNOS) and inducible NOS (iNOS) gene expression and enzyme activity. Three groups of rats were used: sham-ischemia/reperfusion (I/R), vehicle + I/R and melatonin + I/R. As compared with vehicle + I/R group, administration of melatonin significantly enhanced arteriole diameter, improved capillary perfusion, and attenuated endothelial dysfunction in the microcirculation of skeletal muscle after 4 hr warm ischemia. Prolonged warm ischemia followed by reperfusion significantly depressed eNOS gene expression and constitutive NOS activity and enhanced iNOS gene expression. Administration of melatonin did not significantly alter NOS gene expression or activity in skeletal muscle after prolonged ischemia and reperfusion. Melatonin provided a significant microvascular protection from reperfusion injury in skeletal muscle. This protection is probably attributable to the free radical scavenging effect of melatonin, but not to its anti-inflammatory effect.

Ischaemia-induced tissue injury has wide-ranging clinical implications including myocardial infarction, stroke, compartment syndrome, ischaemic renal failure and replantation and revascularization. However, the restoration of blood flow produces a 'second hit' phenomenon, the effect of which is greater than the initial ischaemic event and characterizes ischaemiareperfusion (IR) injury. Some examples of potential settings of IR injury include: following thrombolytic therapy for stroke, invasive cardiovascular procedures, solid organ transplantation, and major trauma resuscitation. Pathophysiological events of IR injury are the result of reactive oxygen species (ROS) production, microvascular vasoconstriction, and ultimately endothelial cell-neutrophil adhesion with subsequent neutrophil infiltration of the affected tissue. Initially thought to increase the amount of free radical oxygen in the system, hyperbaric oxygen (HBO) has demonstrated a protective effect on tissues by influencing the same mechanisms responsible for IR injury. Consequently, HBO has tremendous therapeutic value. We review the biochemical mechanisms of ischaemia-reperfusion injury and the effects of HBO following ischaemia-reperfusion.

Residents were able to acquire a basic subset of microsurgical skills within a reasonable time period using these drills.

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