Arginine suppletion in free TRAM flap Introduction In recent decades, tremendous progress in free flap surgery has taken place.1 Specifically, improved knowledge of vascular territories and flap design has significantly reduced free flap surgery–associated morbidity.2 Despite these improvements, there is still considerable morbidity associated with either partial or total flap loss. Partial flap loss occurs in free flaps and pedicle flaps and is most commonly the result of microvascular perfusion failure.3,4. Partial flap loss is caused by the incapability of the vascular pedicle to provide sufficient microvascular perfusion in distal segments of the flap on top of the ischemia‐ reperfusion injury that occurs in the whole flap. The subsequent reperfusion injury results from increased leukocyte adhesion and migration into the capillaries, which leads to further tissue injury, increased microvascular permeability, and edema. In addition, elevated tissue pressure and inflammation will reduce microvascular perfusion and result in further deterioration and tissue loss. Because the amount of collateral microcirculation is less at greater distances from the vascular pedicle, the distal part of a free flap is more vulnerable to reduced microvascular circulation and ischemia‐reperfusion injury. Therefore, specifically the distal parts of a free flap are affected by these processes and may lead to distal partial flap loss.5 Because of the superficial localization and accessibility for measurements, free flap surgery provides an ideal opportunity for clinical studies regarding reperfusion injury flap surgery. Several studies have been published with experimental models and have shown improved flap survival with either a systemic approach with pharmacologic interventions or with local procedures.6‐8 It is widely accepted that the arginine–nitric oxide pathway plays a pivotal role in microvascular perfusion and the pathophysiology of ischemia‐reperfusion injury. Therefore, the nitric oxide pathway was studied in numerous studies in relation to its use in reducing ischemia‐reperfusion injury.9–14 The amino acid arginine is the sole precursor of nitric oxide. Arginine can be converted into nitric oxide and the amino acid citrulline by a family of tree isoforms of nitric oxide synthase.15,16 Nitric oxide scavenges free radicals, released during reperfusion. Nitric oxide also is an important and potent vasodilator and prevents aggregation and activation of neutrophils and platelets.17 Therefore, increasing nitric oxide production by stimulating the arginine–nitric oxide pathway may reduce the severity of ischemia‐reperfusion injury. Earlier experimental studies in animals in which arginine was given intravenously showed a substantial reduction of ischemia‐reperfusion injury in cutaneous and musculocutaneous flaps.18,19 Despite promising results in animals, data in humans are lacking. The free transverse rectus abdominis myocutaneous (TRAM) flap is used as a clinical surgical model with which to study the effect of arginine on microcirculatory blood flow and tissue viability. It is a frequently used free flap in breast reconstruction with well‐established surgical 87
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