Carnitine is an endogenous cofactor involved in the transport of long-chain fatty acids into the mitochondria where they undergo beta-oxidation. Through another reaction, carnitine produces free coenzyme A and reduces the ratio of acetyl-coenzyme A to coenzyme A, thereby enhancing oxidative use of glucose, augmenting adenosine triphosphate synthesis, and reducing lactate production and acidosis. Because of its regulatory action on the energy flow from the different oxidative sources, especially under ischemic conditions, carnitine has been used in cardiovascular diseases such as coronary heart disease, congestive heart failure, peripheral vascular disease, dyslipidemia, diabetes, and chronic renal diseases with satisfactory results. A flap is also a relatively ischemic tissue and may obtain benefit from carnitine. To investigate this, 30 rats were divided into three groups of 10 animals: a control group and two carnitine-treated groups. Random dorsal skin flaps were elevated on the rats. In the control group, no pharmacologic agents were used. Of the two treated groups, group 1 was treated with 50 mg/kg/day carnitine for 1 week and group 2 was treated with 100 mg/kg/day carnitine for 1 week. The areas of flap necrosis were measured in each group. The median areas of flap necrosis of the groups were 12.55, 9.23, and 4.9 cm2, respectively. There was a statistically significant improvement of flap necrosis in carnitine-treated groups compared with the control group (group 2, p = 0.001; group 3, p = 0.000). Furthermore, there was less necrosis in the high-dose carnitine-treated group than the low-dose carnitine-treated group. As a conclusion, carnitine may have a dose-dependent effect to increase flap survival in random skin flaps.