Analysis of high-energy phosphometabolites in delayed experimental skin flaps using 31P nuclear magnetic resonance...

Using 31phosphorus magnetic resonance spectroscopy (31P-MRS) and surface coils, we noninvasively assessed the intracellular changes in delayed skin flaps of the high-energy phosphometabolites, ATP and phosphocreatine, which are basic energy sources of living cells. In 5 rats, a 3.5 x 7.5 cm bipedicled skin flap was elevated from the dorsum and its caudal base divided after a delay period of 2 weeks. MRS spectra were collected at four times: immediately, 1 week and 2 weeks after elevation of the bipedicled flap, and 18 hours after division of its caudal base. From the spectra, we calculated the intracellular pH and the following ratios: Pi/PCr, PCr/(PCr + Pi), ATP/(PCr + Pi) (PCr, phosphocreatine; Pi, inorganic phosphate; ATP, adenosine triphosphate). As an undelayed control group, cranially based skin flaps of the same size were elevated in another 5 rats, and MRS spectra were obtained 18 hours later. The length of the surviving area was longer in the delayed flaps than in the undelayed flaps. Intracellular pH and ATP/(PCr + Pi) showed no significant alteration in the delayed skin flaps, not only during the delay period but also after conversion of the flaps into cranially based flaps by division of their caudal base. In contrast, PCr/(PCr + Pi) decreased with each surgical procedure (bipedicled flap elevation and base division). Compared with the necrotic distal portion of the undelayed flaps, the surviving distal portion of the delayed flaps had higher levels of intracellular pH and ATP/(PCr + Pi) and lower levels of PCr/(PCr + Pi). Intracellular pH and ATP/(PCr + Pi) showed a strong correlation with the viability of the delayed and undelayed skin flaps, and they can be prognostic indices for predicting the fate of skin flaps. The reason the surviving distal portions of the delayed flaps maintained their level of ATP despite the low intracellular level of PCr may be that the accumulation of mitochondrial creatine kinase enhances the so-called 'energy transport' function of the creatine kinase/phosphocreatine system.