ANALYSIS OF HIGH-ENERGY PHOSPHOMETABOLITES IN DELAYED EXPERIMENTAL SKIN FLAPS USING P-31 NUCLEAR-MAGNETIC-RESONANCE SPECTROSCOPY

Using (31)phosphorus magnetic resonance spectroscopy (P-31-MRS) and su rface coils, we noninvasively assessed the intracellular changes in de layed skin flaps of the high-energy phosphometabolites, ATP and phosph ocreatine, 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 i ts caudal base divided after a delay period of 2 weeks. MRS spectra we re collected at four times: immediately, 1 week and :! weeks after ele vation of the bipedicled flap, and 18 hours after division of its caud al base. From the spectra, we calculated the intracellular pH and the following ratios: Pi/PCr; PCr/(PCr + Pi), ATP/(PCr + Pi) (PCr, phospho creatine; 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 hour s later. The length of the surviving area was longer in,the delayed fl aps than in the undelayed flaps. Intracellular pH and ATP/(PCr + Pi) s howed no significant alteration in the delayed skin flaps, not only du ring the delay period but also after conversion of the flaps into cran ially based flaps by division of their caudal base. In contrast, PCr/( PCr + Pi) decreased with each surgical procedure (bipedicled flap elev ation and base division). Compared with the necrotic distal portion of the undelayed flaps, the surviving distal portion of the delayed flap s had higher levels of intracellular pH and ATP/(PCr + Pi) and lower l evels of PCr/(PCr + Pi). Intracellular pH and ATP/(PCr + Pi) showed a strong correlation with the viability of the delayed and undelayed ski n flaps, and they can be prognostic indices for predicting the fate of skin flags. The reason the surviving distal portions of the delayed f laps 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 kin ase/phosphocreatine system.