Effect of hypothermia on the ischemic and reperfused rat skeletal muscle, monitored by in vivo ³¹p‐magnetic resonance spectroscopy

Abstract

The aim of this study was to compare the ischemic and postischemic energetic changes of rat skeletal muscle in response to hypothermia or room temperature, monitored noninvasively and continuously by in vivo (31)P-magnetic resonance spectroscopy ((31)P-MRS). A model of pedicled rat rectus femoris muscle was developed and analyzed by in vivo (31)P-MRS at a magnetic field strength of 2.35 T. Measurements were performed at three time points: before ischemia, after 4 hours of ischemia, and after 1 hour of reperfusion. Three groups were studied: (1) sham-operated rats (n = 6); (2) rats subjected to room temperature (24-26 degrees C, n = 6); and (3) rats subjected to hypothermia (9-12 degrees C, n = 6). Blood perfusion was measured by laser Doppler flowmetry (LDF). In the hypothermic group, phosphocreatine (PCr) recovered to 75% and adenosine triphosphate (ATP) to 86%; in the room temperature group, the recovery was 53% and 51%, respectively (P < 0.05). Skeletal muscle subjected to hypothermia (9-12 degrees C) was found to recover to a higher postischemic energetic level compared with skeletal muscle subjected to room temperature. Hypothermia appears to be a simple and effective method with which to reduce the damage related to ischemia and reperfusion.

Ischemic preconditioning of free muscle flaps: An experimental study

“…In rat muscle flaps subjected to hypothermia, the energetic stores (phosphocreatine, adenosine triphosphate) recover to a higher level after ischemia than do flaps subjected to the same conditions but at room temperature; therefore the latter is a negative factor for flap viability to a transfer. 52 Our flaps were kept at room temperature (approximately 23À24°C), and in ischemia groups B (4 h) and C (6 h), there was either partial or total necrosis of flaps due to the ischemia-induced inadequate recovery of the energetic stores and cell death. On the other hand, based on previous studies, in preconditioned groups D and E, we can postulate that in our experiments the influence of temperature was minor, and the viability of flaps was due to the preconditioning protocol, since room temperature is not beneficial for flap storage before a free transfer.…”

Improved energetic recovery of skeletal muscle in response to ischemia and reperfusion injury followed by in vivo 31P‐magnetic resonance spectroscopy

“…This spurred us to investigate the effect of SOE on skeletal muscle subjected to ischemia and reperfusion, followed continuously and noninvasively by 31 P-MRS. A pedicled rat rectus femoris muscle model, developed in an earlier study, was used. 12 In this model, ischemia time was set to 4 h and reperfusion to 1 h, since a moderate deep ischemia, and not a complete recovery, was shown after these time intervals. The muscle was analyzed for phosphorus metabolites by in vivo 31 P-MRS, by placing the rectus femoris muscle on the coil outside the rat body.…”

“…In a previous in vivo rat rectus femoris study, hypothermia-treated animals showed a positive postischemic effect on the energy state in the skeletal muscle. 12 A new noninvasive method might be singlet oxygen energy (SOE). Singlet oxygen, O 2 ( 1 D g ), a highly reactive form of oxygen, can be produced photochemically by energy transfer from an excited photosensitizer.…”

“…12 The rats were anesthetized with mebumal (36 mg/kg body weight) intraperitoneally, and anesthesia supplementation (mebumal, 2 mg/kg body weight) was administered intraperitoneally as required. The left rectus femoris muscle was used in each rat, leaving the right side unexposed.…”