The results indicate that rapid IPC protects the spinal cord against neuronal damage 24 h but not 7 days after reperfusion in a rabbit model of spinal cord ischemia, suggesting that the efficacy of rapid IPC may be transient.

We investigated the influence of induced hypothermia on temperature-adjusted hemostasis function tests in rabbits using Sonoclot Analyzer and Thromboelastography. Induced hypothermia delayed the coagulation cascade and reduced platelet function. The conventional coagulation tests performed at 37 degrees C failed to detect these hypothermia-induced degradations in hemostasis performance.

If a train of pulses were used for transcranial stimulation, low-dose propofol can be effectivelyused as a supplement to ketamine-based anesthesia during intraoperative monitoring of myogenic MEPs. Addition of propofol significantly reduced the ketamine-induced psychedelic effects.

The results in the current study show that SCI induced white matter injury as well as gray matter injury in a rabbit model of SCI. The time course for 14 days after reperfusion may differ among the gray and white matter damages and hind-limb motor function in rabbits subjected to SCI.

The aim of the current study was to investigate whether there are differences in amplitudes and intrapatient variability of motor evoked potentials to five pulses of transcranial electrical stimulation between ketamine/N2O- and propofol/N2O-based anesthesia. Patients in the propofol group (n = 13) and the ketamine group (n = 13) were anesthetized with 50% N2O in oxygen, fentanyl, and 4 mg/kg/hr of propofol or 1 mg/kg/hr of ketamine, respectively. The level of neuromuscular blockade was maintained at an M-response amplitude of approximately 50% of control. Motor evoked potentials in response to multipulse transcranial electrical stimulation were recorded from the right adductor pollicis brevis muscle, and peak-to-peak amplitude and onset latency of motor evoked potentials were evaluated. To estimate intrapatient variability, the coefficient of variation (standard deviation/mean x 100%) of 24 consecutive responses was determined. Motor evoked potential amplitudes in the ketamine group were significantly larger than in the propofol group (mean, 10th-90th percentile: 380 microV, 129-953 microV; 135 microV, 38-658 microV, respectively; P <.05). There were no significant differences in motor evoked potential latency (mean +/- standard deviation: 20.9 +/- 2.2 msec and 21.4 +/- 2.2 msec, respectively) and coefficient of variation of amplitudes (median [range]: 32% [22-42%] and 26% [18-41%], respectively) and latencies (mean +/- standard deviation: 2.1 +/- 0.7% and 2.1 +/- 0.7%, respectively) between the ketamine and propofol groups. In conclusion, intrapatient variability of motor evoked potentials to multipulse transcranial stimulation is similar between ketamine/N2O- and propofol/N2O-based anesthesia, although motor evoked potential amplitudes are lower during propofol/N2O-based anesthesia than ketamine/N2O-based anesthesia.

No abstract

Intraoperative monitoring of myogenic motor-evoked potentials (MEPs) may be required under hypothermic conditions because of its neuroprotective efficacy. However, data on the influence of hypothermia on myogenic MEPs are limited. The results indicate that multipulse stimulation may be better than single-pulse stimulation when monitoring MEPs during hypothermia.

The results indicate that TS of the peripheral nerve before transcranial stimulation can enlarge the amplitude of MEPs during general anesthesia with neuromuscular blockade. TS of the peripheral nerve can be intraoperatively applied as a method to augment myogenic MEP responses.