Anesthesia and analgesia
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Anesthesia and analgesia · Jun 2003
The effect of hypothermia on myogenic motor-evoked potentials to electrical stimulation with a single pulse and a train of pulses under propofol/ketamine/fentanyl anesthesia in rabbits.
In the present study, we investigated the effect of hypothermia on myogenic motor-evoked potentials (MEPs) in rabbits. The influence of stimulation paradigms to induce MEPs was evaluated. Twelve rabbits anesthetized with ketamine, fentanyl, and propofol were used for the study. Myogenic MEPs in response to electrical stimulation of the motor cortex with a single pulse and a train of three and five pulses were recorded from the soleus muscle. After the control recording of MEPs at 38 degrees C of esophageal temperature, the rabbits were cooled by surface cooling. Esophageal temperature was maintained at 35 degrees C, 32 degrees C, 30 degrees C, and 28 degrees C, and MEPs were recorded at each point. MEP amplitude to single- pulse stimulation was significantly reduced with a re-duction of core temperature to 28 degrees C compared with the control value at 38 degrees C (0.8 +/- 0.4 mV versus 2.3 +/- 0.3 mV; P < 0.05), whereas MEP amplitude to train-pulse stimulation did not change significantly during the cooling. MEP latency was increased linearly with a reduction of core temperature regardless of stimulation paradigms. In conclusion, these results indicate that a reduction of core temperature to 28 degrees C did not influence MEP amplitudes as long as a train of pulses, but not a single pulse, was used for stimulation in rabbits under propofol/ketamine/fentanyl anesthesia. ⋯ 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.
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Anesthesia and analgesia · Jun 2003
Knowledge and practice regarding prophylactic perioperative beta blockade in patients undergoing noncardiac surgery: a survey of Canadian anesthesiologists.
A lack of awareness of the "best" current practice is frequently cited as a major barrier to the practice of evidence-based medicine. The purpose of this study was to survey Canadian anesthesiologists to determine their knowledge and practices associated with prophylactic perioperative beta blockade, a therapy that has been widely discussed in the literature and has the potential for a significant positive impact on patient outcomes. We sent questionnaires to 1234 members of the Canadian Anesthesiologists' Society. The overall response rate was 54%. Ninety-five percent of respondents were aware of the perioperative beta blocker literature, and of these, 93% agreed that beta blockers were beneficial in patients with known coronary artery disease (CAD). Fifty-seven percent reported always or usually administering prophylactic beta blockers in patients with known CAD, and 34% of these regular users continued therapy beyond the early postoperative period. Only 9% of respondents reported that a formal protocol existed at their facility. This study suggests that barriers to the translation of research to practice were not related to a lack of awareness of the current best evidence. With respect to perioperative beta blockers, controversies within the literature as well as practical considerations may be greater barriers to implementation of best evidence. ⋯ This survey found that anesthesiologists were aware of and supported the use of prophylactic perioperative beta blockers in patients with risk factors or known coronary artery disease; however, only 57% frequently prescribed perioperative beta blockers. A lack of awareness of the current "best" evidence was not a barrier to use.
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Anesthesia and analgesia · Jun 2003
Antinociceptive potentiation and attenuation of tolerance by intrathecal electric stimulation in rats.
We tested whether intrathecal electric stimulation would reduce the tolerance to chronic morphine use and the severity of precipitated morphine withdrawal. Rats received intrathecal electrode catheter implantation and a continuous intrathecal infusion of morphine (2 nmol/h) or saline for 7 days. Intrathecal electric stimulations (0, 20, or 200 V) were performed once daily during the same period. Daily tail-flick and intrathecal morphine challenge tests were performed to assess the effect of intrathecal electric stimulation on antinociception and tolerance to morphine. Naloxone withdrawal (2 mg/kg) was performed to assess morphine dependence, and changes in spinal neurotransmitters were monitored by microdialysis. The antinociceptive effect of intrathecal morphine was increased by 200 V of electric stimulation. The magnitude of tolerance was decreased in the rats receiving the 2 nmol/h infusion with 200 V of intrathecal electric stimulation compared with the control group (morphine 2 nmol/h alone) (AD(50), 13.6 vs 124.7 nmol). The severity of naloxone-induced withdrawal was less in the rats receiving 200 V of stimulation. Intrathecal stimulation thus enhances analgesia and attenuates naloxone-induced withdrawal symptoms in rats receiving chronic intrathecal morphine infusion. Increases in spinal glycine release may be the underlying mechanism. This method may merit further investigation in the context of the long-term use of intrathecal opioids for controlling chronic pain. ⋯ Control of chronic pain is a major health problem. We show here that direct electrical stimulation of the spinal cord in rats enhances analgesia and attenuates naloxone-induced withdrawal symptoms. This may warrant further investigation in the context of long-term use of intrathecal opioids for controlling chronic pain.
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Anesthesia and analgesia · Jun 2003
Olprinone for the treatment, but not prevention, of fatigue-induced changes in guinea-pig diaphragmatic contractility.
Olprinone, a phosphodiesterase III inhibitor, improves the contractility in fatigued diaphragm in vivo, but no data are available for the treatment and prevention of fatigue-induced changes in vitro. We therefore examined the efficacy of Olprinone for the treatment and prevention of fatigue-induced changes in guinea-pig diaphragmatic contractility. The guinea-pig diaphragm strips were randomly allocated according to dose of Olprinone (0, 10(-6), 10(-5), and 10(-4) M) (n = 7 each) and were stimulated directly in an organ bath. Diaphragmatic contractility was measured by assessing twitch tension and force at 20-Hz and 100-Hz stimulation. Diaphragmatic fatigue was induced by generating rhythmic, repetitive contractions produced by 20-Hz stimulation for 5 min. In the first experiment, after the fatigue-producing period, Olprinone was administered to the organ bath for 5 min. In the second experiment, Olprinone was pretreated for 5 min, and then diaphragmatic fatigue was produced. In Experiment 1, after a fatigue-producing period, tetanic force to each stimulus decreased from baseline values (P < 0.05). Olprinone 10(-5)-10(-4) M caused an increase in force at both stimuli from fatigued values (P < 0.05). In Experiment 2, no change in tetanic force was observed by pretreatment with Olprinone (0-10(-4) M). After producing fatigue, tetanic force to each stimulus decreased from baseline values (P < 0.05). These results suggest that Olprinone 10(-5)-10(-4) M improves the fatigue-induced changes in guinea-pig diaphragmatic contractility and that pretreatment with Olprinone does not prevent diaphragmatic fatigability. ⋯ Olprinone is effective for the treatment, but not prevention, of fatigue-induced changes in guinea-pig diaphragmatic contractility.