Anesthesiology
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Randomized Controlled Trial Clinical Trial
The role of epidural morphine in the postcesarean patient: efficacy and effects on bonding.
This study was designed to determine in postcesarean patients whether in addition to superior analgesic effects, epidural morphine administration results in secondary benefits in maternal well-being and maternal-infant interaction. Following elective cesarean section with bupivacaine epidural anesthesia, 40 healthy mothers received 5 mg preservative-free morphine sulfate in 10 ml of saline, either by the epidural (Group 1, n = 20) or the intravenous (Group 2, n = 20) route, in a randomized, double-blind fashion. Each received a simultaneous injection of saline by the alternate route. ⋯ Itching occurred in 58% of Group 1 patients and only 16% of Group 2 patients (P less than 0.01); the incidences of nausea, vomiting, and urinary retention were not statistically different between the groups. No respiratory depression was observed. Benefits of epidural morphine in this patient population appear limited to the provision of improved analgesia and earlier mobility.
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Randomized Controlled Trial Clinical Trial
Potentiation of succinylcholine phase II block with isoflurane.
To determine the effect of isoflurane upon phase II block 20 patients were given succinylcholine by infusion at a rate which maintained the twitch tension of the adductor pollicis muscle at 10% of control for 2 to 4 h. The patients were assigned randomly to either nitrous-oxide-isoflurane (0.75-1.5% inspired) or nitrous-oxide-fentanyl for maintenance of anesthesia, and neuromuscular activity was monitored using train-of-four stimulation. ⋯ This decrease was related to the extent of phase II block present. It is concluded that isoflurane potentiates succinylcholine phase II block although the mechanisms involved are not necessarily the same as in the potentiation of nondepolarizing neuromuscular blocking drugs.
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To determine the effects of cardiopulmonary bypass (CPB) and hypothermia on the neuromuscular blockade produced by pancuronium, this relaxant was infused intravenously into 10 anesthetized patients to produce and maintain 90% depression of the twitch tension of the adductor pollicis muscle following supramaximal ulnar nerve stimulation. Infusion rates, plasma concentration of pancuronium, and adductor pollicis temperature were measured every 15 min. During the normothermic period preceding the start of CPB, the pancuronium requirement, the pancuronium plasma concentration, and muscle temperature were mean (mean +/- SEM): 238 +/- 12 micrograms . m-2 . 15 min-1, 0.31 +/- 0.01 microgram/ml, and 33.9 +/- 0.1 degrees C, respectively. ⋯ After the muscle temperature was returned to 34 +/- 0.6 degrees C, the plasma pancuronium concentration and requirements increased to 0.35 +/- 0.05 microgram/ml and 392 +/- 32 micrograms . m-2 . 15 min-1 (P less than 0.001), respectively. After CPB, these values were 0.39 +/- 0.04 microgram/ml and 239 +/- 25 microgram . m-2 . 15 min-1. These results demonstrate that pancuronium requirements are increased at the beginning of CPB because of circulatory volume changes and again during rewarming of the patient once muscle temperature reaches about 34 degrees C.
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The present study examined the influence of spinally administered fentanyl on the spontaneous and noxiously evoked activity of wide dynamic range (WDR) neurons in the dorsal horn of decerebrate, spinal cord-transected cats. This work was performed in order to evaluate the dose-response relationship, time course, and naloxone reversibility of fentanyl suppression of neurons that are involved with the transmission of information about pain. Extracellular single neuron recordings were obtained from 18 WDR neurons in the lumbar enlargement. ⋯ Such results support the concept that fentanyl is acting through a specific drug-receptor interaction. The onset of neuronal suppression occurred more rapidly, and the duration of the suppression was longer following fentanyl than that seen following spinal morphine. The onset and duration of this suppression correlates well with human clinical data, providing further evidence that alterations of WDR neuronal activity may be important in the production of spinal opioid analgesia.