Propofol and etomidate were compared as hypnotics in total intravenous anaesthesia for microlaryngeal surgery combined with jet ventilation. Two groups of 15 patients were studied. In group 1, propofol 2.0 mg/kg was used for induction. For maintenance a continuous infusion of 12 mg/kg/hour was used for the first 10 minutes, followed by 9 mg/kg/hour for the next 10 minutes and 6 mg/kg/hour thereafter. In group 2, the induction dose of etomidate was 0.3 mg/kg followed by continuous infusion of 1.8 mg/kg/hour for 10 minutes, 1.5 mg/kg/hour for the next 10 minutes and 1.0 mg/kg/hour thereafter. Alfentanil was given for analgesia and suxamethonium for muscle relaxation. The propofol group showed better surgical conditions, more stable anaesthesia and better recovery according to the Steward score. Recovery times to opening eyes on command were comparable for both groups.
The clinical effects and pharmacokinetics of 24 h infusion of midazolam (MDZ) during major maxillofacial surgery and postoperative observation in an Intensive Care Unit (ICU) were studied in 20 patients. During anaesthesia, infusion of MDZ at 5 mg/h combined with 67% nitrous oxide, 1.8 (s.d. = 0.8) mg of fentanyl, and 26.5 (s.d. = 11.4) mg of vecuronium, adequately suppressed clinical responses to surgical nociceptive stimuli. Postoperatively, infusion of MDZ was continued in the ICU at 5 mg/h until 9 a.m. of the first postoperative day for sedation of the intubated but spontaneously breathing patients. The depth of sedation in the ICU was scored from 1-5 (1 = "awake and tense", 5 = "unable to communicate"). During infusion the sedation score decreased from 3.8 after ICU arrival to 2.2 at 8 a.m. of the first postoperative day. Neither ventilatory nor circulatory depression were observed. After cessation of MDZ, recovery from sedation was fast. The degree of amnesia was low. During constant rate infusion no increase in plasma concentration of either MDZ or metabolites occurred. T1/2 beta of MDZ after cessation was 125 min (range 90-320) and its total body clearance was 10.5 ml/kg/min (s.d. = 3.1). The volume of distribution, clearance and T1/2 beta were significantly longer in women than in men. It was concluded that 24 h of MDZ infusion at 5 mg/h caused satisfactory ICU sedation with fast recovery, but that individual tailoring of the infusion rate may still improve the quality of sedation.
The effect of the acetylcholine releaser 4-aminopyridine on ventilation was studied by recording and quantifying the efferent phrenic nerve activity in 40 paralysed and vagotomized cats; with arterial Po2, PCO2 and pH kept constant. 4-Aminopyridine, given intravenously or in the vertebral artery, stimulates the phrenic nerve activity in a dose dependent manner. The stimulatory effects of 4-aminopyridine on the phrenic nerve activity could be abolished completely by administration of high doses of atropine. We conclude that 4-aminopyridine, which is used clinically for the reversal of a neuromuscular block, stimulates the phrenic nerve activity. Since the role of cholinergic mechanisms in the central chemoreception has been well established, the effect on the phrenic nerve activity is most probably by an increased release of acetylcholine at the site of the central chemoreceptors.
In vitro (rat hemidiaphragm) and in vivo (rat and cat tibialis anterior muscle preparation) studies of the interactions between Org NC 45 and some i.v. anaesthetics and antibiotics were carried out. With the exception of ketamine 1 mg kg-1 none of the drugs tested in vivo significantly changed the time course of an Org NC 45 bolus injection. All of the drugs caused an enhancement of the neuromuscular block using infusions in vivo and also in the in vitro preparations. Org NC 45 seems to be potentiated in a manner similar to pancuronium.
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