PubMed · 8371872
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H L Hamburg. Amplification.. https://pubmed.ncbi.nlm.nih.gov/8371872/
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OBJECTIVE: To evaluate cardiorespiratory and anesthetic effects of a microdose of medetomidine hydrochloride on diazepam-ketamine (DK) hydrochloride induced anesthesia in dogs. DESIGN: Randomized crossover study. ANIMALS: 6 two-year-old healthy female dogs. PROCEDURE: A study was designed to compare quality of anesthetic induction, recovery, analgesia, muscle relaxation, duration of immobilization, and ease of endotracheal intubation between diazepam-ketamine-medetomidine (DKM) and diazepam-ketamine induced anesthesia in 6 dogs. Diazepam (0.25 mg/kg [0.114 mg/lb] of body weight, i.v.) and ketamine (5 mg/kg [2.27 mg/lb], i.v.) with or without a microdose of medetomidine (5 micrograms/kg, i.v.) were administered to dogs. A baseline ECG was obtained, and baseline measurements of arterial blood gas tensions, arterial pressures, heart and respiratory rates, and minute volume were taken before drug administration. All measurements were repeated again 5, 10, 20, and 30 minutes after drug administration. Endotracheal intubation was attempted 1 minute after drug administration and then again 5, 10, 20, and 30 minutes after drug administration. Analgesia was evaluated by tail clamp and needle prick testing. RESULTS: Medetomidine improved quality of anesthetic induction, ease of endotracheal intubation, and extended duration of analgesia and lateral recumbency in anesthetized dogs. The addition of medetomidine to DK increased blood pressure and decreased heart and respiratory rates and minute volume. Hypoxemia was observed in 1 dog after DKM induced anesthesia. CLINICAL IMPLICATIONS: Administration of a microdose of medetomidine provides a useful adjunct to DK induced anesthesia in dogs. Oxygen insufflation is recommended for a minimum of the first 5 minutes of DKM induced anesthesia.
A high-dose (0.75 to 2.8 mg/kg) pharmacokinetic study of droperidol was undertaken in patients during the recovery phase after cardiac surgery involving hypothermic cardiopulmonary bypass (CPB). The elimination half-life of droperidol in these patients, determined from concentration-time data obtained after CPB, was significantly prolonged relative to previously reported mean values in younger surgical patients not undergoing CPB and receiving lower doses of the drug (0.05-0.20 mg/kg). On stratification of the patients by droperidol dose, there was an inverse correlation between the size of the dose and the elimination half-life of droperidol: mean half-life decreased as mean dose increased. This difference in elimination half-life was not related to the duration of the CPB procedure, or the total anesthetic time, both of which were not significantly different between the patient groups receiving the three different doses of droperidol. The magnitude or duration of hypothermia after CPB did not differ between the three patient groups. The differences in half-lives are more likely due to the clinical condition of the patients, such that the patients who received the higher doses of droperidol were also judged clinically to be less ill and thus eliminated droperidol more efficiently. This hypothesis, however, could not be supported due to the small number of patients studied. The results obtained in this study indicate that droperidol elimination is significantly prolonged after high-dose administration to elderly patients undergoing hypothermic CPB procedures during cardiac surgery.
Arrhythmia due to ischaemia and/or reperfusion is an important problem, especially in open heart surgery and for patients with ischaemic heart diseases undergoing non-cardiac surgery. This experimental study is planned to evaluate the effects of midazolam on ischaemia and/or reperfusion-induced arrhythmias by comparison with thiopentone in two sets of experiments (n = 20 for every group). In total ischaemia-reperfusion experiments, hearts were perfused in constant pressure conditions. In the control group, after a stabilisation period, perfusion was totally stopped for 30 min and the hearts were reperfused for 10 min. For the experimental groups, hearts were pretreated for 5 min with either 10-6 mol 1-1 midazolam or 10-5 mol 1-1 thiopentone before total ischaemia and reperfused for 10 min with the same concentrations of the drugs. In low-flow ischaemia-reperfusion experiments, hearts were perfused at a constant flow of 10 ml g-1 heart per min initially. In the control group, after a stabilisation period, perfusion rate was decreased successively 1 ml g-1 heart per min for 10 min (mild ischaemia) and to 0.2 ml g-1 heart per min for another 10 min (severe ischaemia). The ischaemic hearts were then reperfused for an additional 10 min at a flow rate of 10 ml g-1 heart per min. Electrogram recordings were evaluated before ischaemia and at the 5th and 10th min of mild ischaemia, severe ischaemia and reperfusion. Midazolam, 10-6 mol 1-1, or thiopentone, 10-5 mol 1-1, were added to the perfusion solution in the midazolam and thiopentone groups, respectively. In these two groups, hearts were perfused according to perfusion rates mentioned above in the control group. As a commonly used i.v. anaesthetic, thiopentone was arrhythmogenic for hearts exposed to ischaemia-reperfusion by increasing ventricular premature beat (% incidences for control, midazolam and thiopental groups in the 10th min of reperfusion were 25, 15 and 65 in total ischaemia-reperfusion experiments, P < 0.01) and ventricular tachycardia (respective % incidences were 0, 5, 25, P < 0.05) incidences, but in our experiments were found out that the new agent midazolam does not have more arrhythmia incidence than the respective control group in any criteria evaluated. None of the agents exerted atrioventricular conductance abnormalities. So we conclude that midazolam is a safe agent for ischaemic hearts and might also be antiarrhythmic and the mechanism of action of this effect remains to be further investigated.