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We examined the effects of midazolam and flumazenil on cardiac function and metabolism in the isolated rat heart-lung preparation. Wistar rats were divided into five groups (each group:n=8) as follows: (1) control (saline); (2) flumazenil (1.3×10(-5)M); (3) flumazenil (10(-4)M); (4) midazolam (60μg·ml(-1)); and (5) midazolam (60μg·ml(-1)) and flumazenil (1.3×10(-5)M). Systolic blood pressure and calculated left ventricular dP/dt maximum in the midazolam or midazolam conbined with flumazenil groups increased significantly in comparison with those in the control group. Heart rate in the midazolam group was lower than that in the control group. However, in the flumazenil group, there were no effects on the hemodynamics. There were no significant differences in the myocardial tissue concentration of ATP, lactate, and glycogen in all groups. In this study, midazolam decreased heart rate; however, flumazenil had no effect on the heart, nor did it antagonize the cardiac effects of midazolam. These results suggest that flumazenil has no effect on the peripheraltype benzodiazepine receptor of the myocardium.
We examined the effects of midazolam and flumazenil on cardiac function and metabolism in the isolated rat heart-lung preparation. Wistar rats were divided into five groups (each group:n=8) as follows: (1) control (saline); (2) flumazenil (1.3×10(-5)M); (3) flumazenil (10(-4)M); (4) midazolam (60μg·ml(-1)); and (5) midazolam (60μg·ml(-1)) and flumazenil (1.3×10(-5)M). Systolic blood pressure and calculated left ventricular dP/dt maximum in the midazolam or midazolam conbined with flumazenil groups increased significantly in comparison with those in the control group. Heart rate in the midazolam group was lower than that in the control group. However, in the flumazenil group, there were no effects on the hemodynamics. There were no significant differences in the myocardial tissue concentration of ATP, lactate, and glycogen in all groups. In this study, midazolam decreased heart rate; however, flumazenil had no effect on the heart, nor did it antagonize the cardiac effects of midazolam. These results suggest that flumazenil has no effect on the peripheraltype benzodiazepine receptor of the myocardium.
In anaesthesia and in the intensive care unit, benzodiazepines have proven safe and effective agents for the induction and maintenance of sedation for a variety of therapeutic goals. However, in these contexts, or in benzodiazepine overdose, it is often desirable to be able to terminate or interrupt sedation without waiting for the effect of the benzodiazepine to become dissipated by normal metabolism and excretion. Flumazenil, a 1,4-imidazobenzodiazepine, is a highly effective, specific benzodiazepine antagonist which is indicated for use when the effect of a benzodiazepine must be attenuated or terminated at short notice. It acts by displacing other benzodiazepines from the receptor site by competitive inhibition. The onset of effect after intravenous administration occurs within 1 to 3 minutes. The optimal dosage is determined for each patient by a dose titration procedure and lies in the range 0.2 to 1.0mg in anaesthesiology, and 0.1 to 2.0mg in intensive care use. Despite its short elimination half-life of around 1 hour, after general anaesthesia or conscious to moderate sedation for short procedures, a single dose of flumazenil is usually sufficient to attain and maintain the desired level of consciousness. After intoxication with high benzodiazepine doses, the duration of effect of a single dose of flumazenil is not expected to exceed 1 hour. In such cases, the period of wakefulness can be prolonged as necessary by repeated low intravenous doses of flumazenil or by infusion (0.1 mg/hour). Flumazenil is well tolerated both systemically and locally. The only adverse events seen with greater frequency after flumazenil compared with placebo were nausea and/or vomiting after general anaesthesia, although the incidence of actual vomiting was not significantly different between the 2 groups. Since these effects were virtually absent in studies of intensive care patients and after sedation for short procedures, and were not seen in tolerability studies in healthy volunteers receiving intravenous bolus doses of up to 100mg, there may be a link between these symptoms and the other agents used in general anaesthesia, some of which have well-known emetic properties. Thus, flumazenil provides a safe and effective means of attenuating or reversing the CNS-depressant effects of benzodiazepines whenever indicated, e.g. following benzodiazepine-induced general anaesthesia, conscious sedation, or after benzodiazepine overdose, either alone or in combination with other agents.(ABSTRACT TRUNCATED AT 400 WORDS)
Benzodiazepines are known to cause central nervous system and centrally mediated cardiovascular depression. The benzodiazepine antagonist flumazenil has been shown to antagonize benzodiazepine-induced central nervous system depression. We report a case in which cardiovascular depression secondary to benzodiazepine use was reversed by this agent.
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