The effects of magnesium salts on the duration of epinephrine-induced ventricular tachyarrhythmias in anesthetized rats.

The effects of MgSO4 or MgCl2 infusion on the duration of epinephrine-induced cardiac arrhythmia were evaluated in male rats anesthetized with either halothane or pentobarbital. In addition, the duration of epinephrine-induced arrhythmia in pentobarbital (50 mg/kg) anesthetized rats was compared with the duration of arrhythmia in halothane (1.5%) anesthetized rats. During halothane anesthesia MgSO4 or MgCl2 infused at a dose rate of 8 mg.kg-1.min-1 for 20 min caused a significant reduction in the duration of arrhythmia (100% and 80%, respectively) following a 4-microgram/kg injection of epinephrine and a significant threefold reduction in arrhythmia duration for each salt following an 8- or 16-micrograms/kg injection of epinephrine. Significantly shorter periods of arrhythmia after each dose of epinephrine were seen in rats anesthetized with pentobarbital than were seen in rats anesthetized with halothane. No significant difference was seen between MgSO4 or MgCl2 infusions in any of these studies. Twenty-minute infusions of MgSO4 (8 mg.kg-1.min-1) were compared with propranolol (0.03 mg.kg-1.min-1) and verapamil (0.5 micrograms.kg-1.min-1) infusions on the duration of arrhythmia after epinephrine (8 micrograms/kg) injections in halothane anesthetized rats. MgSO4 and propranolol infusion caused a significant reduction in the duration of arrhythmia (81% and 70%, respectively). Verapamil infusion caused only a 48% reduction in arrhythmia duration. While there was no significant difference between MgSO4 or propranolol, both caused a significantly greater reduction in arrhythmia than verapamil. CaCl2 (0.15 mM.kg-1.min-1) infusion for 5 min caused a significant fivefold increase in the duration of arrhythmia during halothane anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Respiratory sinus arrhythmia during recovery from isoflurane-nitrous oxide anesthesia.

Heart rate and respiratory patterns were monitored in ten ambulatory female patients undergoing elective laparoscopy. The patients were anesthetized with isoflurane-nitrous oxide. An index of cardiac vagal tone determined from the heart rate pattern by quantifying the amplitude of respiratory sinus arrhythmia was elevated over four 10-min periods: before induction of anesthesia; during maintenance of anesthesia; upon arrival in the recovery room; and 20-30 min later when the patient was fully conscious. All ten patients' vagal tones were lowest during maintenance of anesthesia. During the recovery periods vagal tone increased and approached the conscious level. On-line analysis of respiratory sinus arrhythmia may provide a physiological index of the level of anesthesia and the rate of recovery.

Cerebrovascular and cerebral metabolic effects of flurazepam and a benzodiazepine antagonist, 3-hydroxymethyl-beta-carboline.

There is a need in clinical practice for an antagonist which can reverse the sedative action of benzodiazepines. Recently, 3-hydroxymethyl-beta-carboline (3-HMC) has been reported to inhibit the sleep inducing effects of flurazepam. The effects of flurazepam (0.5, 5 and 50 mg/kg) on cerebral blood flow (CBF) and cerebral O2 consumption (CMRO2) were evaluated in rats and the ability of 3-HMC to reverse these changes was determined. Regional CBF was measured with radioactive microspheres and cortical CMRO2 was calculated from sagittal sinus-arterial O2 content differences and cortical CBF. Flurazepam produced dose dependent decreases in CBF and CMRO2 which were significant at 5 and 50 mg/kg. 3-HMC (5 mg/kg) inhibited flurazepam induced changes at the 5 mg/kg dose but had little effect on the CBF and CMRO2 depression produced by 50 mg/kg flurazepam. At a dose of 25 mg/kg, 3-HMC inhibited the effects of both 5 and 50 mg/kg flurazepam. Blood pressure and heart rate were also decreased by flurazepam but these variables were not reversed as effectively by 3-HMC treatment. The results indicate that 3-HMC is an active antagonist of the cerebrovascular and cerebral metabolic depression produced by flurazepam and can stimulate CBF and CMRO2 at high doses when given alone.