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ニトログリセリン(TNG)低血圧麻酔にジルチアゼム(DZ)を併用した場合の心血管系に及ぼす効果を,エンフルラン麻酔下の17名の婦人科手術患者を対象に検討した。収縮期血圧は,TNG単独投与のA群では目標とする90mmHgに到達するのに15分以上を要したが,DZを2μg/kg/min (B群),5μg/kg/min (C群)で併用すると5分後に目標値となり,中止後の復圧も容易であった。C群の心拍数は投与60分でA群に比較し有意に低値となり,中止15分後も低下した。中心静脈圧,肺動脈圧,肺動脈楔入圧は3群とも有意に低下したが,心拍出量はC群で低血圧開始前に比べ有意に減少した。収縮期血圧を90mmHg前後に維持させるTNGの投与量は,DZの併用により量依存性に減少した。DZを2μg/kg/minで同時投与すれば,調節性に優れ心血管系を抑制することなくTNGの投与量を節減できる。

Hemodynamic effects of nicardipine-induced hypotension during enflurane/nitrous oxide were evaluated in 10 surgical patients. An infusion of nicardipine was titrated to maintain mean arterial pressure at 60 to 70 mmHg under enflurane 1.5 to 2.0 vol% and nitrous oxide 60 vol%. Mean arterial pressure was well controlled with the nicardipine infusion, whereas cardiac index increased with decreased systemic vascular resistance. Heart rate increased concomitantly with decreased blood pressure, which indicated that enflurane 1.5 to 2.0 vol% did not suppress baroreceptor reflex during nicardipine administration. However, rate-pressure-product was not increased by the nicardipine. Right and left ventricular systolic work indices were not increased by the nicardipine. Right ventricular ejection fraction was not also changed by the nicardipine. Although serum norepinephrine level increased during the nicardipine infusion, the values remained within physiological ranges. Our results suggest that nicardipine-induced hypotension may be safely performed during enflurane/nitrous oxide anesthesia because neither ventricular work nor myocardial oxygen demand was increased by nicardipine.

The effects of anesthetic induction by diazepam, flunitrazepam and midazolam on cardiac performance were evaluated in 33 ASA class I surgical patients (average age was 36 years). The patients were divided according to the 3 drug groups, and the effects of each drug assessed utilizing measurements of systolic time intervals. An increase in heart rate and decrease in blood pressure was observed following flunitrazepam and midazolam induction. There was no changes in PEPI (pre-ejection period index) and LVETI (left ventricular ejection time index) by benzodiazepines induction. The PEP/LVET ratio was increased by diazepam while the DPTI (diastolic pressure time index)/TTI (tension time index) was reduced by flunitrazepam and midazolam. However, these changes in PEP/LVET and DPTI/TTI were within normal limits. These data indicate that in healthy humans the induction dose of either diazepam, flunitrazepam or midazolam does not extremely influence either PEP/LVET for cardiac performance or DPTI/TTI for cardiac oxygen balance. The results also suggest that the simultaneous use of PEP/LVET and DPTI/TTI is more informative than any single variable for the evaluation of cardiac effects of anesthetics.

The combined negative inotropic effects ofisoflurane and calcium entry blockers (verapamil, diltiazem, nifedipine, nicardipine) were studied utilizing isolated heart preparations of ventricular muscles from dogs. All of these calcium entry blockers exerted dose-dependent decreases in maximal velocity of shortening (Vmax), maximal developed isometric force (Fm), and the maximal first derivative of Fm (maximal dF/dt). Dose-dependent decreases of these variables of muscle mechanics were augmented in isoflurane-depressed myocardium. At equimolar concentrations, direct myocardial depression was demonstrated in the following order of severity: nifedipine > diltiazem = verapamil > nicardipine. Percent depressions of Vmax, Fm and maximal dF/dt were significantly greater in muscles when calcium entry blockers were combined with 1MAC isoflurane than in muscles of calcium entry blockers alone. These data suggest that the negative inotropic effects of verapamil, diltiazem, nifedipine, and nicardipine were potentiated by isoflurane

Effects of CM7857 on electrophysiologic properties in canine Purkinje fibers and inotropic effects in canine ventricular muscle were studied. As CM7857 is a derivative of disopyramide phosphate, the effects of CM7857 (5 mg/L, 1.5 X 10(-5) M) were compared with those of disopyramide phosphate (5 mg/L, 1.4 X 10(-5) M). CM7857 significantly lowered the maximum rate of rise of phase 0 (Vmax) from 351.5 +/- 50.6 V/s (mean +/- SE, n = 5) to 283.6 +/- 33.0 V/s, and conduction velocity from 2.68 +/- 0.56 m/s to 1.70 +/- 0.28 m/s. The automaticity of Purkinje fibers was depressed by CM7857 as the result of reduction in the slope of phase 4. These effects were comparable to those of disopyramide. A marked difference between CM7857 and disopyramide was observed in the effect on action potential duration. APD90 was significantly shortened from 327.4 +/- 14.8 ms (n = 8) to 279.9 +/- 12.9 ms by CM7857, whereas disopyramide did not show any significant changes in APD90. As the CM7857-induced shortening of APD disappeared in low [Na+]o or low [K+]o concentration, it may be attributed to the lowering effect of "window current," a steady-state sodium current, maintaining action potential plateau. Effective refractory period (ERP) did not show any significant change. An acetylstrophanthidin-induced oscillatory afterpotential was significantly depressed by disopyramide, but not by CM7857. Isotonic contraction and isometric contraction of the right ventricular trabecullae were depressed by both drugs.

The direct inotropic action of seven local anesthetics: procaine, mapivacaine, lidocaine, tetracaine, chloroprocaine, bupivacaine and etidocaine were compared in isolated cat papillary muscles. All of the local anesthetics produced a doserelated depression of maximal velocity of shortening (Vmax), maximal developed force (Fm) and maximal dF /dt. The more potent local anesthetics such as bupivacaine and etidocaine depressed myocardial contractility at significantly lower concentrations than the less potent local anesthetics such as lidocaine and mepivacaine. Depression of Vmax by bupivacaine or etidocaine was three times greater than that by lidocaine and ten times greater than that by procaine. At the same concentration (10−4M), direct myocardial depression was demonstrated in the following order of severity: etidocaine ≥ bupivacaine > tetracaine > chloroprocaine ≥ lidocaine > mepivacaine > procaine.

Inotropic effects of 7 anesthetics (procaine, chloroprocaine, tetracaine, mepivacaine, lidocaine, bupivacaine and etido-caine) were compared by measurements of both isometric and isotonic contractions in isolated cat papillary muscles.