Potentiation of pancuronium induced neuromuscular blockade by calcium channel blockers in vitro.

The calcium channel blockers verapamil, methoxyverapamil, diltiazem, and nisoldipine have been tested for interactions with the nondepolarizing muscle relaxant pancuronium bromide by using the indirectly stimulated in vitro preparation of the rat hemidiaphragm. Dose response curves of each calcium channel blocker, pancuronium bromide, and combinations of both were determined. Each of the four calcium channel blocking drugs showed agonistic interaction in potentiating pancuronium induced neuromuscular blockade.

[Interaction of the calcium antagonists nifedipine and nisoldipine with the nondepolarizing muscle relaxant vecuronium bromide in an vivo rat preparation]. / Zur Wechselwirkung der Ca-Antagonisten Nifedipin und Nisoldipin mit dem nichtdepolarisierenden Muskelrelaxans Vecuroniumbromid im "in vivo" Rattenpräparat.

The interaction of two orally administered Ca-channel blockers, the dihydropyridines nisoldipine and nifedipine, with the non-depolarizing muscle relaxant, vecuronium bromide, was tested in the indirectly stimulated tibialis anterior muscle of anesthetized and ventilated Sprague-Dawley rats. In both the nisoldipine and the nifedipine group, depression of twitch tension and duration of vecuronium-induced neuromuscular blockade was potentiated when compared with a control group. The possible clinical relevance of these findings is discussed.

[Nifedipine and vecuronium bromide. How does a patient treated with calcium antagonists react to nondepolarizing muscle relaxants? Brief scientific communication]. / Nifedipin und Vecuroniumbromid. Wie reagiert der mit Ca-Antagonisten behandelte Patient auf nichtdepolarisierende Muskelrelaxantien? Kurze wissenschaftliche Mitteilung.

The muscle-relaxation reactions of Ca-antagonist (nifedipine) pretreated patients and a control group (5 in each group) were observed after administration of vecuronium bromide using the "priming principle." Twitch depression induced by the "priming dose" of vecuronium bromide (20 micrograms/kg body weight and T4/T1 ratio in the Ca-antagonist-treated patients (35 +/- 13% and 0.42 +/- 0.14%, respectively), was significantly different (P less than 0.01) when compared with the control group (1.2 +/- 2.7% and 0.75 +/- 0.15%). Similarly, the onset time to maximum blockade after the intubating dose of vecuronium bromide (60 micrograms/kg body wt.) was significantly shorter in the nifedipine group (40 +/- 21 s) when compared with the controls (100 +/- 17 s). The duration of the effect observed clinically (until 25% recovery) in the nifedipine group 32.9 +/- 7.3 min versus 25 +/- 8.15 min was enhanced; however, the difference between the treated group and the control group was not significant.

Comparative investigations on the cardiovascular effects of Org NC45 and pancuronium in dogs.

Cardiovascular effects of Org NC 45 and pancuronium were examined in seven anaesthetized dogs. Systemic circulatory effects were measured after increasing doses administered as a single i.v. bolus. Cardiac effects were measured after intracoronary (i.c.) injection of the equivalent dose of the respective neuromuscular blocking agent, which produced 90% neuromuscular blockade. Org NC 45 i.v. did not cause any significant cardiovascular changes, whereas pancuronium i.v. produced significant and dose-related increases in heart rate, left ventricular (LV) dP/dtmax and cardiac output (CO). After i.c. injection of equipotent doses, neither drug induced any significant change in haemodynamic measurements. This implies that neither drug exerted a direct influence on cardiac contractility, the increases in LV dP/dt max and CO following pancuronium being dependent on heart rate.

Rapid tracheal intubation with vecuronium: the priming principle.

Following the administration of a single 0.1 mg/kg dose of vecuronium bromide, satisfactory conditions for tracheal intubation developed in 156 +/- 12 s (mean +/- SEM), and the clinical duration of the initial dose was 36 +/- 2 min. When the initial dose of vecuronium was administered in two increments, a 0.015 mg/kg "priming" dose, followed 6 min later by a 0.050 mg/kg "intubating" dose, intubation time decreased to 61 +/- 3 s and clinical duration to 21 +/- 1 min. The priming dose that had no unpleasant effect on premedicated, awake patients could be administered 3-4 min before, and the intubating dose 2 to 3 min after induction of anesthesia. With the described technique, comparable intubating conditions could be obtained just as rapidly with vecuronium as with succinylcholine chloride, without subjecting the patients to the side effects of and the complications occasionally encountered with succinylcholine. An added advantage of the use of a priming dose is that it will reveal undiagnosed, pathologic, or idiopathic increase of sensitivity to nondepolarizing muscle relaxants.