We investigated the concentration-time-effect relationship of the relaxant rapacuronium and the contribution of its metabolite. Clearance, rate constant of transport between plasma and the biophase, and modeled concentration in the biophase at 50% effect of rapacuronium are consistent with its rapid onset and short to intermediate duration. The lower clearance of the metabolite will gradually prolong the time course of the neuromuscular blockade during maintenance with rapacuronium.

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We have studied, in adult patients, ASA I-II, the cardiovascular effects of an intubating dose of rocuronium 0.6 mg kg-1. After induction, patients were paralysed with vecuronium and the trachea intubated. Heart rate (HR) and non-invasive mean arterial pressure (MAP) were measured every 1 min. After stabilization of HR and MAP, defined as < 3% change over three measurements, rocuronium (n = 20) or saline (n = 10) was injected at random. Mean HR increased initially from 66.6 to 72.1 beat min-1, 4 min after rocuronium, and then decreased gradually to 69.6 beat min-1, that is a net increase of 3.3 beat min-1 over 10 min (P < 0.001), whereas after saline there was a gradual decrease from 65.8 to 60.9 beat min-1 (P < 0.001) over 10 min. From the third minute, HR was significantly higher in the rocuronium group. Mean MAP decreased in both groups within 10 min to a similar extent after rocuronium and saline, that is from 74.9 to 72.1 mm Hg and from 74.7 to 72.2 mm Hg, respectively (both P < 0.001). There were no differences in MAP at any time between the rocuronium and saline groups. We conclude that an intubating dose of rocuronium, in the absence of haemodynamic effects related to paralysis itself, resulted in a limited increase in HR without change in MAP, probably because of its weak vagolytic activity.