PANCURONIUM BROMIDE IS AN amino steroid muscle relaxant (Figure 1) which was synthesized in 1964 by Hewett and Savage and has been studied and evaluated clinically in Europe during the past four years2 -5 It is an odourless, white, crystalline powder with a bitter astringent taste, melts at 215~ with decomposition, and is soluble in 50 parts of chloroform and one part water at 20~ The co]ourless solution is stable while sealed, but breaks down in a few hours after exposure to air. In Europe it is available in 2-ml ampoules containing 4 mg pancuronium bromide, 18 nag sodium chloride B.P. and water for injection B.P. to 2 mls. The preparation which was used in this study contains preservatives (acetic acid and sodium acetate) to buffer the solution to pH 4.0. Pharmacological studies have shown that it has no hormonal action but is a potent non-depolarizing skeletal muscle relaxant like'tubocurarine and gallamine. It has a more rapid onset of action than tubocurarine with a similar duration of action. It has a somewhat longer action than gallamine. It has no significant effect on the blood pressure or the tracheobronchial tree due to the very. slight ganglionblocking action and the claim is that no histamine is released, a It does not affect OOC. CH
THE CUBItENT CONTROVERSY regarding the role of succinylcholine in producing cardiovascular disturbances deserves the careful attention of every anaesthesiologist. These changes, which may be catastrophic in nature, can occur after a single intravenous dose 1-~ as well as following repeated administrations. 4-9 The disturbances range from mild, transient changes in rate or rhythm through severe bradycardia and serious arrhythmias to cardiac arrest.Several theories have been offered to explain the causes, but none of them seems adequate. One of the most recent concerns the increase of plasma potassium immediately following the intravenous administration of succinylcholine.The release of plasma potassium as a result of damage to myofibrillae has been described. The occurrence of haemoglobinuria or myoglobinaemia after vigorous muscular exercises like forced marches, karate, 1~ or football 11,12 has been well documented, and several authors have described myoglobinaemia or myoglobinuria after the administration of succinylcho]ine. 13-15 A case of acute renal failure following the use of succinylcholine in a patient with idiopathic myoglobinuria was described by Bennike. 14 These phenomena (myoglobinuria, myoglobinaemia) after succinylcholine indicate myofibrillar damage and presumably the release of intracellular potassium.This study was designed to determine the incidence, magnitude and timing of plasma potassium changes and their correlation with electrocardiographic abnormalities following the administration of succinylcholine. MATERIALS AND METI-IODSOne hundred anaesthetics were studied in patients undergoing surgical procedures requiring only a single, short period of muscular relaxation and no endotracheal intubation. The reason for avoiding patients in whom intubation or other forms of pharyngeal or laryngeal manipulation would become necessary was to eliminate the likelihood of electrocardiographic abnormalities that frequently accompany such events.Eighty-nine of the one hundred patients studied were females, most of whom were undergoing vaginal gynaecological procedures; ten male patients were operated on for relatively minor orthopedic or urological problems, and one for debridement of burns. From the point of view of anaesthetic risk, the patients seemed to represent a fair sample of the usual surgical material and age groups
ONE OF THE COMMONEST COMPLICATIONS Of anaesthesia and surgery is the occurrence of nausea, retching, and vomiting. The action of anaesthetic and associated drugs directly upon the digestive tract and its central and peripheral innervation probably play a prominent role on its incidence (see Table I). 1,2 Many nonspecific prophylactic and therapeutic measures have been employed to prevent or reduce its occurrence with but variable success (see Table I1). 3.4 Numerous drugs have been shown to have a depressant effect on the vomiting induced by chemical agents in dogs and other animals? Unfortunately, it is not as easy to reproduce the usual clinical factors which appear to initiate vomiting in man, so that it is practically useless to attempt to prove the eflqcacy of an anti-emetic drug by animal experiments alone?-7 Several other factors must be considered before it is decided to use an antiemetic agent in man in order to be sure that it is indeed useful following anaesthesia. First, the anti-emetic drug should be free of an appreciable depressant effect on the circulation and on respiration in the dose which might suppress postanaesthetic vomiting. The agent should be non-toxic to vital organs, and it should not prolong the hypnotic effect of anaesthetics or itself cause marked drowsiness. Very few of the drugs currently available as anti-emetics have such a limited action. Furthermore, the brief duration of the anti-emetic effect of these drugs substantially limits the optimum time for their administration, s-x~ Metoclopramide (MK 745) was developed in France in 1963, where it is known as Primp6ran. Its anti-emetic action was said to be powerhfl whether vomiting is of central or peripheral origin in a variety of clinical conditions in man. The formula is shown in Figure 1. 0 II CI-.~C-NHCH2CH2N(C2Hs)2 9 HCI H~N~OCH3 Metoclopramide hydrochloride 4-amino.5-chloro-N-[2-(diethylamino) ethyl]-o-anisamide hydrochloride CI,~H22CIN302 .HCI FIctrl~ 1. Structural formula of metoclopramide.
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