Blocking Action of Decamethonium at Different Sites in the Autonomic Nervous System of the Cat

Abstract

Doses of decamethonium sufficient to paralyse skeletal and respiratory muscles in the cat for 20 to 30 min can reversibly block transmission at several sites in the autonomic nervous system. The sympathetic vasodilator outflow to skeletal muscle was blocked at the post-ganglionic nerve endings, probably by preventing the release of acetylcholine. The effects of vagal stimulation on heart-rate and intestinal contraction were blocked in most experiments, possibly by an action on pre-ganglionic as well as post-ganglionic nerve endings. However, decamethonium did-not block all cholinergic nerve endings-for example, it did not diminish either the effects of stimulation of the chorda tympani on the submandibular salivary gland or those of pelvic nerve stimulation on the bladder.Decamethonium iodide is extensively used as a neuromuscular blocking agent in animal experiments. It was being used for this purpose, during experiments on the activation of cholinergic vasodilator nerves to skeletal muscle in decerebrate cats (Abrahams, Hilton & Zbrozyna, 1960), when it was found that the dose used to paralyse skeletal and respiratory muscles for 20 to 30 min also abolished the action of the vasodilator nerve fibres. Further experiments have shown that these doses of decamethonium affect transmission at a number of sites in the autonomic nervous system of the cat. METHODSThe experiments were performed on cats anaesthetized with chloralose (70 mg/kg) given intravenously after the induction of anaesthesia with ethyl chloride and ether.Regional blood flows were registered by the venous outflow technique using a transistorized drop recorder. The preparations for muscle, skin and submandibular salivary gland blood flow were those previously described (Hilton & Lewis, 1955;Abrahams, Hilton & Zbrozyna, 1960). Salivary secretion was recorded from the cannulated duct of one submandibular salivary gland: the gland was stimulated via a fluid electrode attached to the cut chordolingual nerve. The heart rate was recorded by means of a Statham strain gauge transducer connected to a cannula in one femoral artery, records being made with a high-speed pen recorder.Records of intestinal activity were made in situ by introducing a small rubber bag into a loop of small intestine through a small slit. About 1 ml. of normal saline was introduced into the rubber bag, which was then connected by polythene tubing to a Statham strain gauge. One vagus nerve was dissected free in the neck, divided, and the peripheral stump placed on platinum stimulating electrodes and immersed in liquid paraffin. Stimuli were supramaximal square waves, 10/sec, with a pulse width of 1 msec.

The heart rate responses to carotid body chemoreceptor stimulation in the cat

“…It may be argued that the cardiac response to carotid body stimulation was in some way dependent on the fact that decamethonium was given to paralyse any spontaneous respiratory movements. In this connexion Abrahams & Hilton (1961) found that decamethonium paralysed vagal post-ganglionic nerve endings in the cat. In experiments in which a bilateral pneumothorax was made before applying positive pressure ventilation, similar results were obtained on stimulation of the carotid bodies.…”

“…In this connexion Abrahams & Hilton (1961) found that decamethonium paralysed vagal post-ganglionic nerve endings in the cat. In experiments in which a bilateral pneumothorax was made before applying positive pressure ventilation, similar results were obtained on stimulation of the carotid bodies.…”

Heart rate changes evoked by hypoxia in the anaesthetized, artificially ventilated cat

“…Tachycardia could also be caused by increased secretion of adrenal catecholamines, which has been observed in both the cat and the dog (Anichkov, Malyghina, Poskalenko & Ryzhenkov, 1960;Critchley, Ellis & Ungar, 1980). Interpretation of some experiments is further complicated by non-specific actions of muscle relaxants used for control of respiratory movements (Abrahams & Hilton, 1962;Clark & Mitchelson, 1976;Birmingham & Husain, 1980); newer, steroid-based relaxants, especially vecuronium, are more specific (Sutherland, Squire, Gibb & Marshall, 1983;Saxena, Dhasmana & Prakash, 1983).…”