Acceleration of the heart by the vagus in cats after complete sympathectomy

Abstract

In the course of experiments on totally sympathectomized cats, we had occasion to observe the effects on the heart of stimulation, after the administration of atropine, of the peripheral ends of the vagus nerves cut in the neck.In the normal cat, stimulation of the vagus after atropine does not affect the heart frequency, but in some of the sympathectomized cats we have observed accelerator effects. The existence of accelerator fibres has been demonstrated in the dog's vagus [Morgan & Goland, 1932], but there appears to be general agreement that the vagus of the cat does not contain such fibres [Hering, 1924], and our observations on normal cats confirmed this. We have therefore undertaken some experiments to explain this anomalous acceleration which we observed in the sympathectomized animals. RESULTSThose cats in which we observed the abnormal acceleration by the vagus had, in all cases, been subjected to complete sympathectomy by the method of Cannon, Newton, Bright, Menken & Moore [1929], with the slight modification that, in completing the operation at the upper end of each thoracic chain, we gripped the stellate ganglia with forceps, and removed them by forcible avulsion, breaking the rami communicantes, the nervi accelerantes and the two branches of the annulus Vieussenii near their junction below the middle cervical sympathetic ganglion, leaving the latter in situ. Two to two and a half months had in all cases elapsed between the first stage of the operation and the final experiment.In one of our experiments on a sympathectomized cat, after decerebration, we observed that the normal fall of blood pressure produced by stimulation of the peripheral end of the cut right vagus nerve in the neck was followed, when the stimulation was ended, by a rise of blood pressure and an acceleration of the heart. The administration of atropine, in a dose sufficient to abolish 1 Leverhulme Scholar. PH. CI. 25

The influence of acute sympathetic denervation, reserpine and choline xylyl ether on vagal escape

“…The intrinsic myocardial mechanism for vagal escape is unmasked when the influence of these fibres is eliminated (Brown & Maycock, 1942). In the present study it was found that acute stellate ganglionectomy combined with spinal transection does not alter significantly the pre-stimulation heart rate or its restoration during vagal stimulation, which suggests that the primary mechanism of ventricular escape is localized in the heart and the influence of peripheral sympathetic nerves is secondary.…”

“…Moreover, the fact that tachycardia can be induced by acetylcholine or by vagal stimulation in the atropinized heart (Jourdan & Nowak, 1936; Kabat, 1939;Brown & Maycock, 1942; Hoffmann, Hoffmann, Middleton & Talesnik, 1945;Heymans & Bennati, 1949) suggests the possibility that acceleration occurs through the activation of sympathetic structures (ganglia and/or chromaffin tissue) located in the myocardium (Heymans & Bennati, 1949;Ginzel & Kottegoda, 1953; Burn, Leach, Rand & Thompson, 1959). Other findings suggesting a possible peripheral activation of adrenergic structures by acetylcholine have been presented by Burn & Rand (1959).…”

The inhibitory nerve fibres in the vagal supply to the guinea‐pig stomach

“…Directly contradictory results concerning their central connexions have been obtained by a number ofworkers (for instance, compare the results obtained on cats by Dale, Laidlaw & Symons (1910), Brown & Maycock (1942) and Pannier (1946)). But it is interesting to note that, at least in guinea-pig atria, the vagal cardio-acceleration is not prevented by guanethidine (Greeff et at.…”

Visceral Functions of the Nervous System

“…The effect was abolished when the middle cervical ganglion was paralysed by nicotine. They conclude that the accelerated response to stimulation of the vagus is probably due to the formation of synaptic connections between pregang lionic vagus fibres and the denervated cells of the middle cervical ganglion (61).…”