An action of adrenaline on transmission in sympathetic ganglia, which may play a part in shock

Abstract

We have had two reasons for approaching this problem. One of us [Burn, 1932] showed that when the hindleg of a dog was perfused with defibrinated blood through a cannula tied in the abdominal aorta 34 cm. above the bifurcation, the vasoconstriction produced by stimulating the lumbar sympathetic chain was very small. When adrenaline was added to the perfusing blood, however, the effect of the same stimulation was greater, and this augmentation outlasted the effect of the added adrenaline on the vascular tone. The observations were taken to mean that sympathetic stimulation was effected by the liberation of adrenaline from the post-ganglionic endings, and that in the preparation used the necessary store of this adrenaline was depleted, until it was restored by addition of adrenaline to the blood. Thus, the augmentation of the effect of sympathetic stimulation was thought to be due to a change at the post-ganglionic terminations.Recently, Dr P. Glees called our attention to a paper by Stohr [1939] in which large-scale drawings of sympathetic ganglia showed the ganglion cells surrounded by what St6hr described as chromaffine tissue. Dr Glees himself obtained phlotographs showing similar small cells. Reflexion suggested that if chromaffine celLs were present in sympathetic ganglia, they presumably exerted some function. What function could adrenaline have in sympathetic ganglia? The question recalled the observations which have just been described, in which the stimulation was applied to the preganglionic fibres of the sympathetic chain. It was clear that the augmentation of the effect of stimulation produced by adrenaline might have been due to a change in the ganglion whereby transmission was improved.Our second reason for studying this question was that we have recently [Biilbring & Burn, 1941] made observations on the transmission of impulses in the spinal cord, and have observed three effects of adrenaline. We found that adrenaline facilitated the action of small doses of acetylcholine in causing PH. CI. 20

Observations on the action of acetylcholine and adrenaline on the hypothalamus

“…There is now a considerable body of evidence (Marrazzi, 1939;Bulbring & Burn, 1939, 1942Luco, 1939;Biilbring, 1944) that adrenaline can, according to dose, potentiate or inhibit the effect of ACh peripherally both at neuromuscular junctions and in autonomic ganglia, and more centrally in the spinal cord. Verney's work (1947) has shown that adrenaline can prevent the emotional inhibition of renal activity by a central action, and Pickford (1939,1947) and Duke et at.…”

The Electrogenesis of Adrenaline-Hyper-Polarization of Sympathetic Ganglion Cells in Bullfrogs

“…ECCLES and LIBET(1961)suggested that a catecholamine may be the mediator of a slow surface positive potential, which corresponds to the slow inhibitory postsynaptic potential(slow IPSP).In fact,a membrane hyperpolarization is produced by the direct action of catecholamines (LUNDBERG, 1952;DEGROAT and VOLLE, 1966), and it has been recorded by the sucrose-gap method (LIBET, 1970;LIBET and TOSAKA, 1970) and also using intracellular microelectrodes (LIBET and KOBAYASHI, 1969;KOBAYASHI and LIBET, 1970;CHRIST and Man, 1971) in mammalian sympathetic ganglia. On the other hand,membrane depolarization produced by the direct action of catecholamines (BULBRING and BURN, 1942) has also been recorded using extracellular electrodes (DEGROAT and VOLLE, 1966) and intracellular microelectrodes (CHRIST and NISHI, 1971) in these ganglia.…”

The Effect of Sympathomimetic Amines on Femoral Arterial Blood Flow in the Cat

“…Marrazzi (1939) and Bulbring & Burn (1942) showed that adrenaline may inhibit ganglionic transmission but again this effect was produced only by doses greatly in excess of those required to produce femoral vasodilation.…”