RECENTLY two of us [W. F. and B. M., 1933] have shown that a substance pharmacologically indistinguishable from acetylcholine can be detected in the venous blood collected from the suprarenals during splanchnic stimulation, when eserine is present, but that no such substance is present in the absence of stimulation. It seemed to us that it should be possible to demonstrate the effects of this liberated acetylcholine either on the arterial blood-pressure or on a distant organ of the same animal, if the blood from the suprarenals containing it were allowed to flow normally into the general circulation. This possibility was tested in the experiments described in the first part of this paper. To detect the acetylcholine by its action on a distant organ we used the submaxillary gland.Experiments thus to detect acetylcholine, by its action on other systems of the animal into the blood of which it is liberated, are complicated by the actions of adrenaline, the output of which from the medullary cells is the main and more obvious effect of the splanchnic stimulation. It is necessary in some way to suppress the actions of this adrenaline, or, allowing it to produce its normal effects, to demonstrate the action of acetylcholine only as a complication or phase of the total effect. Both methods have been used.The demonstration that acetylcholine is liberated from the suprarenal bodies during splanchnic stimulation does not, however, provide a direct proof that acetylcholine is the direct cause of the adrenaline discharge. As evidence of this function of acetylcholine, we consider, in the second part of this paper, the effect of eserine on the response of the suprarenals to splanchnic stimulation by the discharge of adrenaline.
Studies on the simultaneous influence of the reticular formation of the brain stem on the patellar and jaw reflexes showed that stimulation of the medial portion of the medulla oblongata dorsal to the pyramids consistently inhibited the patellar reflex as had been described by Magoun ('44) and Magoun and Rhines ( '45 ; '46) but simultaneously facilitated the linguomandibular reflex. Stimulation of the more lateral and rostra1 regions of the reticular formation, on the other hand, which facilitated the patellar reflex as had been shown by Rhines and Magoun ( '46) simultaneously inhibited the reflex lowering of the mandible. These preliminary results (King, Minz and Unna, '52) indicated a reciprocal relationship between the extensor-type (patellar) and the flexor-type (linguomandibular) reflexes which was not in accord with the conclusion of Magoun and his co-workers that areas in the brain stem reticular formation either facilitated all reflex and cortically-o r subcortically-induced motor activity or inhibited it. Extensive studies were therefore undertaken
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