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• The concentration of gastrin in serum and antral mucosa was studied in anesthetized dogs after electrical stimulation of the antral branch vagus nerve. Vagal stimulation caused immediate and sustained release of gastrin into the circulation. After stimulation for one hour, the gastrin concentration of antral mucosa increased significantly. This suggests that vagal release of gastrin triggers its rapid synthesis. (Arch Surg113: 87-89, 1978)

A 68-year-old patient with syncope associated with an urge to urinate differed from other cases of micturition syncope with respect to age, presence of cardiovascular and urinary disease, lack of association with recumbency, and loss of consciousness before onset of micturition. Investigation incriminated vagal stimulation from the distended bladder with transient blocking of the atrioventricular node as the likely mechanism. The patient was successfully treated with a permanent demand pacemaker. Micturition syncope is probably not a single entity, but a symptom complex arising as a result of several mechanisms. (JAMA229:1631-1633, 1974)

• Pancreatic polypeptide (PP), a 36-amino acid peptide, may function as an important feedback inhibitor of pancreatic secretion after a meal. It arises from both islet and acinar cells of the pancreas. Release of PP by a meal, primarily protein, occurs in a biphasic manner. The first rapid release occurs as a result of vagal stimulation; the second, more prolonged rise (the so-called intestinal phase) occurs in response to hormonal stimulation, predominantly cholecystokinin. Plasma PP levels increase with age; PP levels are elevated above those of age-controlled normal subjects in diabetic patients and in some patients with pancreatic amine precursor uptake decarboxylase tumors. The value of plasma PP as a possible marker for pancreatic tumors is as yet unsettled but may be a valuable tool. ( Arch Surg 1981;116:1256-1264)

Stimulation of the left efferent vagal nerve (2 msec, 5 V, 10 Hz), for up to 60 min in rats infected with 11-day-old Hymenolepis diminuta induced anteriad migration of worm scolex and biomass in the small intestine. Ligation at the pyloric sphincter prior to vagal stimulation shortened the length of time before significant relocation occurred and increased the migrational response. The results support the hypothesis that worm migration is mediated via vagal stimulation of gastrointestinal function, and is unrelated to actual feeding.

The influence of respiration and of vagal stimulation on the location of the cardiac pacemaker and on the form of the ventricular electrocardiogram has been reviewed by Wilson, 1 and need not be detailed here. In brief, so far as man is concerned, the pacemaker may be displaced from its normal location at the sino-auricular node to the auriculoventricular node, and vagal stimulation may affect the form of the ventricular electrocardiogram by producing a bundle branch block. In the case described below, marked alterations in the cardiac mechanism were associated with Cheyne-Stokes respiration and were brought about by vagal stimulation. In this instance, changes in the form of the ventricular complexes were due to displacement of the pacemaker into the branches of the His bundle, and it is the purpose of this paper to report such a disturbance in the cardiac mechanism. REPORT OF CASE The patient, a colored man, aged

Excerpt In routine electrocardiograms taken on healthy young adults without clinical evidence of heart disease, bundle branch block is a rare finding, occurring in less than 1 per cent.1, 2, 3, 4Ap...

In 1866 Czermack 1 demonstrated that digital pressure of the neck in the region of the vagus nerve caused a slowing of the heart rate in man. He attributed this effect to a mechanical excitation of the vagus nerve. Hering, 2 while making observations on this phenomenon, noted that very slight pressure resulted in marked cardiac inhibition in some instances. These observations led him to doubt the theory of direct vagal stimulation. Hering and his co-workers demonstrated conclusively that the slowing of the heart by digital pressure in the neck was the result of a reflex which originated in a specialized portion of the internal carotid artery, the carotid sinus. It has been observed that the usual response to pressure on the carotid sinus is a moderate slowing of the heart rate, but that in some instances there results a complete arrest of the heart for many seconds. The present

In 1876 Ferrier 1 stated: "There is no reason to suppose that one part of the brain is excitable and another not. The question is, how the stimulation manifests itself." As one is prone to look for active responses, one may fail to observe other manifestations elicited by electrical stimulation of nerve tissue. In 1845, biologic inhibition was first experimentally demonstrated by the Weber brothers, 2 who showed that vagal stimulation slowed the heart. For their studies a background of cardiac activity was necessary. Similarly, a background of activity is necessary for any studies of inhibition, whether central or peripheral. Setschenow 3 (1863) employed the "withdrawal" response of the frog's hindlimb as the background of activity for his attempts to localize inhibition within the central nervous system. Bubnoff and Heidenhain 4 (1881) showed that inhibition of a muscular contraction may be brought about through tactile stimulation of an ipsilateral member.