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Vagally denervated (Heidenhain) pouch acid outputs and serum gastrin concentrations, basal and in response to feeding, were measured in dogs before and after massive intestinal resection. Both 24-hr and postprandial Heidenhain pouch acid outputs increased (P less than 0.01) after intestinal resection. Increases in serum gastrin concentrations following feeding were greater after massive resection of the small intestine. There was an excellent correlation (r= 0.967; P less than 0.005) between increases in serum gastrin concentrations and Heidenhain pouch acid outputs after intestinal resection. These studies support and are consistent with the hypothesis that the polypeptide hormone gastrin plays a role in the production of the gastric acid hypersecretion which, in both dogs and man, frequently results from massive resection of the small intestine.

1. A double sucrose gap method to clamp small bundles (diameter 0.8-1.2 mm) of sheep or calf ventricular fibres is described.2. Comparison between micro-electrode recordings from the central gap and the externally recorded potentials showed good agreement between the time course and amplitude of the action potentials. The rapid sodium inward current was not controlled on depolarizing clamp steps. On repolarization, control was obtained within 20 msec. The method is regarded as only suitable for a study of slow currents.3. During clamps of several seconds duration slow changes in outward current can be demonstrated. The potential, where the instantaneous current-voltage relationship crosses the voltage axis, shifted in a positive direction as the clamp duration was increased (clamp amplitude constant), and did not alter much if the clamp amplitude was increased while the duration remained constant. For these reasons it is concluded that K ions accumulate round the cells.4. A comparison between the instantaneous current-voltage relationship in various K solutions and after a depolarizing clamp, showed that an increase in external K could not exactly mimic the changes during a clamp. Because of this, a conductance change, unrelated to accumulation, is also postulated.5. To measure the influence of the slowly increasing outward current during an action potential, slowly increasing inward current (to reduce net outward current) was applied during an action potential and the prolongation of the action potential measured. In the same experiment the increase in outward current during a clamp in a solution with tetrodotoxin and Mn was measured. From these experiments it is concluded that the slow increase in outward current does not contribute much to repolarization in sheep or calf.6. Equations are derived for the voltage distribution and leakage current in the double sucrose gap. From the equations it is possible to calculate an optimal gap width. Too small a gap causes the membrane current to be swamped by the leakage current. Too wide a gap gives unequal potential distribution.

Canines with vagally innervated fundic pouches and chronic esophageal fistulas were subjected to sham feeding experiments during which pouch acid output and peripheral serum gastrin levels were measured. These dogs then underwent construction of vagally innervated antral pouches. The sham feeding experiments were repeated after recovery. Preoperatively sham feeding provoked a substantial increase in acid output accompanied by a small serum gastrin increase which did not achieve statistical significance. After creation of the innervated antral pouches, sham feeding evoked an acid secretory response similar to control values. Serum gastrins, however, increased nearly 500 percent in response to sham feeding. Our data support the concept that direct vagal stimulation of the parietal cell mass is the major mechanism by which sham feeding increased acid secretion.

Macrophage migration inhibition factor produced in response to purified hepatitis Bs antigen has been demonstrated in patients with and recovering from hepatitis B antigen-positive acute viral hepatitis. These results suggest that cell-mediated immunity against this antigen occurs concomitantly with the illness, and may be important in its pathogenesis. In addition, patients with chronic aggressive hepatitis, whether serologically positive or negative for hepatitis Bs antigen, were also found to have positive macrophage migration inhibition tests. This observation suggests a role for hepatitis B virus in the majority of patients with chronic aggressive hepatitis. Negative macrophage migration inhibition tests in response to the antigen were noted in acute viral hepatitis seronegative for the hepatitis B antigen, alcoholic hepatitis, normal controls, and carriers of the antigen.

Foregut endocrine polypeptide-secreting APUD cells (Amine-Precursor-Uptake and Decarboxylation), in their embryologic migration from neural crest to foregut may become "arrested" in the mesoderm or in other ectopic locations. They may become hyperplastic, adenomatous or malignant. Eight illustrative patients are reported. One patient had "pancreatic hyperparathyroidism" with hypercalcemic crises, pancreatic apudocarcinoma, normal parathyroids, biologically active parathormone, but inert immunochemically to the usual parathyroid antisera. Two had gastrin-secreting malignancies in the mesoderm. Remission after excision, but eventual recurrence of the syndrome due to islet cell hyperplasia required total gastrectomy. One patient had a gastric corpus apudocarcinoma found prospectively with hypergastrinemia which required excision of the tumor. One patient had acromegaly with hypergastrinemia and antral gastrinosis treated by pituitary irradiation, One patient had the antral or intermediary type of the Zollinger-Ellison syndrome with moderate hypergastrinemia, duodenal ulcer and antral gastrinosis, treated by vagotomy and antrectomy. One patient had hyperparathyroidism with antral gastrinosis, treated by parathyroidectomy. One patient had malignant Zollinger-Ellison syndrome and developed associated thyroid parafollicular cell hyperplasia and parathyroid chief cell hyperplasia, treated by total gastrectomy and multiple endocrine excisions. These investigative observations demonstrate ectopic loci and associated hyperplasias which support the concept of migration and bizarre potentiality of polypeptide-secreting cells of the foregut.

The Exalto-Mann-Williamson procedure produces peptic ulceration in nearly 100% of experimental animals but the mechanism is unknown. To investigate the possible hormonal role of the gastric acid hypersecretion seen after this procedure, we investigated preoperative and postoperative serum gastrin and secretin concentrations. There was no significant change in serum gastrin; however, serum secretin concentrations increased to 2 1/2 times the preoperatve value, most likely secondary to the enhanced secretion of gastric acid. These data do not suppport the theory that alterations in circulating secretin or gastrin levels are responsible for the gastric acid hypersecretion following the Exalto-Mann-Williamson operation.

The modern view of the mammalian ventricular action potential is that Na-ions are responsible for depolarization, the plateau is maintained by an inward Ca current and repolarization is due to the inactivation of this inward Ca current against a background outward K current. The electrical activity spreads over the surface and T-tubules of the cell and the inflow of Ca-ions, and possibly also the electrical signal, cause, a further release of Ca from internal stores, the lateral cisternae of the sarcoplasmic reticulum (SR). This released Ca, by triggering the splitting of ATP, induces contraction. The released Ca is pumped back into the longitudinal SR and, as the Ca concentration is reduced, relaxation occurs. The Ca in the longitudinal SR is transported back to the storage site in the cisternae. This completes the cycle, release, uptake, transport back to the releasing site. On the basis of this scheme, the action of various drugs is briefly discussed.

In seven dogs, prepared with gastrostomies and femoral and portal vein cannulas, insulin hypoglycemia was accompanied by an average of fivefold increase in the rate of acid secretion and the release of gastrin into the portal vein as measured by radioimmunoassay. The average peak of portal vein gastrin was 225 pg. per milliliter (range, 74 to 520). Gastrin release appeared to be triggered abruptly at glucose concentrations of 43 +/- 11 mg. percent. Vagal release of gastrin has been documented by direct measurement of this hormone.