Total thyroidectomy showed a marked diuretic effect to McKee's dog and its ascitic fluid considerably decreased or disappeared. The titre of serum antidiuretic activity in McKee's dogs was generally high. On the contrary, a diuretic activity was observed in the thyroidectomized group. The existence of some unknown substance which promotes diuresis was suggested. The intrahepatic portogram of the normal dog and thyroidectomized group showed the gregular pattern of vascular branching and fine foliage, but in McKee's dog, the portogram showed such as “leafless tree” without fine foliage. In McKee's dog, liver lymphangiography revealed the existence of intrahepatic lymph duct and its dilatation, and the dilatation of the thoracic duct was also observed. There was no appreciable difference between normal and thyroidectomized dog. Administration of antithyroid drugs to the McKee's dog showed no evidence of loss of ascites. No influence of various diuretics on water excretion was observed. All the dogs subjected to caval constriction after thyroidectomy developed ascites. The thoracic inferior vena cava was constricted 4 weeks after preliminary hypophysectomy in 22 dogs. In all of these dogs, the urine volume progressively decreased after constriction and the girth increased remarkably. In 5 thyroidectomized dogs of this group, the effect of thyroidectomy was not seemed at all. The mechanism of effect of thyroidectomy on ascitic fluid may be ascribed, at least in part, to a certain substance which might be diuretic activator.
The behaviours of amylase in the bile were examined in rats under various experimental conditions. The results obtained were as follows: 1) Biliary amylase output of the normal rats was 0.275±0.048 (Mean±S.E.) I. U./hour. Biliary amylase output was positively correlated with amylase activity in the bile (P<0.01). 2) The intravenous infusion of dehydrocholic acid caused an increase (P<0.01) of the bile flow and a decrease (P<0.05) of the amylase activity in the bile. Thus, the biliary amylase output was virtually unchanged.3) The intravenous injection of hog pancreatic amylase produced increase of both the plasma amylase activity (P<0.01) and the biliary amylase output (P<0.01). 4) The intravenous injection of hog amylase produced an abrupt rise followed by slow decrease of plasma amylase activity. In the nephrectomized rats, the decay of plasma amylase activity developed later than that in the controls (P<0.05), and the biliary amylase output showed gradual increase during this phase. 5) In the bile-duct-ligated rats, hog amylase was injected intravenously and the similar behaviour of plasma amylase activity as described in (4) was observed. The decay of plasma amylase activity developed later in these rats than that in the controls (P<0.01). 6) Pancreatic damage was produced by the obstruction of the pancreatic duct. In these rats, plasma amylase activity (P<0.01) and biliary amylase output (P<0.01) were increased. There was a positive correlation between the former and the latter (P<0.01). 7) Acute hepatic damage was produced by the CCl-intoxication. In these rats, neither amylase activity in plasma and in bile nor biliary amylase output showed any significant change, compared to those in control rats. 8) Chronic hepatic damage was produced by the CCl- intoxication. In these rats, amylase activity in plasma and in bile increased (P<0.05) but bile flow slightly decreased. Therefore amylase output increased insignificantly compared to that in control rats. Thus in hepatic damage of correlation was found between plasma amylase activity and biliary amylase output and this finding was quite different from the phenomenon observed in pancreatic damage. These findings suggested that amylase in the bile originated from blood amylase, and that the regulation of plasma amylase activity was influenced by the biliary amylase excretion.
In order to investigate the relation between the morphology and function of gastric secretory cells, gastro-endoscopic biopsy was performed on 9 subjects. They were divided into 2 groups, namely, 5 essentially intact gastric mucosa and 4 advanced atrophic gastric mucosa. The fine structural changes between 2 groups of parietal cells induced by Histalog were comparatively analysed. In this study, parietal cells to be examined were obtained from middle portion of the gastric corpus in greater curvature. Moreover, the part of gastric gland examined was restricted to the middle region. Morphological changes appeared mainly in basal and lateral cell membranes, mitochondria, Golgi apparatus, nucleus, vesicular component, intra-cellular canaliculus and microvillus. These alterations became prominent at 10 minutes after stimulation in normal gastric group, and at 20 minutes in advanced atrophic gastritis group. In addition to alterations in the above mentioned organellae, the changes in lysosome and vacuole containing body were especially prominent in advanced atrophic gastritis group. These morphological changes in advanced atrophic gastritis group were more diffuse than in normal gastric group. The above results may well be correlated with the assumption that the function in advanced atrophic gastritis group is very much disturbed. As to the secretory mechanism of HCl in parietal cells, I would say conclusively that eccrine secretion is seen in most cases, while micro-apocrine secretion is seen in only a few cases.