Riboflavin and Thiamine Absorption

For the purpose of estimating the maximum absorption of riboflavin and thiamine from the intestine, large test doses of riboflavin and thiamine were administered orally to apparently normal male subjects, receiving normal Korean diets, and their maximum absorption were estimated by determining the excretion in urine. The maximum absorption of riboflavin and thiamine were estimated 10.700 and 3.800 mg. respectively.

The Development of the Ruminal Ulcer in the Albino Rats Fed with Low Protein Diet associated with Rocking Stress

The pathological changes of the gastric rumen produced by rocking stress in 38 young male albino rats fed on low protein diet for a short period and in 20 young male albino rats fed on low protein diet only as the control rats, were investigated macroscopically and histologically. The ulcerative lesions of the gastric rumen were observed in 17 out of 38 experimental rats accompanied with hyperplasia and cornification of the ruminal epithelial layer and more or less edematous changes of the tunica propria near the ulcer site. The authors, finding of the ruminal ulcer in albino rats produced by rocking stress associated with feeding on a low protein diet for a short period were compared with the results of others. The authors discussed other opinions concerning of the gastric ruminal ulcer of the albino rats produced in various ways.

The L-Ascorbic acid Absorption

When about 300mg of L-ascorbic acid was given intravenously to the adults saturated with the vitamin, the increased blood level returned to almost the original level in 3 hours. Also the amounts of the vitamin absorbed by the tissue cells and metabolized in the body or excreted into the gastrointestinal tract were found to average 74.1mg in 3 hours. When about 300mg of L-ascorbic acid was given intravenously twice at intervals of 3 hours, an average of 101 mg of the vitamin was absorbed by the tissue cells and metabolized in the body or excreted into the gastrointestinal tract in 6 hours. When the vitamin was given orally to the saturated adults, the absorption rate increased as the test does increased. When large amounts (3.0gm) of the vitamin were given, the absorption rate reached the maximum. The maximum absorption in 6 hours was estimated as 681 mg of the vitamin.

A Blood Anticoagulant Substance from Garlic (Allium Sativum); I. Its Preparation and Studies on its Anticoagulant Effect

The blood eanticoagulant factor (G. E.) in garlic was isolated. This substance was precipitated at a neutral pH as the calcium salt in water, and then the calcium salt was dissolved at a pH of 3.0. Calcium was removed by adding sodium oxalate. Then G. E. was precipitated by adding two volumes of 95% ethanol. The effect of G. E. on blood coagulation was studied; prothrombin time, blood clotting time, antithrombin, anti-Ac-globulin and fibrinolysis. A half mg of G. E. completely inhibited one ml of blood from coagulating. The blood specimen containing G.E. showed a prolongation of the prothrombin time. As the calcium ion concentration increased, the prothrombin time of the plasma containing G. E. was reduced, but not to that of the control(oxalated plasma). This indicated that G. E. inhibited the prothrombin time by precipitating calcium ions, and, in addition to this calcium precipitation, another means of G. E. inhibition may be present. G. E. showed fibrinolytic effects and, in the prothrombin time tests, the plasma containing G. E. always showed less fibrin formation than was shown with oxalated plasma. G. E. showed inhibition of fibrin formation in experiments on its antithrombic effect. But this action may not be due to the antithrombin effect of G. E. but to the fibrinolytic effect of G. E. In in-vivo experiments G. E. did not show any anticoagulant effect. From these facts, it may be said that G. E. has an anticoagulant effect in at least two ways in vitro; first by precipitating calcium ions and secondly by causing fibrinolysis.

A B1ood Anticoagulant Substance from Garlic(Allium Sativum); II. Chemical Analysis and Studies on the Biochemical and Pharmacological Effects

G. E. as prepared in our laboratory is a non-volatile white substance, which is odorless and water soluble. Only in vivo does it have a hypotensive effect, while both in vivo and in vitro it has a hypo-calcemic effect. We determined the chemical analysis, toxicity, lethal dose, and the effect on isolated intestinal and auricular movements of rabbits of G. E. The sodium salt of G. E. contains 18.7% Phosphorus and l5.7% Sodium. It contains inositol and a small amount of sulfur and nitrogen. The ratio of inositol: phosphorus: sodium is 1:6:6.7. Also G. E. may contain phytic acid and other mat erials which have not been identified. Toxicity tests of G. E. done on mice. The first symptoms of toxicity in mice began with irritability and unstable walking, which were followed by dyspnea and sluggish movement, and finally by coma. Mice LD 50 was 222mg/kg. As the dose of G. E. was increased in successive injections in the rabbits, the rabbits died, when the total dose reached 100-200 mg%. Probably G. E. is not destroyed quickly nor excreted rapidly. The blood pressure in the rabbits continued to fall at each injection indicating no development of tachyphylaxis. If 70mg. of G. E. was injected intravenously, as one dose, the rabbit died with muscular hyperactivity. On post mortem examination, we found G. E. had a hypocalcemic effect. However if the calcium salt of G. E. was injected no muscular hyperactivity developed, but severe hypotension was observed. The hypocalcemic effect of G. E. is due to the combining of G. E. with the blood calcium and the muscular activity may be secondary to hypocalcemic. The G. E. hypotensive effect in atropinized rabbits and in ganglionic blocked rabbits (Hexamethonium) was the same as the effect found in rabbits which had not been drugged. Epinephrine also did not change the hypotensive effect of G. E., G. E. itself showed no effect on the isolated intestinal and auricular movements of a rabbit as long as there were enough calcium ions in the solution. Hence we can not say that the hypotension of G. E. is due to vagus stimulation and or to paralysis of sympathetic nerve endings. The mechanism of the hypotensive effect of G. E. is not yet clear.