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.
Animals ; Anticoagulants/*pharmacology ; Chemistry, Analytical ; *Garlic ; In Vitro ; *Plants, Medicinal ; Rabbits