Guanidine

GUANIDINE, NH = C(NH₂)₂, the diamide-imide of carbonic acid, in its free form consists of colorless crystals that greedily attract CO₂ and H₂O from the air and therefore deliquesce. With acids, guanidine forms salts, among which the sparingly soluble picric acid salt may be noted, which serves for the detection and isolation of guanidine. From solutions, guanidine is precipitated by phosphotungstic acid. It was discovered by Strecker in guano (bird droppings), from which it received its name. Under the influence of alkalis, as well as putrefactive bacteria, it converts into urea. It is part of the diamino acid arginine, as well as one of the purine bases, guanine, from which it can be obtained by oxidation. In nature, it is found in etiolated vetch leaves, in sugar beet juice; it has been found in Swiss cheese and in the products of autolysis of the pancreas. Among the derivatives of guanidine, the following should be noted: methylguanidine, found along with dimethylguanidine in the urine of dogs after extirpation of the parathyroid glands. Agmatine (aminobutylene-guanidine) has been found in herring sperm and in ergot. The alkaloid galegine, which is isoamylene-guanidine, has been detected in the seeds of Galega officinalis. Guanidine can be considered as urea in which oxygen is replaced by the imide group NH. This substitution is accompanied by very significant changes in both chemical and physiological properties. While urea is practically devoid of basic properties and is physiologically neutral, guanidine is a base whose strength approaches that of caustic alkalis and which possesses an extremely strong effect on the organism. The latter consists chiefly in the excitation of motor nerve endings and manifests itself in the form of fibrillary or bundle (fascicular) twitchings of the musculature, passing at higher degrees of poisoning into strong convulsions. On smooth musculature, guanidine in high concentrations (1:1,000) causes an increase in tone. Regarding the central nervous system, excitation is observed first (dyspnea, vomiting), followed by depression (apathy). Blood pressure changes insignificantly. The antagonist of guanidine is primarily curare, followed by calcium salts. Barium and quinine are synergists, enhancing the action of guanidine. When introduced into the organism, guanidine partially disappears, while a significant portion is excreted unchanged in the urine. Guanidine-acetic acid, glycocyamine, is methylated in the organism, turning into creatine. The picture of guanidine poisoning in many respects resembles the symptom complex of tetany occurring after the removal of or in case of insufficiency of the parathyroid glands: in addition to convulsions, hypoglycemia and a decrease in the calcium content of the blood are observed. Since the content of guanidine and methylguanidine in the blood increases during parathyroidectomy, this gave grounds to ascribe an important role to guanidine in the genesis of tetany (Noel Paton). The ability of guanidine and its derivatives to lower blood sugar content served as the basis for the development of a synthetic insulin surrogate, "synthalin" (decamethylene-diguanidine). Apparently, the action of "gluchorment" obtained by von Noorden from the pancreas is based on the presence of the same guanidine derivative. Quantitative microdetermination of guanidine in the blood can be performed colorimetrically by means of the following reagent (Weber): equal volumes of 10% solutions of sodium nitroprusside, potassium ferricyanide, and NaOH are mixed and diluted with three volumes of water. After 20 minutes, when the solution turns slightly yellow, it is ready for use; 1 cm³ of this reagent is taken per 5 cm³ of the fluid under study. The normal blood content found is 0.07–0.15 mg%; in hypertension, the content rises to 0.6 mg%.

V. Engelhardt.