Abstract

Widal was the first to stress the blood changes occurring during anaphylactic shock. These changes included leucopenia, modifications in the blood clotting time and low blood pressure. Later, D'Amato and Zappacosta1, stated that in patients with tuberculosis and syphilis, the hemoclastic shock provoked by tuberculin or antisyphilitic drugs was followed by changes in the distribution of the different blood proteins, affecting mainly the globulin fraction. Aubry, Thiodet, and Ribere2-', studied the blood protein equilibrium in allergic patients. They claimed that there was a definite change in the concentration and in the distribution of the protein fractions, and that variations might be closely related to sensitization phenomena and its intensity. Determinations made in the same individual, but in different phases of activity of the allergic process, showed a decrease in the blood globulin concentration, closely paralleling the activity and intensity of the allergic symtpoms, resulting in an increased A: G ratio. After the parxoysmal crisis the total proteins and the ablumin and globulin fractions returned to normal levels or close to the normal. More recently the gold curves obtained by Anderson6 using allergic sera suggested that some chemical mechanism is involved in allergic phenomena with its accompanying edema and discharge of serum and mucus. It was thought tha~ disturbances in the water balance, or in the combination of water with protein molecules might be at fault. Instead of the presence of an abnormal substance, there may be an absence of some factor which maintains complete solution of the body proteins in the water of the living cells. A combination of both factors is probably responsible for allergic lesions. . SomogyiG thinks that changes in water metabolism leading to edema are the result of a depletion of serum albumin subsequent to allergic shock. The loss of albumin with its capacity to fix inorganic ions would result in the escape from the blood to the tissues of the necessary amount of water to keep the osmotic pressure balanced. According to Widal and others7, shock could be the result of a definite disturbance in the blood colloids (hemoclasis and colloidoclasia), characterized by an impairment of the liver which normally acts as a barrier against the entrance into the general circulation of foreign proteins (proteopexis). Walzer&, however, has shown that the portal injection of a protein equivalent

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