The effect of chlorpromazine on haemostasis

Abstract

RECENT STtrDmS INDICATE that the lethal effect of experimental, traumatic and chronic haemorrhagic shock is decreased or prevented by pre-treatment with chlorpromazine (1,2). In animals this treatment also attenuates the deleterious influence of bacterial invasion, and when bacterial contamination does occur, congestion and haemorrhage in the bowel does not develop (8). In a clinical study of patients undergoing surgical treatment for pulmonary tuberculosis, it was found also that pre-treatment with chlorpromazine possibly prevented or minimized the decompensatory uptake of blood following severe or prolonged haemorrhage and improved the postoperative course of these patients (4).This protective action of chlorpromazine has been partially explained on physiological, pharmacological and psychological grounds. Physiologically, the major known effect of the drug is to decrease peripheral vascular resistance. This causes hypotension and reduces the head of pressure in the peripheral circulation (5, 6). Zweifach and associates believe that the protection afforded by chlorpromazine is due to the block of neurogenic peripheral vascular control and a hyper-reactive response by the arterioles and venulc~ to vaso-active materials in the circulation during sh'ess (7). This hyper-reactivity sustains regional blood flow in the presence of a decreased circulating blood volume more effectively than sympathetic over-compensation in response to stress as seen in the unprotected or unblocked peripheral circulation. This effect is noted both in the visceral and in the peripheral (sldn) circulation. The hyper-reactivity of arterioles and venules is considered a favourable sign, indicating that tJhe deleterious pooling of blood in the splanchnic area, as seen in irreversible shock, has been eliminated and that a sustained circulation of the skin and peripheral vascular bed is present in spite of depletion of the blood volume.Pharmacologically, there is a potent anti-adrena~u effect, a protective action on the heart against epinephrine-induced arrhythmias of chloroform, cyclopropane and trichlorethylene; a slight anti-histaminic effect, an anti-acetytcholine (parasympatholytic) effect; and a potent anti-5-hych'oxytryptamine effect. There is also a moderate local anaesthetic effect and a "pharmacological leucotomy" which extends from the level of the cortex to the brain 'stem and to the cervical ganglia (8, 9, i0, 11, 12, 18).Psychologically, chlorpromazine suppresses primary epinephrine-precipitable subcortical warning or tension anxiety. It exerts only an indirect influence on the secondary cortical manifestations, consisting of the traumatic state of the ego, ir~ inverse proportion to the degree to which important ego functions have been

Are metabolic disorders part of a severe mental illness? Historical and current perspective

“…As early as in 1954, Dobkin et al published the results of an experiment in which 7 healthy volunteers were administered chlorpromazine. It was noticed that in these people the level of glucose in blood significantly increased [36]. It is now known that some antipsychotic drugs disturb the carbohydrate metabolism, which in turn contributes to the development of type 2 diabetes.…”