Abstract

Vasovagal syncope, although often seen as a disease, is the result of a neurophysiological reflex which can be induced in most healthy people after a 30 % reduction in blood volume either by venous pooling or by hemorrhage. Studies in mammals showed that the activation of certain brainstem nuclei including the caudal midline medulla is responsible for hypotension and bradycardia following central hypovolemia. The hypothesis is presented that vasovagal fainting developed during the evolution in order to support hemostasis. Bleeding animals with a central mechanism for the initiation of hypotension had presumably a better chance for blood clot formation and hemostasis than animals with normal blood pressure. In the context of this hypothesis, vasavagal fainting with blood or injury displaying stimuli can be understood as an early attempt to support hemostasis before the development of larger blood losses.

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