Diehl Rolf R
Autonomic Laboratory, Dept. of Neurology, Krupp Hospital, Alfried-Krupp-Str. 21, 45117, Essen, Germany.
Clin Auton Res. 2005 Apr;15(2):126-9. doi: 10.1007/s10286-005-0244-0.
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.
血管迷走性晕厥虽然常被视为一种疾病，但它是一种神经生理反射的结果，在大多数健康人身上，通过静脉淤积或出血导致血容量减少30%后，这种反射就可能被诱发。对哺乳动物的研究表明，包括延髓尾侧中线在内的某些脑干核团的激活，是导致中枢性血容量不足后出现低血压和心动过缓的原因。有人提出一种假说，即血管迷走性昏厥是在进化过程中发展而来，以支持止血。与血压正常的动物相比，具有引发低血压中枢机制的出血动物可能有更好的机会形成血凝块并实现止血。在这一假说的背景下，面对血液或损伤等显示刺激因素时发生的血管迷走性昏厥，可以被理解为在出现更大失血之前支持止血的一种早期尝试。
