Alboni Paolo, Alboni Marco, Bertorelle Giorgio
Divisione di Cardiologia, Ospedale Civile, Cento, FE.
G Ital Cardiol (Rome). 2010 Jan;11(1):20-7.
Vasovagal syncope (VVS) is characterized by sudden hypotension and bradycardia, due to inhibition of the sympathetic system and activation of the vagal system, respectively. Major lines of evidence suggest that classical (emotional and orthostatic) VVS is not a disease, but a characteristic of the individual. It is, therefore, interesting to investigate the factors that can explain its origin and evolution and, to this purpose, we investigated the available literature data on the vasovagal reflex in animals, including humans. We found two processes in vertebrates, which appear relevant to the investigation of VVS evolution: fear and threat bradycardia in animals and vasovagal reflex during hemorrhagic shock, both in animals and humans. The trigger of the latter is thoracic hypovolemia, the same of the vasovagal reflex occurring in humans during orthostatic stress (prolonged standing, tilt testing). During thoracic hypovolemia, the vasovagal reflex in humans seems to share physiological mechanisms similar to those observed in other mammals, that is an activation of the vagal system and an inhibition of the sympathetic system, preceded by an activation of the same system. Even emotional VVS in humans seems to share physiological mechanisms similar to those observed in other vertebrates during fear/threat bradycardia. Therefore, the vasovagal reflex appears to be predisposed in humans and other vertebrates with the same mechanisms and this may indicate a common evolutionary root. If the vasovagal reflex persisted for millions of years along the vertebrates evolutionary history, we can reasonably assume that it has (or it maybe had in the past) a function. Also, since this reflex is sporadically displayed, a role as a "defense mechanism" appears likely. The most likely hypothesis is a defense mechanism of the heart during stressful and possible dangerous heart conditions. The slowing of heart rate induced by the vasovagal reflex may constitute a beneficial break of cardiac pump (thereby reducing myocardial oxygen consumption) and permit better diastolic filling and coronary perfusion.
血管迷走性晕厥（VVS）的特征是突然出现低血压和心动过缓，分别是由于交感神经系统受到抑制和迷走神经系统被激活。主要证据表明，典型的（情绪性和直立性）血管迷走性晕厥不是一种疾病，而是个体的一种特征。因此，研究能够解释其起源和演变的因素很有意思，为此，我们研究了包括人类在内的动物血管迷走反射的现有文献数据。我们在脊椎动物中发现了两个与血管迷走性晕厥演变研究相关的过程：动物的恐惧和威胁性心动过缓以及动物和人类失血性休克期间的血管迷走反射。后者的触发因素是胸腔血容量减少，这与人类在直立应激（长时间站立、倾斜试验）期间发生的血管迷走反射相同。在胸腔血容量减少期间，人类的血管迷走反射似乎与其他哺乳动物观察到的生理机制相似，即在同一系统激活之前，迷走神经系统被激活，交感神经系统受到抑制。甚至人类的情绪性血管迷走性晕厥似乎也与其他脊椎动物在恐惧/威胁性心动过缓期间观察到的生理机制相似。因此，血管迷走反射在人类和其他脊椎动物中似乎具有相同的易感性机制，这可能表明存在共同的进化根源。如果血管迷走反射在脊椎动物的进化历史中持续了数百万年，我们可以合理地假设它具有（或者过去可能具有）一种功能。此外，由于这种反射是偶尔表现出来的，它作为一种“防御机制”的作用似乎很可能存在。最有可能的假说是在应激和可能危险的心脏状况下对心脏的一种防御机制。血管迷走反射引起的心率减慢可能构成心脏泵的有益中断（从而减少心肌耗氧量），并允许更好的舒张期充盈和冠状动脉灌注。
