Isbister J P
Haematology and Transfusion Medicine Department, Royal North Shore Hospital of Sydney, St Leonards, NSW, Australia.
Transfus Sci. 1997 Sep;18(3):409-23. doi: 10.1016/S0955-3886(97)00040-4.
Adequate cardiac output and tissue perfusion is dependent on intravascular blood volume and its adequate return to the heart. Considering the overall functions of the cardiovascular system in ensuring appropriate flow to the peripheral microcirculation, it is not surprising that conflicts of interest may occur when an organism is exposed to stresses. Of particular importance are the stresses in which there are increased oxygen demands, decreased oxygen availability and concomitant requirements for thermoregulation. When there is depletion of intravascular blood volume, the splanchnic circulation is in effect an "autologous blood bank" for maintaining venous return until trans-capillary refill and haemodilution occurs. With the acute haematological stress response centralisation of blood, secondary contraction of the venous capacitance occurs, as seen with acute hypoxia. This results in overfilling of the heart, activation of atrial volume receptors, release of atrial natriuretic peptide and subsequent reduction of the plasma volume by rapid shifting of plasma into the lymphatic capacitance (via spleen) and transcapillary efflux throughout the circulation. In this overview the physiology and pathophysiology of blood volume, red cell mass and plasma volume regulation is reviewed.
充足的心输出量和组织灌注取决于血管内容量及其回心的充足程度。考虑到心血管系统在确保外周微循环适当血流方面的整体功能,当机体受到应激时可能出现利益冲突就不足为奇了。特别重要的是那些氧需求增加、氧供应减少以及伴有体温调节需求的应激情况。当血管内容量耗竭时,内脏循环实际上是一个“自体血库”,用于维持静脉回流,直到发生跨毛细血管再充盈和血液稀释。随着急性血液学应激反应导致血液集中,静脉容量会继发收缩,如急性缺氧时所见。这会导致心脏过度充盈、心房容量感受器激活、心房利钠肽释放,随后通过血浆快速转移至淋巴容量(经脾脏)以及整个循环中的跨毛细血管外流,使血浆量减少。在本综述中,将对血容量、红细胞量和血浆量调节的生理学和病理生理学进行回顾。