Woodson R D, Auerbach S
J Appl Physiol Respir Environ Exerc Physiol. 1982 Nov;53(5):1299-306. doi: 10.1152/jappl.1982.53.5.1299.
Effect of increased blood O2 affinity on cardiac output and its distribution was studied in conscious sedated rats by the microsphere-reference sample method. After a preliminary measurement of cardiac output and its distribution, rats were exchange transfused with normal blood or low-P50 (PO2 at which hemoglobin is half-saturated with O2) blood; other groups were made anemic with and without a simultaneous reduction in P50. Reduction in P50 from 38 to 17 Torr did not change cardiac output, pulse, or blood pressure but caused, after allowance for changes in controls, a 102% increase in coronary blood flow and an 88% increase in cerebral blood flow. Anemia (hematocrit = 22%) produced similar changes in coronary and cerebral flow. When anemia was combined with a 12-Torr reduction in P50, coronary and cerebral flow increased by 297 and 209%, respectively. These increases in coronary and cerebral flow were not attributable to increased cardiac work or hypercapnia. It is concluded that a left shift of the O2 dissociation curve induces increased blood flow to brain and heart, probably in compensation for decreased tissue O2 pressure.
采用微球-参比样品法，在清醒镇静大鼠中研究了血液氧亲和力增加对心输出量及其分布的影响。在初步测量心输出量及其分布后，给大鼠换输正常血液或低P50（血红蛋白氧饱和度为50%时的氧分压）血液；其他组造成贫血，同时或不同时降低P50。P50从38 Torr降至17 Torr，心输出量、脉搏或血压未发生变化，但在考虑对照组变化后，冠状动脉血流量增加了102%，脑血流量增加了88%。贫血（血细胞比容=22%）使冠状动脉和脑血流量发生类似变化。当贫血与P50降低12 Torr同时存在时，冠状动脉和脑血流量分别增加了297%和209%。冠状动脉和脑血流量的这些增加并非由于心脏做功增加或高碳酸血症所致。得出结论：氧解离曲线左移导致脑和心脏的血流量增加，这可能是对组织氧分压降低的一种代偿。
