Effect of increased blood-oxygen affinity on oxygen transport in hemorrhagic shock.
Effect of increased blood-oxygen affinity on tolerance of hemorrhagic shock was studied in pentobarbital-anesthetized rats. Rats were first exchanged transfused with blood whose P50 had been reduced by various methods by 4-21 Torr. Hypotension (BP = 30 Torr) was induced and maintained at this level by controlled hemorrhage; it was terminated when reinfusion of shed blood became necessary to sustain this blood pressure. Initial rate of bleeding during shock was inversely proportional to P50, varying from 0.52 ml.min-1.kg-1 in controls to 1.5 ml.min-1.kg-1 in the group with the lowest P50, a reaction probably indicating increased sympathetic output in the latter group. Duration of shock tolerance varied from 50 +/- 16 min in controls to 28 +/- 11 min (SD, P less than 0.001) in the group with the lowest P50. Central venous SO2 (SCVO2) and PO2 (PCVO2) were significantly higher and lower, respectively, in low-P50 animals than in controls, probably because of limited oxygen extraction due to increased blood oxygen affinity. VO2 and cardiac output were significantly lower, and mortality was significantly greater, in low-P50 animals. The data suggest that a left shift of the oxygen dissociation curve limits oxygen delivery during hemorrhagic shock.
D000818:Animals; D002248:Carbon Monoxide; D002302:Cardiac Output; D005078:Exchange Transfusion, Whole Blood; D006863:Hydrogen-Ion Concentration; D007022:Hypotension / Q000150:complications; D008297:Male; D010100:Oxygen / Q000097:blood; D010108:Oxyhemoglobins / Q000378:metabolism*; D051381:Rats; D012771:Shock, Hemorrhagic / Q000097:blood* / Q000150:complications / Q000401:mortality
D010108:Oxyhemoglobins; D002248:Carbon Monoxide; D010100:Oxygen