Blood affinity for oxygen in experimental hemorrhagic shock with metabolic acidosis.
This study was designed to evaluate, in vivo, the effect of a severe non-respiratory acidosis on hemoglobin oxygen transport. Oxygen affinity of hemoglobin, Bohr effect, Hill's number and red cell 2,3-DPG were evaluated during experimental hemorrhagic shock in dogs. Three periods were considered: control, hypotension (mean arterial pressure 60 mm Hg for 2 hr 30 min) and blood replacement. There was no significant change in erythrocyte 2,3-DPG following hemorrhagic hypotension but ATP increased significantly. n, the Hill number (2.6), was not changed by in vivo acidosis (pH 7.1). Respiratory Bohr coefficient (BCO2) corresponding to pHe variations was drastically reduced (control BCO2 = 0.55, acidosis BCO2 = 0.31, blood replacement BCO2 = 0.35). P50(7.4) was not modified significantly by hemorrhagic acidosis. It is unlikely that variations of blood affinity for oxygen play a major role in oxygen delivery during early experimental hemorrhagic shock.
D000138:Acidosis / Q000097:blood*; D000255:Adenosine Triphosphate / Q000097:blood; D000818:Animals; D001692:Biological Transport; D002245:Carbon Dioxide / Q000097:blood; D004163:Diphosphoglyceric Acids / Q000097:blood; D004285:Dogs; D004912:Erythrocytes / Q000378:metabolism*; D006454:Hemoglobins / Q000378:metabolism*; D010100:Oxygen / Q000097:blood*; D012771:Shock, Hemorrhagic / Q000097:blood*
D004163:Diphosphoglyceric Acids; D006454:Hemoglobins; D002245:Carbon Dioxide; D000255:Adenosine Triphosphate; D010100:Oxygen