Diaspirin cross-linked Hb and norepinephrine prevent the sepsis-induced increase in critical O2 delivery

Andreas W. Sielenkämper, Pei Yu, Otto Eichelbrönner, Tammy MacDonald, Claudio M. Martin, Ian H. Chin-Yee, William J. Sibbald
2000 American Journal of Physiology. Heart and Circulatory Physiology  
Diaspirin cross-linked Hb and norepinephrine prevent the sepsis-induced increase in critical O 2 delivery. Am J Physiol Heart Circ Physiol 279: H1922-H1930, 2000.-We hypothesized that support of arterial perfusion pressure with diaspirin cross-linked Hb (DCLHb) would prevent the sepsis-induced attenuation in the systemic O 2 delivery-O 2 uptake relationship. Awake septic rats were treated with a chronic infusion of DCLHb or a reference treatment [norepinephrine (NE)] to increase mean arterial
more » ... ase mean arterial pressure by 10-20% over 18 h. Septic and sham control groups received normal saline. Isovolemic hemodilution to create anemic hypoxia was then performed in a metabolic box during continuous measurement of systemic O 2 uptake. O 2 delivery was calculated from hemodynamic variables, and the critical point of O 2 delivery (Ḋ O 2 crit ) was determined using piecewise regression analysis of the O 2 delivery-O 2 uptake relationship. Sepsis increased Ḋ O 2 crit from 4.99 Ϯ 0.17 to 6.69 Ϯ 0.42 ml ⅐ min Ϫ1 ⅐ 100 g Ϫ1 (P Ͻ 0.01), while O 2 extraction capacity was decreased (P Ͻ 0.05). DCLHb and NE infusion prevented the sepsis-induced increase in Ḋ O 2 crit [4.56 Ϯ 0.42 ml ⅐ min Ϫ1 ⅐ 100 g Ϫ1 (P Ͻ 0.01) and 5.04 Ϯ 0.56 ml ⅐ min Ϫ1 ⅐ 100 g Ϫ1 (P Ͻ 0.05), respectively]. This was explained by a 59% increase in O 2 extraction capacity in the DCLHb group compared with septic controls (P Ͻ 0.05), whereas NE treatment decreased systemic O 2 uptake in anemic hypoxia (1.51 Ϯ 0.08 vs. 1.87 Ϯ 0.1 ml ⅐ min Ϫ1 ⅐ 100 g Ϫ1 in septic controls, P Ͻ 0.05). We conclude that DCLHb ameliorated O 2 extraction capacity in the septic microcirculation, whereas NE decreased the metabolic demands of the tissues. blood substitute; anemic hypoxia; cardiovascular; rat
doi:10.1152/ajpheart.2000.279.4.h1922 pmid:11009481 fatcat:n5c2npcf7fa3bghno73w2rct4y