Volume expansion with modified hemoglobin solution, colloids, or crystalloid after hemorrhagic shock in rabbits: effects in skeletal muscle oxygen pressure and use versus arterial blood velocity and resistance.
Therapeutic goals for hemorrhagic shock resuscitation are the increase of cardiac output and oxygen delivery. The possibility exists that because of microcirculatory effects, different volume expanders result in different tissue oxygen delivery and oxygen use. In a rabbit model of resuscitation from hemorrhagic shock (50% blood loss), we compared the effects of an hemoglobin-based O2-carrying solution (HbOC) with those elicited by albumin, hydroxyethyl starch (HES), or saline on systemic hemodynamics, skeletal muscle O2 pressure (PtiO2), and interstitial concentration of lactate (LACi) through the combined implantation of a microdialysis probe and a sensitive O2 electrode into the hind limb. Hemorrhagic shock induced a 50% decrease in mean arterial pressure (MAP), femoral artery blood flow (BF), and PtiO2. After resuscitation, there were statistically significant differences among the volume expanders. The increase in MAP was faster with HbOC and colloids, and slower with saline, mainly obtained by vasoconstriction for HbOC and by increased BF with albumin and HES. The maximum MAP values were significantly higher for HbOC compared with the other volume expanders. HbOC and colloids induced a faster increase in PtiO2 as compared with saline, but maximum PtiO2 values were not different among the volume expanders. Tissue oxygen use as estimated by LACi increased transiently at the beginning of volume expansion with similar maximum values. Animals resuscitated with saline had significantly higher LACi concentrations after the onset of volume expansion as compared with HbOC but not with colloids. Our results demonstrate that there are measurable differences in MAP and BF upon resuscitation with the four different solutions and there is a slower increase in tissue PtiO2 with saline than with colloids associated with significantly increased LACi consistent with delayed reoxygenation upon resuscitation with saline.
Boura
Cédric
C
Laboratoire d'hématologie et physiologie, Faculté de Pharmacie, Université Henri Poincaré, Nancy, France.
Caron
Alexis
A
Longrois
Dan
D
Mertes
Paul Michel
PM
Labrude
Pierre
P
Menu
Patrick
P
D000818:Animals; D001158:Arteries / Q000473:pathology; D001783:Blood Flow Velocity / Q000187:drug effects; D003102:Colloids / Q000378:metabolism* / Q000494:pharmacology; D000077324:Crystalloid Solutions; D005263:Femoral Artery / Q000473:pathology; D006400:Hematocrit; D006439:Hemodynamics; D006454:Hemoglobins / Q000378:metabolism* / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia; D007552:Isotonic Solutions; D007773:Lactates / Q000378:metabolism; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D010952:Plasma Substitutes / Q000378:metabolism* / Q000494:pharmacology; D011312:Pressure; D011817:Rabbits; D012771:Shock, Hemorrhagic / Q000188:drug therapy*; D013997:Time Factors
D003102:Colloids; D000077324:Crystalloid Solutions; D006454:Hemoglobins; D007552:Isotonic Solutions; D007773:Lactates; D010952:Plasma Substitutes; D010100:Oxygen