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Augmented Oxygen Offloading by the Hemoglobin-Based Oxygen Carrier Hemoglobin Glutamer-200 Following Resuscitation in a Canine Hypovolemia Model



Augmented Oxygen Offloading by the Hemoglobin-Based Oxygen Carrier Hemoglobin Glutamer-200 Following Resuscitation in a Canine Hypovolemia Model



Anesthesiology Abstracts of Scientific Papers Annual Meeting: Abstract No. A-679



Introduction: Hemoglobin-based oxygen carriers (HBOC) have been linked to reduction of blood viscosity, vasoconstriction, decreased functional capillary/arteriole density, and impaired microvascular function. How much O2 is delivered to tissue and to what extent is total systemic O2 demand met by HBOCs? This study was designed to compare the contribution of Hemoglobin glutamer-200 (Hb-200; Oxyglobin(R), Biopure) to native red blood cell (RBC) Hb in relation to the amount of O2 contributed by each to total system O2 consumption index (VO2) in a canine model of acute hemorrhage. Methods: Six dogs (27.7 +- 1 kg) were anesthetized and ventilated mechanically (Fi O2:0.21)with isoflurane and sufentanil infusion. After splenectomy and insertion of arterial, venous, and balloon-tipped pulmonary arterial catheters, vascular pressures and cardiac output index (CI) were monitored and arterial and mixed venous blood samples collected. After recording baseline values, dogs were bled to a MAP of 50 mmHg and maintained hypovolemic for 1 h. Measurements were repeated and dogs were resuscitated with 30 ml/kg Hb-200. Measurements were repeated immediately following (Resuscitation I) and again at 3 h post resuscitation (Resuscitation II). Arterial and venous samples were evaluated on a cooximeter for oxygen saturation and total Hb (HbTot) and on a blood gas machine to determine PaO2 and PvO2. Plasma Hb (HbPla) concentration was determined after centrifugation using the HemoCue(R). Oxygen content in venous (CvO2) and arterial (CaO2) blood was determined directly using a LEXO2CON. Total systemic oxygen delivery index (DO2) was calculated as CI x CaO2. The RBC contribution to total DO2 was calculated as DRBCO2 = ((SaO2) x (1.39 HbRBC)+PaO2 x .003) x CI while the Hb-200 contribution was calculated as DHb-200O2 = DO2 - DRBCO2. The VO2 was calculated as (CaO2- CvO2) x CI. The RBC contribution to VO2 was calculated as VRBCO2 = DRBCO2 - (((SvO2) x (1.39 HbRBC)+PvO2 x .003) x CI) while the Hb-200 contribution was calculated as VHb-200O2 = VO2 - VRBCO2. HbRBC was calculated as the difference between HbTot and HbPla. Results: Data are mean +- SEM and expressed in (mLcntdotm-2cntdotmin-1). After Resuscitation I, Hb-200 constituted 48% of HbTot and provided 39% of the DO2 (278+-24) while HbRBC provided 61% (442+-35). At 3 h post resuscitation the pattern was similar. At Resuscitation I HbRBC provided only 43% of the total VO2 (78+-7) while Hb-200 provided 57% (104+-23). At 3 h post resuscitation, when Hb-200 constituted 44% of HbTot, the differences decreased with HbRBC providing 51% (83+-7) and Hb-200 49% (81+-10) of the total VO2. Conclusions: Unique O2 affinity of Hb-200 may allow it to offload a disproportionately large amount of O2 as it passes through the circulation. This may be advantageous in restoring normal tissue oxygen following hypovolemia. .

Accession: 034459311

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