INFUSION OF STROMA-FREE CROSS-LINKED HEMOGLOBIN DURING ACUTE GRAM-NEGATIVE BACTEREMIA

Citation
Jp. Crowley et al., INFUSION OF STROMA-FREE CROSS-LINKED HEMOGLOBIN DURING ACUTE GRAM-NEGATIVE BACTEREMIA, Circulatory shock, 41(3), 1993, pp. 144-149
Citations number
18
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
00926213
Volume
41
Issue
3
Year of publication
1993
Pages
144 - 149
Database
ISI
SICI code
0092-6213(1993)41:3<144:IOSCHD>2.0.ZU;2-V
Abstract
Twelve dogs were divided into two groups of six each, and were infused with bis-3,5-dibromosalicyl fumarate stroma-free hemoglobin (DBBF-Hb) or albumin. Their responses to an intravenous bolus of Escherichia co li were followed for 4 hr. Bacterial clearance from the blood stream w as studied using standard colony counting methodology as well as blood counts, blood chemistries, and clotting factor analysis. There was a significant difference in mean arterial pressure (MAP) over time betwe en DBBF-Hb-treated dogs and those treated with albumin (P < 0.02). Whi le the DBBF-treated dogs had a higher MAP during the 1 0 min of bacter emia, after 1 hr, there were no longer any appreciable differences bet ween septic dogs treated with DBBF-Hb vs. albumin. Consumption of clot ting and natural anticoagulant factors was observed to be similar in b oth groups, as were endotoxin levels. Blood urea nitrogen (BUN) increa sed slightly in both groups, while white blood cell counts and clottin g factor levels fell in both groups in a similar fashion. There was a more pronounced fall (P < 0.04) in platelet counts in the animals trea ted with DBBF-Hb. In the dogs treated with DBBF-Hb, there was also a l ate rise in pCO2 (P < 0.01), a more pronounced fall in pO2, and greate r acidosis, which suggested that ventilation perfusion abnormalities m ay have been exacerbated by DBBF-Hb treatment. Since the exacerbation of respiratory abnormalities was not related to diminished bacterial o r endotoxin clearance, the possibility is raised that DBBF-Hb interfer es with compensatory respiratory changes during sepsis. (C) 1993 Wiley -Liss, Inc.