Document Detail


Increased hemoglobin O2 affinity protects during acute hypoxia.
MedLine Citation:
PMID:  22636677     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Acclimatization to hypoxia requires time to complete the adaptation mechanisms that influence oxygen (O(2)) transport and O(2) utilization. Although decreasing hemoglobin (Hb) O(2) affinity would favor the release of O(2) to the tissues, increasing Hb O(2) affinity would augment arterial O(2) saturation during hypoxia. This study was designed to test the hypothesis that pharmacologically increasing the Hb O(2) affinity will augment O(2) transport during severe hypoxia (10 and 5% inspired O(2)) compared with normal Hb O(2) affinity. RBC Hb O(2) affinity was increased by infusion of 20 mg/kg of 5-hydroxymethyl-2-furfural (5HMF). Control animals received only the vehicle. The effects of increasing Hb O(2) affinity were studied in the hamster window chamber model, in terms of systemic and microvascular hemodynamics and partial pressures of O(2) (Po(2)). Pimonidazole binding to hypoxic areas of mice heart and brain was also studied. 5HMF decreased the Po(2) at which the Hb is 50% saturated with O(2) by 12.6 mmHg. During 10 and 5% O(2) hypoxia, 5HMF increased arterial blood O(2) saturation by 35 and 48% from the vehicle group, respectively. During 5% O(2) hypoxia, blood pressure and heart rate were 58 and 30% higher for 5HMF compared with the vehicle. In addition, 5HMF preserved microvascular blood flow, whereas blood flow decreased to 40% of baseline in the vehicle group. Consequently, perivascular Po(2) was three times higher in the 5HMF group compared with the control group at 5% O(2) hypoxia. 5HMF also reduced heart and brain hypoxic areas in mice. Therefore, increased Hb O(2) affinity resulted in hemodynamics and oxygenation benefits during severe hypoxia. This acute acclimatization process may have implications in survival during severe environmental hypoxia when logistic constraints prevent chronic acclimatization.
Authors:
Ozlem Yalcin; Pedro Cabrales
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-05-25
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  303     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2012 Aug 
Date Detail:
Created Date:  2012-08-02     Completed Date:  2012-10-10     Revised Date:  2013-08-14    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H271-81     Citation Subset:  IM    
Affiliation:
Department of Bioengineering, University of California, San Diego, La Jolla, USA.
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MeSH Terms
Descriptor/Qualifier:
Acute Disease
Animals
Anoxia / blood,  drug therapy*,  pathology,  physiopathology
Biological Transport
Brain / drug effects,  metabolism,  pathology
Capillaries / drug effects,  physiopathology
Cerebrovascular Circulation / drug effects
Coronary Circulation / drug effects
Cricetinae
Disease Models, Animal
Furaldehyde / administration & dosage,  analogs & derivatives*,  pharmacology
Hemodynamics / drug effects*
Hemoglobins / metabolism*
Immunohistochemistry
Infusions, Parenteral
Male
Mesocricetus
Mice
Mice, Inbred C57BL
Microcirculation / drug effects
Microscopy, Video
Myocardium / metabolism,  pathology
Oxygen / blood*
Partial Pressure
Regional Blood Flow / drug effects
Skin / blood supply*
Time Factors
Grant Support
ID/Acronym/Agency:
P01-HL-071064/HL/NHLBI NIH HHS; R01-HL-52684/HL/NHLBI NIH HHS; R01-HL-62318/HL/NHLBI NIH HHS; R01-HL-62354/HL/NHLBI NIH HHS; R24-HL-64395/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Hemoglobins; 70ETD81LF0/5-hydroxymethylfurfural; 7782-44-7/Oxygen; 98-01-1/Furaldehyde
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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