Bibliographic Citation
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Title | Disassociation of reversal of cyanide (CN) toxicity and methemoglobin (MH) formation by nitrite (N) in the isolated heart |
Creator/Author | Baskin, S.I. ; Froehlich, H.L. ; Groff, W.A. |
Publication Date | 1986 Mar 01 |
OSTI Identifier | OSTI ID: 5524659 |
Report Number(s) | CONF-8604222- |
Other Number(s) | CODEN: FEPRA |
Resource Type | Conference |
Specific Type | Journal Article |
Resource Relation | Fed. Proc., Fed. Am. Soc. Exp. Biol. ; Vol/Issue: 45:3; 70. annual meeting of the Federation of American Society for Experimental Biology; 13 Apr 1986; St. Louis, MO, USA |
Subject | 560301 -- Chemicals Metabolism & Toxicology-- Cells-- (-1987); CYANIDES-- TOXICITY;NITRITES-- BIOLOGICAL EFFECTS; BLOOD FLOW;BLOOD PRESSURE;HEART;HEMOGLOBIN;PERFUSED ORGANS |
Related Subject | BODY;CARBOXYLIC ACIDS;CARDIOVASCULAR SYSTEM;GLOBIN;HETEROCYCLIC ACIDS;HETEROCYCLIC COMPOUNDS;NITROGEN COMPOUNDS;ORGANIC ACIDS;ORGANIC COMPOUNDS;ORGANIC NITROGEN COMPOUNDS;ORGANS;OXYGEN COMPOUNDS;PIGMENTS;PORPHYRINS;PROTEINS |
Description/Abstract | It has been proposed that the mechanism by which N reverses CN toxicity is due to its ability to convert hemoglobin to MH.^However, the reversal of CN toxicity does not appear to parallel the appearance of MH formed by N. The authors sought to determine whether N could reverse the toxicity of CN in a MH-free system.^After a 20 min stabilization period, blood or Krebs/Henseleit (KH) perfused isolated hearts were administered sodium CN (4.5 x 10/sup -4/ M).^Following a 40-50% reduction of contractile force, sodium N (2.9 x 10/sup -3/ M) was added to the perfusate.^Hemoglobin, MH, total and free CN levels in the perfusate were measured periodically.^Although N reversed the CN responses, there were no differences in contractile force, perfusion pressure or heart rate between the blood and KH perfused hearts (p > 0.05).^MH and free CN levels differed between the blood and KH-perfused hearts (p < 0.05), while the total CN levels in the perfusate were constant for the 60 min period.^Their data suggest that the formation of MH by N is not responsible for the therapeutic action of N to reverse the cardiac CN toxicity.^Similar perfusion pressures following CN and N in blood and KH-perfused hearts suggest that blood flow is not responsible for the N effect.^The direct antagonism of CN by N at a myocardial site is proposed. |
Country of Publication | United States |
Language | English |
Format | Pages: 196 |
System Entry Date | 2001 May 13 |
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