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- W246532479 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 CNmore » 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.« less" @default.
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- W246532479 date "1986-03-01" @default.
- W246532479 modified "2023-09-23" @default.
- W246532479 title "Disassociation of reversal of cyanide (CN) toxicity and methemoglobin (MH) formation by nitrite (N) in the isolated heart" @default.
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