11/1/2023 0 Comments Methylene blue cyanide![]() ![]() Food and Drug Administration, ameliorates cyanide toxicity by normalizing oxidation-reduction state and Ca 2+ channel function.Ĭyanide (CN) has been used by physiologists for more than a century ( 27) as a surrogate for anoxia in many experimental settings, assuming that the inhibition by CN of the metalloenzymes present in the mitochondrial complexes ( 13) would mimic the acute effects of a reduction in O 2 supply. Methylene blue, a drug approved by the U.S. In the early stage of cyanide exposure, adenosine triphosphate levels are normal but myocyte contractility is reduced, largely due to alterations in Ca 2+ homeostasis because of changes in oxidation-reduction environment of ion channels. NEW & NOTEWORTHY Cyanide poisoning due to industrial exposure, smoke inhalation, and bioterrorism manifests as cardiogenic shock and requires rapidly effective antidote. We conclude that MB reversed NaCN-induced cardiotoxicity by preserving intracellular Ca 2+ homeostasis and excitation-contraction coupling ( I Ca), minimizing risks of arrhythmias ( E m, AP configuration, and depolarization-activated K + currents), and reducing O 2 Methylene blue (MB 20 µg/ml) added 3 min after NaCN restored contraction and i transient amplitudes, systolic i, E m, AP amplitude, APD 50, APD 90, I Ca, depolarization-activated K + currents, ΔΨ m, and O 2 NaCN did not affect cellular adenosine triphosphate levels but depolarized mitochondrial membrane potential (ΔΨ m) and increased superoxide (O 2 In addition, NaCN depolarized resting membrane potential ( E m), reduced action potential (AP) amplitude, prolonged AP duration at 50% (APD 50) and 90% repolarization (APD 90), and suppressed depolarization-activated K + currents but had no effect on Na +-Ca 2+ exchange current ( I NaCa). ![]() NaCN (100 µM) exposure for 10 min significantly decreased contraction and intracellular Ca 2+ concentration ( i) transient amplitudes, systolic but not diastolic i, and maximal L-type Ca 2+ current ( I Ca) amplitude, indicating acute alteration of i homeostasis largely accounted for the observed excitation-contraction abnormalities. In adult left ventricular mouse myocytes, exposure to sodium cyanide (NaCN) in the presence of glucose dose-dependently reduced contraction amplitude, with ~80% of maximal inhibitory effect attained at 100 µM. ![]()
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