Effect of sodium nitrite on ischaemia and reperfusion-induced arrhythmias in anaesthetized dogs: is protein S-nitrosylation involved?

Effect of sodium nitrite on ischaemia and reperfusion-induced arrhythmias in anaesthetized dogs: is protein S-nitrosylation involved?

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To provide evidence for the protective role of inorganic nitrite against acute ischaemia and reperfusion-induced ventricular arrhythmias in a large animal model.Dogs, anaesthetized with chloralose and urethane, were administered intravenously with sodium nitrite (0.2 µmol kg(-1) min(-1)) in two protocols.In protocol 1 nitrite was infused 10 min prior to and during a 25 min occlusion of the left anterior descending (LAD) coronary artery (NaNO2-PO; n = 14), whereas in protocol 2 the infusion was KYOLIC EXTRA STRENGTH started 10 min prior to reperfusion of the occluded vessel (NaNO2-PR; n = 12).

Control dogs (n = 15) were infused with saline and subjected to the same period of ischaemia and reperfusion.Severities of ischaemia and ventricular arrhythmias, as well as changes in plasma nitrate/nitrite (NOx) levels in the coronary sinus blood, were assessed throughout the experiment.Myocardial superoxide and nitrotyrosine (NT) levels were determined during reperfusion.Changes in protein S-nitrosylation (SNO) and S-glutathionylation were also examined.

Compared with controls, sodium nitrite administered either pre-occlusion or pre-reperfusion markedly suppressed the number and severity of ventricular arrhythmias during occlusion and increased survival (0% vs.50 and 92%) upon reperfusion.There were also significant decreases in superoxide and NT levels in the nitrite treated dogs.Compared with controls, increased SNO was found only in NaNO2-PR dogs, whereas S-glutathionylation occurred integrated dryer primarily in NaNO2-PO dogs.

Intravenous infusion of nitrite profoundly reduced the severity of ventricular arrhythmias resulting from acute ischaemia and reperfusion in anaesthetized dogs.This effect, among several others, may result from an NO-mediated reduction in oxidative stress, perhaps through protein SNO and/or S-glutathionylation.