Antiarrhythmic effects of preconditioning in anaesthetised dogs and rats

Abstract

Short preconditioning periods of myocardial ischaemia protect the myocardium against the arrhythmogenic effects of a more prolonged occlusion. The optimum time for this preconditioning occlusion in rats is 3 min and protection is still apparent 30 min later. In dogs, the protective effect is especially clear with two short (5 min) coronary artery occlusions. The protection in this species lasts for less than 1 h.

The effect of acute simvastatin administration on the severity of arrhythmias resulting from ischaemia and reperfusion in the canine: Is there a role for nitric oxide?

“…This protection against arrhythmias was similar to that we have obtained previously in the same model with ischaemic preconditioning (Végh et al, 1992a), and with the administration of NO donors (Gyorgy et al, 2000;Gonczi et al, 2009;Kiss et al, 2010). Furthermore, the present study confirmed the role of eNOS activation in the antiarrhythmic effect of simvastatin, since both the phosphorylation of eNOS (determined by Western blot) and Fluorescence intensity (arbitrary units) Fig.…”

“…Under light anaesthesia (30 mg/kg intravenous sodium pentobarbitone, Sigma, St. Louis, MO, USA) the right femoral artery was prepared and catheterized, through which the dogs were further anaesthetized with a mixture of chloralose and urethane (60 and 200 mg/kg, respectively; Sigma, St. Louis, MO, USA) to maintain anaesthesia. The animals were then intubated and ventilated with room air using a Harvard respirator (Harvard Apparatus, Natick, MA, USA) at a rate and volume sufficient to maintain arterial blood gases and pH within physiological limits (Végh et al, 1992a). Body temperature was measured from the mid-oesophagus and maintained by a heating pad at 37 70.5 1C.…”

“…These were measured by a composite electrode (containing also four unipolar electrodes by which changes in ST-segment [mV] were detected) positioned within the potentially ischaemic area as described previously (Végh et al, 1992a). The greatest delay in activation within the ischaemic area following coronary artery occlusion was expressed in ms. All parameters, together with a chest lead electrocardiogram, were measured with a Plugsys Haemodynamic Apparatus (Hugo Sachs Electronics, Germany) and recorded on a Graphtec Thermal Array Recorder (Hugo Sachs Electronics, Germany).…”

“…Ventricular arrhythmias were assessed according to the Lambeth conventions (Walker et al, 1988) with that modification as outlined previously (Végh et al, 1992a). In brief, the total number of ventricular premature beats (VPBs), the incidence and the number of episodes of ventricular tachycardia (VT; defined as a run of four or more consecutive VPBs at a rate faster than the resting heart rate), and the incidence of ventricular fibrillation (VF) were assessed during the occlusion period.…”

“…The risk area following coronary artery occlusion was assessed by injecting Patent Blue V dye into the re-occluded artery using the same method that has been described in detail elsewhere (Végh et al, 1992a).…”