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Cardiac alternans is a promising predictor of sudden death, yet its role in the mechanism of hypothermic arrhythmia induction is unclear. We aimed to investigate the effect of hypothermia on spatial-temporal characteristics of repolarization pattern in the Langendorff-perfused hearts of summer active (SA, n = 6) and winter hibernating (WH, n = 7) ground squirrels Spermophilus undulatus and rabbits (n = 5), who were immobilized with the excitation-contraction uncoupler BDM (10 mM) and optically mapped using the voltage sensitive dye di-4-ANNEPS and CCD camera (128 x 128 pixels; 500 frames/sec). Action potential duration (APD) restitution was quantified over the posterior epicardial heart surface and estimated using Nolasco-Dahlen criterion. In rabbit hearts, hypothermia resulted in arrhythmogenic overshoots of APD alternans as well as increase of APD restitution curve steepness. In contrast, significant APD alternans were observed in SA hearts at 27 degrees C, and at 17 degrees C in WH hearts. Moreover, slope of APD restitution curve in ground squirrels hearts did not reached arrhythmogenic threshold (43 +/- 9 degrees and 39 +/- 5 degrees for SA and WH respectively). Our results demonstrate different resistance of hibernating and non-hibernating mammals against induction of arrhythmogenic cardiac alternans which is closely associated with adaptive changes in intracellular Ca2+ cycling during hibernation.

Arrhythmias developing in isolated Langendorff-perfused heart following the cooling of the perfusion solution from +37 to +3 degrees C were studied in rats and winter hibernating ground squirrels Citellus undulatus with application of no drugs. In rats, hypothermia significantly increased the probability of ventricular arrhythmias (from 22 +/- 6 % at 37 degrees C to 56 +/- 14 % at 17 degrees C). Excitation failure was observed in the rat hearts below 10 +/- 1 degrees C. The appearance of arrhythmias was closely correlated with a decrease in the wavelength which strongly suggests a reentrant mechanism of the hypothermic arrhythmias. In contrast, ground squirrels showed insensibility of the wavelength to cooling and were resistant to arrhythmias during hypothermia.

In anaesthetised dogs with open chest (n = 10), against the background of the Gd3+ (a blocking agent of mechano-sensitive ion channels), acetylcholine perfusion induced no significant changes either in probability of atrial fibrillation occurrence or in the paroxysm duration. The Gd3+ did not alter the deceleration of the sinus rhythm either. Therefore the mechanism of spontaneous occurrence of atrial cholinergic fibrillation seems not to be associated with the trigger activity induced by an increased blood pressure in the right atrium.