Due to the obvious difficulties in obtaining serial human tissue samples, we used porcine model of pacing-induced (nonischaemic) dilated cardiomyopathy (DCM) [ 16].
Similar to our findings, prior work in a canine model of pacing-induced HF [ 9], where HF progression was monitored with either an LAP pressure sensor or LVEDV (LV end-diastolic volume) measurements via echocardiography, demonstrated that intrathoracic impedance using the LVring-case vector had the fastest and largest change in response to HF severity and increasing LAP.
The activities of complexes III and V have also been reported to decrease in the same experimental model of pacing-induced left ventricular failure in dogs; this paper also reported increased aldehyde levels in left failing ventricles as indirect measure of increased oxidative stress [ 53, 54].
The proposed mechanistic hypothesis is further supported by an earlier study performed using a canine model of pacing-induced HF where LVEDV exhibited a delayed response to rapid RV pacing in comparison with the response seen in pulmonary capillary wedge pressure [ 17].
In a canine rapid atrial pacing (RAP) model of AF, pacing-induced reduction of AERP was attenuated by ascorbate, a potent antioxidant.
In a model of tachycardia pacing-induced severe heart failure, BAY 58-2667 causedose dependentdent reduction in BP, right atrial, pulmonary artery pressure, and PWP an increase in cardiac output and renal blood flow, with no change in glomerular filtration rate, urine flow and urine sodium excretion [ 55].
The isolated Ca2+ clock model has been previously investigated in detail (50) and produces a wide range of pacing rates suitable for the rabbit SAN cell model.
Patel, et al, performed a study in which dogs were paced for 21 days at rates 10%15%15% above the normal sinus rate [ 11], in contrast to canine models of pacing-induced heart failure in which the ventricles are paced at more than twice the normal sinus rate [ 30- 32].
Recommencement of pacing on each day restored LAP promptly to levels observed prior to pacing termination.
Hypercholesterolemia was the first comorbidity reported to alter responses to preconditioning, with hypercholesterolemic rabbits unable to respond to IPC in a model of pacing-induced preconditioning (Ferdinandy et al., 1998; Szilvassy et al., 1995).
In a rabbit model of pacing-induced heart failure, Aker et al. [ 42] have shown that sabiporide significantly reduced myocardial apoptosis, fibrosis, myocyte cross-sectional area, p38MAPK phosphorylation, and iNOS protein expression.
