Rapid pacemaker stimulation in dogs for 14 days induced low output heart failure, reducing cardiac output by 54% and elevating levels of renin, angiotensin II, aldosterone, catecholamines, and ADH.
Rapid ventricular pacing in dogs provides a reversible model of low-output heart failure characterized by fluid retention and activation of the renin-angiotensin-aldosterone, sympathetic, and antidiuretic hormone systems.
Congestive heart failure was induced in dogs by rapid pacemaker stimulation of the heart (240-280/min) for 14 days. This represents a model of low output heart failure which permits the study of the development and reversal of congestive heart failure in an anatomically intact circulation in the unanaesthetized animal. 2. Cardiac output was reduced by 54%. Pulmonary artery pressure gradually increased by a factor of 2.4 and pulmonary capillary pressure rose to 4.6 times basal values. The animals retained a mean of 1.1 litres of fluid. 3. At the same time there was a gradual increase of plasma levels of renin, angiotension II, aldosterone, noradrenaline and adrenaline. After the pacemaker stimulation was discontinued all hormone levels returned to normal, the retained fluid was excreted, and intracardiac pressures and cardiac output returned to baseline values. 4. When heart failure was established at the end of the pacemaker stimulation period an inappropriately high secretion of antidiuretic hormone in relation to plasma osmolality was observed in five of six dogs. 5. It is concluded that beside the well-known non-hormonal renal factors, these hormone systems may be involved in the formation of oedema in congestive heart failure. The inappropriately high levels of antidiuretic hormone may cause hyponatraemia by water retention, representing a state of 'dilutional hypo-osmolality'.
Riegger et al. (1982) studied Congestive heart failure (n=6). Rapid pacemaker stimulation vs. Baseline (within-subject) was evaluated on Cardiac output, pulmonary pressures, fluid retention, and hormone levels. Rapid pacemaker stimulation in dogs for 14 days induced low output heart failure, reducing cardiac output by 54% and elevating levels of renin, angiotensin II, aldosterone, catecholamines, and ADH.