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Ventriculographic evaluation in three rat models of cardiac dysfunction
X P Yang1, H N Sabbah, Y H Liu
1Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, Michigan.
Insights
Coronary ligation and embolization effectively induce chronic cardiac dysfunction in rats, significantly reducing left ventricular ejection fraction (LVEF). Aorto-caval fistula models myocardial hypertrophy with minimal cardiac dysfunction.
Area of Science:
- Cardiovascular Research
- Animal Models of Disease
- Heart Failure Pathophysiology
Background:
- Chronic cardiac dysfunction is a significant health concern.
- Developing reliable animal models is crucial for studying heart failure.
- Understanding the distinct pathophysiological changes induced by different models is essential.
Purpose of the Study:
- To evaluate and compare three distinct rat models for inducing chronic cardiac dysfunction: aorto-caval fistula, coronary ligation, and coronary embolization.
- To assess the impact of each model on cardiac function, hemodynamics, and neurohormonal markers.
- To determine the most effective models for studying specific aspects of cardiac dysfunction.
Main Methods:
- Induction of chronic cardiac dysfunction in rats via aorto-caval fistula, coronary ligation, or coronary embolization.
- Assessment of left ventricular ejection fraction (LVEF) using ventriculography 11-12 weeks post-induction.
- Measurement of cardiac output (CO), systemic vascular resistance (SVR), left ventricular volumes, pressures, and plasma atrial natriuretic factor (ANF), renin activity, and catecholamines.
Main Results:
- Coronary ligation and embolization significantly decreased LVEF (-36%, -30%) and CO, while increasing SVR. Aorto-caval fistula mildly decreased LVEF (-13%) but markedly increased CO (+82%) and decreased SVR (-47%).
- All models showed increased left ventricular end-systolic volume and end-diastolic pressure. Aorto-caval fistula and ligation increased left ventricular end-diastolic volume, unlike embolization.
- Plasma ANF increased substantially in all models, with the highest increase in the aorto-caval fistula group. Renin activity and catecholamines remained unchanged.
Conclusions:
- Coronary embolization and ligation are effective models for inducing significant chronic left ventricular dysfunction in rats, characterized by reduced LVEF.
- Aorto-caval fistula serves as a suitable model for studying myocardial hypertrophy and elevated plasma ANF, with only mild cardiac dysfunction.
- The distinct hemodynamic and functional profiles of these models allow for targeted research into specific aspects of cardiac disease.
Abstract:
Chronic cardiac dysfunction was produced in rats by means of 1) aorto-caval fistula (A-V fistula), 2) coronary ligation, or 3) coronary embolization. Eleven to twelve weeks later, left ventricular ejection fraction (LVEF) was evaluated by ventriculography and compared with normal controls. A-V fistula decreased LVEF by 13% and increased cardiac output (CO) by 82%. Coronary ligation and embolization produced a greater decrease in LVEF (-36% and -30%) and a decrease in CO (-36% and -29%). Systemic vascular resistance was significantly decreased in the A-V fistula (-47%) model but increased in both ligation and embolization models (by 99 and 87%). LV end-diastolic volume was increased in fistula or ligation (by 68 and 36%), whereas there was no change in rats with embolization. LV end-systolic volume and LV end-diastolic pressure were significantly increased in all three models. Plasma atrial natriuretic factor was increased by 676% with fistula, 212% with ligation, and 113% with embolization. There was no significant change in plasma renin activity or catecholamines in any of the models. We concluded that coronary embolization and ligation are effective methods of producing chronic LV dysfunction in rats, as evidenced by the significant decrease in LVEF. On the other hand, A-V fistula is an appropriate model of myocardial hypertrophy with greatly increased plasma atrial natriuretic factor, but cardiac dysfunction was minimal as indicated by the mild decrease in LVEF.