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Pressure overload induced in newborn rats: effects on left ventricular growth, morphology, and function
F Kolár1, F Papousek, V Pelouch
1Department of Developmental Cardiology, Institute of Physiology Academy of Sciences of the Czech Republic, Prague.
Insights
Pressure overload in young rats causes cardiac hypertrophy, but functional reserve remains unchanged. Capillary and collagen growth adapt proportionally to ventricular hypertrophy, suggesting these are not limiting factors in this model.
Area of Science:
- Cardiovascular Physiology
- Developmental Biology
- Cardiac Remodeling
Background:
- Cardiac hypertrophy is a response to increased workload.
- Understanding the developmental impact of pressure overload is crucial for pediatric cardiology.
- Early-life cardiac stress can influence long-term heart function.
Purpose of the Study:
- To investigate the effects of early-life abdominal aortic constriction on cardiac hypertrophy and function in rats.
- To compare the cardiac remodeling response to pressure overload induced at different early postnatal ages.
- To assess the relationship between hypertrophy, contractile performance, and microvascular/collagen changes.
Main Methods:
- Induction of gradual pressure overload via abdominal aortic constriction in male rats at postnatal day 2 (AC2) or day 6 (AC6).
- Assessment of systemic blood pressure, left ventricular (LV) contractile performance, and right ventricular weight at 8 weeks.
- Histomorphometric analysis of LV myocytes, capillaries, and collagen concentration.
Main Results:
- Aortic constriction induced significant LV hypertrophy, more pronounced in the AC2 group (71%) than AC6 (34%).
- Contractile performance was elevated, but functional reserve remained unchanged in both groups.
- Myocyte density decreased, myocyte size increased, while capillary density and collagen concentration remained constant, adapting proportionally to hypertrophy.
Conclusions:
- Early-life pressure overload leads to proportional cardiac growth and remodeling, with unchanged functional reserve.
- Capillary and collagen adaptations are proportional to ventricular hypertrophy, indicating they are not limiting factors.
- This model is valuable for studying myocardial growth, differentiation, and the transition to decompensated hypertrophy.
Abstract:
Gradual pressure overload was induced by abdominal aortic constriction in male rats on postnatal d 6 (AC6) or 2 (AC2). At the age of 8 wk, the systemic blood pressure was measured, and the contractile performance of the left ventricle (LV) was assessed after acute ligation of the ascending aorta in open chest anesthetized animals. The LV free wall was used for the determination of collagen concentration and morphometric analysis of cardiac myocytes and capillaries. Aortic constriction resulted in LV hypertrophy, which was more pronounced in AC2 (by 71%) as compared with AC6 (by 34%) groups and correlated closely with the degree of pressure overload (r = 0.88 and 0.80, respectively). The right ventricular weight was increased by 13% in the AC2 group only. Contractile performance of the LV of aortic constricted rats was significantly higher before as well as after the acute load, but the average functional reserve was unchanged in both experimental groups. Although the maximum value of the rate of pressure development increased linearly with the degree of ventricular hypertrophy in the AC6 group (r = 0.82), a negative correlation was observed in the AC2 animals (r = -0.61). The density of myocytes was decreased, and the calculated average myocyte cross-sectional area was increased in aortic constricted rats, but the coronary capillary density and myocardial concentration of collagen remained constant. Thus, in spite of the larger cardiac growth response in the younger age group, the capillary proliferation and collagen formation were proportional to the ventricular hypertrophy. Therefore, the degrees of overload and hypertrophy do not seem to be limiting factors. Pressure overload induced in newborn rats can be a useful model for the study of mechanisms that control either the growth and differentiation of myocardium soon after birth, as well as the transition from compensated to decompensated hypertrophy at later stages.