Efecto de la ovariectomía sobre la estructura y función cardiovascular en ratas hipertensas

Introducción

El objetivo del presente estudio es investigar los efectos de la ovariectomía en el remodelado vascular miocárdico y en la función cardíaca en ratas hipertensas.

Material y métodos

Los experimentos se realizaron en animales de 18 semanas: ratas ovariectomizadas en la semana 10 espontáneamente hipertensas (SHR-OVX), hipertensas intactas (SHR) y controles normotensos (WKY). El remodelado vascular miocárdico se evaluó por medio de la medida del grosor de la pared vascular y el grado de fibrosis perivascular de arteriolas miocárdica. Para valorar la función sistólica in vivo se realizaron curvas de gasto cardíaco a diferentes niveles de presión auricular derecha por sobrecarga aguda de volumen. Como un índice de la función diastólica se estudió in vitro la distensibilidad pasiva de la pared ventricular, utilizando curvas de sobrecarga de volumen intraventricular frente a cambios en la presión intraventricular.

Resultados

Los SHR presentan, en comparación con el grupo WKY, un aumento del grosor de la pared vascular (p < 0,05) y del grado de fibrosis de los vasos miocárdicos (p < 0,01); ambos cambios vasculares se agravan con la ovariectomía (p < 0,01). Frente a aumentos de presión en aurícula derecha a 3, 6 y 9 cmH2O se produce en todos los grupos experimentales un aumento del índice cardíaco. Este aumento de la función sistólica es, comparado con el grupo WKY, significativamente mayor (p < 0,01) en SHR y SHR-OVX.

Discusión

Sin embargo, dado que entre ambos grupos no existen diferencias significativas parece que la ovariectomía no modifica la función sistólica. La medida de la distensibilidad pasiva ventricular, valorada por nuestra técnica, indica que ésta es significativamente (p < 0,05) menor en los animales ovariectomizados. Estos resultados sugieren que en los animales hipertensos la insuficiencia ovárica experimental agrava el remodelado vascular que ya está presente en la hipertensión y que disminuye la distensibilidad pasiva ventricular sin modificar la función sistólica cardíaca.

Introduction

The aim of the present study is to investigate the effects of ovariectomy on myocardial vascular remodeling and cardiac function in hypertensive rats.

Material and methods

Experiments were performed in 18- week-old rats. There were included animals spontaneously hypertensive which were ovariectomized at 10 weeks (SHROVX), intact hypertensive (SHR) and normotensive controls (WKY). Myocardial vascular remodeling was evaluated by measuring vascular wall thickness and degree of perivascular fibrosis in myocardial arterioles. In order to evaluate in vivo systolic function, cardiac output curves were constructed for differing values of right atrial pressure induced by acute volume loading. In order to provide an index for diastolic function, in vitro passive distensibility of the vascular wall was studied using curves depicting intraventricular volume loading versus changes in intraventricular pressure.

Results

In comparison to the normotensive (WKY) animals, the hypertensive (SHR) group presented increases in both vascular wall thickness (p < 0.05) and degree of myocardial vascular fibrosis (p < 0.01). Both vascular changes worsen with ovariectomy (p < 0.01). When submitted to right atrial pressure increases of 3, 6, and 9 cm of H20, all experimental groups exhibit increases in cardiac index. This systolic function increase is significantly larger (p < 0.01) in both hypertensive groups (SHR and SHR-OVX) as compared to normotensive (WKY).

Discussion

As both groups show no significant differences between them, however, it would seem that ovariectomy does not modify systolic function. Measurement of passive ventricular distensibility, as evaluated by our technique, indicates that it is significantly (p < 0.05) lower in animals submitted to ovariectomy. These results suggest that in hypertensive animals, experimentally-induced ovarian failure aggravates the vascular remodeling which is already present in hypertension, and that it diminishes passive ventricular distensibility without modifying systolic cardiac functio.