Hg. Zimmer et al., CARDIOVASCULAR-RESPONSE TO TRIIODOTHYRONINE IN SPRAGUE-DAWLEY AND SPONTANEOUSLY HYPERTENSIVE RATS, Cardioscience, 4(3), 1993, pp. 157-162
In this study we have compared the influence of triiodothyronine (T3)
on cardiovascular function and heart weight in Sprague-Dawley and spon
taneously hypertensive rats. We also investigated whether the effects
induced by T3 are reversible. T3 was administered daily (0.2 mg/kg sub
cutaneously) for 14 days in female Sprague-Dawley and spontaneously hy
pertensive rats. Treatment was then stopped for 14 days. At the end of
the treatment and of the period without T3, hemodynamic measurements
were made in the intact, anesthetized animals by catherization of the
left ventricle with a Millar ultraminiature catheter pressure transduc
er. Cardiac output was measured by thermodilution. The development and
regression of myocardial hypertrophy was measured by the ratio of hea
rt to body weight. The systolic pressure in the left ventricle was hig
her in spontaneously hypertensive rats than in Sprague-Dawley rats mat
ched for body weight. At the end of treatment with T3, the heart rate
was increased to exactly the same extent in both groups. Left ventricu
lar systolic pressure was increased by 15 % in Sprague-Dawley rats, bu
t was not altered significantly in spontaneously hypertensive rats. T3
induced an increase in left ventricular dp/dt(max) by 106 % in Spragu
e-Dawley rats, but by only 32 % in spontaneously hypertensive rats, Ca
rdiac output increased by 63 % in Sprague-Dawley rats, but by only 31
% in spontaneously hypertensive rats (statistically not significant).
When T3 treatment was stopped for 14 days, all the functional changes
returned to control values. T3 induced an increase in the ratio of hea
rt to body weight by 57 % in Sprague-Dawley rats, but by only 38 % in
spontaneously hypertensive rats, which bad already developed a signifi
cant degree of cardiac hypertrophy at the beginning of T3 treatment. T
hus, except for the heart rate, the functional and growth response of
the heart to T3 was attenuated in spontaneously hypertensive rats.