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or -
: an echocardiograph study
Departments of 1 Medicine and 2 Pathology, University of Chicago, Chicago, Illinois 60637; and 3 Laboratoire de Biologie Moleculaire et Cellulaire de l'Ecole Normale Supérieure de Lyon, 69364 Lyon, France
We investigated the effect of thyroid
hormone (TH) receptor (TR)
and -
isoforms in TH action in the
heart. Noninvasive echocardiographic measurements were made in mice
homozygous for disruption of TR
(TR
0/0) or TR
(TR
/
). Mice were studied at baseline, 4 wk after TH
deprivation (using a low-iodine diet containing propylthiouracil), and
after 4-wk treatment with TH. Baseline heart rates (HR) were similar in
wild-type (WT) and TR
0/0 mice but were greater in
TR
/
mice. With TH deprivation, HR decreased 49% in
WT and 37% in TR
/
mice and decreased only 5% in
TR
0/0 mice from baseline, whereas HR increased in all
genotypes with TH treatment. Cardiac output (CO) and cardiac index (CI)
in WT mice decreased (
31 and
32%, respectively) with TH
deprivation and increased (+69 and +35%, respectively) with TH
treatment. The effects of CO and CI were blunted with TH withdrawal in
both TR
0/0 (+8 and
2%, respectively) and
TR
/
mice (
17 and
18%, respectively). Treatment
with TH resulted in a 64% increase in LV mass in WT and a 44%
increase in TR
0/0 mice but only a 6% increase in
TR
/
mice (ANOVA P < 0.05). Taken
together, these data suggest that TR
and TR
play different roles
in the physiology of TH action on the heart.
left ventricular mass; thyrotropin; cardiac index; cardiac output; shortening fraction
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