Heart hypertrophy induced by levothyroxine aggravates ischemic lesions and reperfusion arrhythmias in rats
Abstract
AIM: To develop a cardiac hypertrophic model in rats.
METHODS: Rats were i.p. levothyroxine 0.5 mg.kg-1.d-1 x 10 d. The action
potentials of right papillary muscles were recorded by standard
glass-microelectrode technique. The left coronary artery was ligated followed by
reperfusion and the apparent infarcted zone (AIZ) was determined by tetracycline
fluoresence, and the superoxide dismutase (SOD) activity and malondialdehyde
(MDA) product in myocardium were also measured.
RESULTS: In the rats treated by levothyroxine, the heart was hypertrophic and the
action potential duration (APD) and effective refractory period (ERP) were
prolonged, the APD20, APD50, APD90, and ERP were prolonged by 80%, 79%, 74%, and
68%, respectively. No changes in resting potential (RP), action potential
amplitude (APA), and Vmax were produced. The incidence of heart arrest (8/8) and
the risk of death (67 +/- 0) induced by ischemia-reperfusion in rats with
hypertrophic heart was higher than those in normal rats (4/10 and 44 +/- 19,
respectively). The AIZ was expanded markedly in hypertrophic heart, and
attenuated by lidocaine and propranolol.
CONCLUSION: Levothyroxine-induced heart hypertrophy is a suitable model for
severe ischemia and arrhythmias in rats.
Keywords:
METHODS: Rats were i.p. levothyroxine 0.5 mg.kg-1.d-1 x 10 d. The action
potentials of right papillary muscles were recorded by standard
glass-microelectrode technique. The left coronary artery was ligated followed by
reperfusion and the apparent infarcted zone (AIZ) was determined by tetracycline
fluoresence, and the superoxide dismutase (SOD) activity and malondialdehyde
(MDA) product in myocardium were also measured.
RESULTS: In the rats treated by levothyroxine, the heart was hypertrophic and the
action potential duration (APD) and effective refractory period (ERP) were
prolonged, the APD20, APD50, APD90, and ERP were prolonged by 80%, 79%, 74%, and
68%, respectively. No changes in resting potential (RP), action potential
amplitude (APA), and Vmax were produced. The incidence of heart arrest (8/8) and
the risk of death (67 +/- 0) induced by ischemia-reperfusion in rats with
hypertrophic heart was higher than those in normal rats (4/10 and 44 +/- 19,
respectively). The AIZ was expanded markedly in hypertrophic heart, and
attenuated by lidocaine and propranolol.
CONCLUSION: Levothyroxine-induced heart hypertrophy is a suitable model for
severe ischemia and arrhythmias in rats.