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Effect of T4-induced cardiac hypertrophy on O2 supply-consumption balance during normoxia and hypoxia



Effect of T4-induced cardiac hypertrophy on O2 supply-consumption balance during normoxia and hypoxia



American Journal of Physiology 246(3 Pt 2): H374-H379



The purpose of this study was to determine if thyroxine-induced hypertrophic hearts can maintain an adequate O2 supply-consumption balance both at rest and under hypoxic stress. New Zealand White rabbits were given 0.5 mg/kg L-thyroxine (T4) for 3 or 16 days, and a third group served as a control. Chests were opened under anesthesia, and myocardial blood flow was determined using microspheres. In half of these animals, microspectrophotometric determinations were made on left ventricular arterial and venous O2 saturation, and by combining this data with blood flows, O2 consumption was determined. The other animals were then subjected to hypoxia (8% O2 in N2), and flows and O2 consumption were again determined. T4 increased arterial pressure and heart rate in normoxic animals and also increased myocardial blood flow 65 and 210% for 3- and 16-day T4 groups, respectively, with no regional differences. O2 extraction was also increased in T4 animals. O2 consumption increased 134 and 280% in 3- and 16-day T4 groups. Only normoxic saline controls had a regional O2 consumption difference with subendocardial O2 consumption higher than subepicardial values. When compared with their respective normoxic groups, blood flow increased 49 and 101% for the hypoxic 3- and 16-day T4 groups. Hypoxia had no effect on saline control blood flow. Hypoxia decreased O2 extraction 29 and 41%, respectively, in the 3- and 16-day T4 groups and was unchanged in saline controls.

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Accession: 017870209

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PMID: 6230939


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