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

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 these 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 goups. 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. The O₂ supply-consumption ratio was depressed to similar values for all groups with hypoxia compared with their respective normoxic group. Thus thyroxine hearts were able to maintain an adequate O₂ supply-consumption balance under hypoxic stress.