Induced fetal hyperthyroidism: cardiac output and oxygen consumption.

In 13 chronically catheterized fetal lambs, we inserted a subcutaneous osmotic minipump that released triiodothyronine (T3) at a rate of 5.9 microgram x h-1. Five days postoperatively, fetal plasma T3 concentration had increased 10-fold from a control value of 18.4 ng x dl-1; reverse T3 and thyroxine had decreased 83 and 61% from control values of 524 ng x dl-1, and 9.5 microgram x dl-1, respectively. Fetal heart rate increased 29% to 210 from 163 beats x min-1, and blood pressure remained constant. Cardiac output measured with radioactive-labeled microspheres increased 22% to 678 +/- 33 from a control value obtained from another group of animals of 554 +/- 16 ml x min-1 x kg-1. Umbilical blood flow also increased 22%, while coronary flow increased 35%, and pulmonary flow increased 90%. In contrast, flow to the thyroid gland decreased 52%. Fetal oxygen consumption increased 28% to 10.5 +/- 0.5 from 8.2 +/- 1.1 ml x min-1 x kg-1. Placental carbon monoxide diffusing capacity and venous and arterial blood gas values remained unchanged. We conclude that 1) sustained fetal T3 infusion is one of the few factors that can increase fetal cardiac output, and may play a role in increasing cardiac output in the newborn infant, 2) T3 infusion results in an increased rate of metabolism with increased oxygen consumption, and 3) placental reserve for oxygen diffusion exceeds normal oxygen requirements.