Key result
Propylthiouracil reduced T3 levels in pregnant mice to nonpregnant values but did not revert the pregnancy-induced increased heart rate (607 vs 556 bpm, P=0.038), indicating T3 does not drive this increase.
Why the study?
Heart rate increases throughout pregnancy alongside up to 50% increases in T3 levels, which regulates cardiac electrophysiology, but the potential contribution of T3 to pregnancy-induced increased heart rate was unknown.
Does altering thyroid hormone levels with T3 or PTU affect pregnancy-induced increased heart rate in mice?
Does altering thyroid hormone levels with T3 or PTU affect pregnancy-induced increased heart rate in mice?
Answers are grounded in this paper and cite their sources.
Triiodothyronine (T3) is unlikely to contribute significantly to the pregnancy-induced increased heart rate, as demonstrated in a mouse model.
Background The heart rate increases by 10–20 beats per minute (bpm) throughout pregnancy in women, reaching maximum heart rate in the third trimester. During pregnancy, important changes in thyroid hormones also occur, with increases of up to 50% in the levels of triiodothyronine (T 3 ), the biological active thyroid hormone. In addition, T 3 has been shown to regulate cardiac electrophysiology. Objective Thus, in the present study the potential contribution of T 3 in pregnancy-induced increased heart rate was explored. Methods We compared the heart rate between nonpregnant and pregnant mice under control conditions and after altering thyroid hormone levels with T 3 and propylthiouracil (PTU, an antithyroid drug) treatments. Results Consistent with the clinical data, we found a 58% rise in T 3 levels during pregnancy in mice. Although pregnant mice had a higher baseline heart rate (607 ± 8 bpm, P = .004) and higher T 3 levels (1.9 ± 0.4 nM, P = .0005) than nonpregnant mice (heart rate: 546 ± 16 bpm; T 3 levels: 1.2 ± 0.1 nM), their heart rate responded similarly to T 3 treatment as nonpregnant mice (nonpregnant: Δ130 ± 22 bpm; pregnant: Δ126 ± 17 bpm, P = .858). Additionally, the heart rate remained significantly elevated (607 ± 11 bpm, P = .038) and comparable to untreated pregnant mice, after the use of the antithyroid drug PTU, although T 3 levels (1.3 ± 0.2 nM, P = .559) returned to nonpregnant values. Conclusion Based on these results, it is unlikely that T 3 contributes significantly to the pregnancy-induced increased heart rate.
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Long et al. (2021) studied Pregnancy-induced increased heart rate (n=35). Propylthiouracil (PTU) and Triiodothyronine (T3) vs. Vehicle / Nonpregnant mice was evaluated on Heart rate (bpm) after PTU treatment in pregnant mice compared to nonpregnant mice (p=.038). Propylthiouracil reduced T3 levels in pregnant mice to nonpregnant values but did not revert the pregnancy-induced increased heart rate (607 vs 556 bpm, P=0.038), indicating T3 does not drive this increase.
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