Tags

Type your tag names separated by a space and hit enter

[Autonomic contribution to the blood pressure and heart rate variability changes in early experimental hyperthyroidism].
Arch Mal Coeur Vaiss. 1998 Aug; 91(8):1003-7.AM

Abstract

A great deal of uncertainty persists regarding the exact nature of the interaction between autonomic nervous activity and thyroid hormones in the control of heart rate (HR) and blood pressure (BP). Thyrotoxicosis was produced by a daily intraperitoneal (i.p.) injection of L-thyroxine (0.5 mg/kg body wt in 1 ml of 5 mM NaOH for 5 days). Control rats received i.p. daily injections of the thyroxine solvant. Autonomic blockers were administered intravenously: atropine (0.5 mg/kg), atenolol (1 mg/kg), atenolol + atropine or prazosin (1 mg/kg). Eight animals were studied in each group. Thyroxine treatment was sufficient to induce a significant degree of tachycardia (423 +/- 6 vs 353 +/- 4 bpm; p < 0.001, unpaired Student's tests), systolic BP elevation (142 +/- 3 vs 127 +/- 2 mmHg; p < 0.001), pulse pressure increase (51 +/- 2 vs 41 +/- 2 mmHg, p < 0.01), cardiac hypertrophy (1.165 +/- 0.017 vs 1.006 +/- 0.012 g, p < 0.001), weight loss (-21 +/- 2 g; p < 0.001) and hyperthermia (37.8 +/- 0.1 vs 37.0 +/- 0.1 degrees C, p < 0.001). The intrinsic HR observed after double blockade (atenolol + atropine) was markedly increased after treatment with thyroxine (497 +/- 16 vs 373 +/- 10 bpm, p < 0.05). Vagal tone (difference between HR obtained after atenolol and intrinsic HR) was positively linearly related to intrinsic HR (r = 0.84; p < 0.01). Atenolol neither modified HR nor BP variability in rats with hyperthyrodism. The thyrotoxicosis was associated with a reduction of the 0.4 Hz component of BP variability (analyses on 102.4 sec segments, modulus 1.10 +/- 0.07 vs 1.41 +/- 0.06 mmHg; p < 0.01). Prazosin was without effect on this 0.4 Hz component in these animals. These data show a functional diminution of the vascular and cardiac sympathetic tone in experimental hyperthyroidism. Increased intrinsic HR resulting from the direct effect of thyroid hormone on the sinoatrial node is the main determinant of a tachycardia leading to a subsequent rise in cardiac output. The resulting BP elevation could reflexly induce a vagal activation and a sympathetic (vascular and cardiac) inhibition.

Authors+Show Affiliations

Laboratoire de pharmacologie, CNRS URA 1482, faculté de médecine Necker, Paris.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article

Language

fre

PubMed ID

9749154

Citation

Safa-Tisseront, V, et al. "[Autonomic Contribution to the Blood Pressure and Heart Rate Variability Changes in Early Experimental Hyperthyroidism]." Archives Des Maladies Du Coeur Et Des Vaisseaux, vol. 91, no. 8, 1998, pp. 1003-7.
Safa-Tisseront V, Ponchon P, Blanc J, et al. [Autonomic contribution to the blood pressure and heart rate variability changes in early experimental hyperthyroidism]. Arch Mal Coeur Vaiss. 1998;91(8):1003-7.
Safa-Tisseront, V., Ponchon, P., Blanc, J., & Elghozi, J. L. (1998). [Autonomic contribution to the blood pressure and heart rate variability changes in early experimental hyperthyroidism]. Archives Des Maladies Du Coeur Et Des Vaisseaux, 91(8), 1003-7.
Safa-Tisseront V, et al. [Autonomic Contribution to the Blood Pressure and Heart Rate Variability Changes in Early Experimental Hyperthyroidism]. Arch Mal Coeur Vaiss. 1998;91(8):1003-7. PubMed PMID: 9749154.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Autonomic contribution to the blood pressure and heart rate variability changes in early experimental hyperthyroidism]. AU - Safa-Tisseront,V, AU - Ponchon,P, AU - Blanc,J, AU - Elghozi,J L, PY - 1998/9/28/pubmed PY - 1998/9/28/medline PY - 1998/9/28/entrez SP - 1003 EP - 7 JF - Archives des maladies du coeur et des vaisseaux JO - Arch Mal Coeur Vaiss VL - 91 IS - 8 N2 - A great deal of uncertainty persists regarding the exact nature of the interaction between autonomic nervous activity and thyroid hormones in the control of heart rate (HR) and blood pressure (BP). Thyrotoxicosis was produced by a daily intraperitoneal (i.p.) injection of L-thyroxine (0.5 mg/kg body wt in 1 ml of 5 mM NaOH for 5 days). Control rats received i.p. daily injections of the thyroxine solvant. Autonomic blockers were administered intravenously: atropine (0.5 mg/kg), atenolol (1 mg/kg), atenolol + atropine or prazosin (1 mg/kg). Eight animals were studied in each group. Thyroxine treatment was sufficient to induce a significant degree of tachycardia (423 +/- 6 vs 353 +/- 4 bpm; p < 0.001, unpaired Student's tests), systolic BP elevation (142 +/- 3 vs 127 +/- 2 mmHg; p < 0.001), pulse pressure increase (51 +/- 2 vs 41 +/- 2 mmHg, p < 0.01), cardiac hypertrophy (1.165 +/- 0.017 vs 1.006 +/- 0.012 g, p < 0.001), weight loss (-21 +/- 2 g; p < 0.001) and hyperthermia (37.8 +/- 0.1 vs 37.0 +/- 0.1 degrees C, p < 0.001). The intrinsic HR observed after double blockade (atenolol + atropine) was markedly increased after treatment with thyroxine (497 +/- 16 vs 373 +/- 10 bpm, p < 0.05). Vagal tone (difference between HR obtained after atenolol and intrinsic HR) was positively linearly related to intrinsic HR (r = 0.84; p < 0.01). Atenolol neither modified HR nor BP variability in rats with hyperthyrodism. The thyrotoxicosis was associated with a reduction of the 0.4 Hz component of BP variability (analyses on 102.4 sec segments, modulus 1.10 +/- 0.07 vs 1.41 +/- 0.06 mmHg; p < 0.01). Prazosin was without effect on this 0.4 Hz component in these animals. These data show a functional diminution of the vascular and cardiac sympathetic tone in experimental hyperthyroidism. Increased intrinsic HR resulting from the direct effect of thyroid hormone on the sinoatrial node is the main determinant of a tachycardia leading to a subsequent rise in cardiac output. The resulting BP elevation could reflexly induce a vagal activation and a sympathetic (vascular and cardiac) inhibition. SN - 0003-9683 UR - https://www.unboundmedicine.com/medline/citation/9749154/[Autonomic_contribution_to_the_blood_pressure_and_heart_rate_variability_changes_in_early_experimental_hyperthyroidism]_ L2 - https://medlineplus.gov/hyperthyroidism.html DB - PRIME DP - Unbound Medicine ER -