Control of cardiac output in thyrotoxic calves. Evaluation of changes in the systemic circulation

Steven Goldman, M. Olajos, E. Morkin

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

The contribution of peripheral vascular factors to the high output state in thyrotoxicosis was examined in 11 calves treated with daily intramuscular injections of L-thyroxine (200 μg/kg) for 12-14 d. Thyroxine treatment increased cardiac output from 14.1±1.4 to 24.7±1.4 liters/min (P < 0.001) and decreased systemic vascular resistance from 562±65 to 386±30 dyns/cm5 (P < 0.01). Blood volume was increased from 65±4 ml/kg in the euthyroid state to 81±6 ml/kg when the animals were thyrotoxic (P < 0.05). The role of low peripheral vascular resistance in maintenance of the high output state was evaluated by infusion of phenylephrine at two dosages (2.5 and 4.0 μg/kg per min). In the euthyroid state, no significant decrease in cardiac output was observed at either level of pressor infusion. In the thyrotoxic state, the higher dosage of phenylephrine increased peripheral resistance to the euthyroid control level and caused a small (6%) decrease in cardiac output (P < 0.05). This small decrease in cardiac output probably could be attributed to the marked increase in left ventricular afterload caused by the pressor infusion as assessed from measurements of intraventricular pressure and dimensions. Changes in the venous circulation were evaluated by measurement of mean circulatory filling pressure and the pressure gradient for venous return in six animals during cardiac arrest induced by injection of acetylcholine into the pulmonary artery. Mean circulatory filling pressure increased from 10±1 mmHg in the euthyroid state to 16±2 mmHg (P < 0.01) during thyrotoxicosis, while pressure gradient for venous return increased from 10±1 to 14±2 mmHg (P < 0.02). These changes in venous return curves were not affected significantly by ganglionic blockade with trimethapan (2.0 mg/kg per min) before cardiac arrest. Thus, the high output state associated with thyrotoxicosis is not dependent upon a low systemic vascular resistance, but is associated with increases in blood volume, mean circulatory filling pressure, and pressure gradient for venous return.

Original languageEnglish (US)
Pages (from-to)358-365
Number of pages8
JournalJournal of Clinical Investigation
Volume73
Issue number2
StatePublished - 1984
Externally publishedYes

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Cardiac Output
Vascular Resistance
Thyrotoxicosis
Venous Pressure
Phenylephrine
Blood Volume
Thyroxine
Pressure
Induced Heart Arrest
Intramuscular Injections
Ventricular Pressure
Heart Arrest
Pulmonary Artery
Acetylcholine
Injections
Therapeutics

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Control of cardiac output in thyrotoxic calves. Evaluation of changes in the systemic circulation. / Goldman, Steven; Olajos, M.; Morkin, E.

In: Journal of Clinical Investigation, Vol. 73, No. 2, 1984, p. 358-365.

Research output: Contribution to journalArticle

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abstract = "The contribution of peripheral vascular factors to the high output state in thyrotoxicosis was examined in 11 calves treated with daily intramuscular injections of L-thyroxine (200 μg/kg) for 12-14 d. Thyroxine treatment increased cardiac output from 14.1±1.4 to 24.7±1.4 liters/min (P < 0.001) and decreased systemic vascular resistance from 562±65 to 386±30 dyns/cm5 (P < 0.01). Blood volume was increased from 65±4 ml/kg in the euthyroid state to 81±6 ml/kg when the animals were thyrotoxic (P < 0.05). The role of low peripheral vascular resistance in maintenance of the high output state was evaluated by infusion of phenylephrine at two dosages (2.5 and 4.0 μg/kg per min). In the euthyroid state, no significant decrease in cardiac output was observed at either level of pressor infusion. In the thyrotoxic state, the higher dosage of phenylephrine increased peripheral resistance to the euthyroid control level and caused a small (6{\%}) decrease in cardiac output (P < 0.05). This small decrease in cardiac output probably could be attributed to the marked increase in left ventricular afterload caused by the pressor infusion as assessed from measurements of intraventricular pressure and dimensions. Changes in the venous circulation were evaluated by measurement of mean circulatory filling pressure and the pressure gradient for venous return in six animals during cardiac arrest induced by injection of acetylcholine into the pulmonary artery. Mean circulatory filling pressure increased from 10±1 mmHg in the euthyroid state to 16±2 mmHg (P < 0.01) during thyrotoxicosis, while pressure gradient for venous return increased from 10±1 to 14±2 mmHg (P < 0.02). These changes in venous return curves were not affected significantly by ganglionic blockade with trimethapan (2.0 mg/kg per min) before cardiac arrest. Thus, the high output state associated with thyrotoxicosis is not dependent upon a low systemic vascular resistance, but is associated with increases in blood volume, mean circulatory filling pressure, and pressure gradient for venous return.",
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