Regulation of breathing in hyperthyroidism: relationship to hormonal and metabolic changes

Pino-García, José M.; García‐Río, Francisco; Díez, Juan J.; Gómez-Mendieta, M.A.; Racionero, Miguel A.; Díaz-Lobato, S; Villamor, J.

doi:10.1183/09031936.98.12020400

Cited by 28 publications

(23 citation statements)

References 31 publications

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“…Both of the above values were reduced, compared to results of the control group, and they also increased after treatment of hyperthyroidism [35]. Similar results were obtained in another study, where MEP and MIP also increased significantly after treatment of hyperthyroidism [37]. A significant correlation was reported between T3, T4 levels and MEP and MIP [35].…”

Section: Hyperthyroidismsupporting

confidence: 75%

Thyroid Gland in Chronic Obstructive Pulmonary Disease

Miłkowska-Dymanowska

Białas

Laskowska

et al. 2017

Advances in Respiratory Medicine

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The risk of chronic obstructive pulmonary disease (COPD), as well as thyroid diseases increases with age. COPD is a common systemic disease associated with chronic inflammation. Many endocrinological disorders, including thyroid gland diseases are related to systemic inflammation. Epidemiological studies suggest that patients with COPD are at higher risk of thyroid disorders. These associations are not well-studied and thyroid gland diseases are not included on the broadly acknowledged list of COPD comorbidities. They may seriously handicap quality of life of COPD patients. Unfortunately, the diagnosis may be difficult, as many signs are masked by the symptoms of the index disease. The comprehension of the correlation between thyroid gland disorders and COPD may contribute to better care of patients. In this review, we attempt to revise available literature describing existing links between COPD and thyroid diseases.

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Section: Hyperthyroidismsupporting

confidence: 75%

Thyroid Gland in Chronic Obstructive Pulmonary Disease

Miłkowska-Dymanowska

Białas

Laskowska

et al. 2017

Advances in Respiratory Medicine

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“…In hyperthyroid human subjects, ventilation is in excess of metabolic demands (20,29). This is especially apparent when the subject exercises.…”

Section: Discussionmentioning

confidence: 99%

“…For example, hyperthyroidism increases the metabolic demands of the body and stresses the cardiovascular and respiratory systems (22,29). In contrast, patients with heart failure can actually exhibit a "sick euthryoid" syndrome, characterized by decreased or normal levels of triiodothyronine (T 3 ) and increased levels of reverse T 3 (9, 23, 35).…”

mentioning

confidence: 99%

Gender-specific effects of thyroid hormones on cardiopulmonary function in SHHF rats

Schlenker

Tamura²,

Gerdes³

2003

Journal of Applied Physiology

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der-specific effects of thyroid hormones on cardiopulmonary function in SHHF rats. J Appl Physiol 95: 2292-2298, 2003. First published August 8, 2003 10.1152/japplphysiol. 00594.2003.-Spontaneously hypertensive heart failure (SHHF) rats develop hypertension and heart failure. We hypothesized that induction of hyperthyroidism should accelerate development of heart failure in male SHHF rats. Male and female SHHF rats received diets containing desiccated thyroid glands (DTG) or a control diet for 8 wk. Male and female Wistar-Kyoto rats were used as normotensive controls. DTG treatment reduced body weight in male, but not female, SHHF rats but increased body temperature and heart weight-to-body weight ratio in both genders. In DTGtreated male SHHF rats, serum triiodothyronine levels doubled relative to SHHF controls, whereas O2 consumption increased in DTG-treated SHHF rats. Frequency of breathing in air increased in DTG-treated female rats, and ventilation increased in DTG-treated male rats. Ventilatory equivalents exhibited gender differences in SHHF rats, were decreased in both genders by DTG treatment, and reached levels similar to those of Wistar-Kyoto rats. DTG increased heart rate, right ventricular pressure, and contractility in both genders and increased left ventricular pressure in SHHF male rats. These results refute our hypothesis and suggest that cardiopulmonary function of SHHF male rats may be improved by DTG treatment.hypertension; sick euthryoid syndrome; hyperthyroidism SPONTANEOUSLY HYPERTENSIVE heart failure (SHHF) rats were originally derived from a cross between the spontaneously hypertensive rat (SHR) and the Koletsky obese rat. Subsequently, these animals were bred with SHR-N (an SHR colony at the National Institutes of Health) (27). Lean male SHHF rats die between 15 and 20 mo of age, and lean females die between 22 and 26 mo of age. Although gender differences in the development of heart failure and hypertension have been examined in this strain (11,12,18,28,36), control of breathing has not been investigated.An additional stressor on the cardiopulmonary system is thyroid hormone dysfunction. For example, hyperthyroidism increases the metabolic demands of the body and stresses the cardiovascular and respiratory systems (22,29). In contrast, patients with heart failure can actually exhibit a "sick euthryoid" syndrome, characterized by decreased or normal levels of triiodothyronine (T 3 ) and increased levels of reverse T 3 (9, 23, 35). The possibility of using thyroid hormone replacement as a therapeutic measure has been approached in patients with heart failure (13, 23). Thus, increasing thyroid levels in SHHF rats may actually improve their cardiopulmonary status.In this study, we investigated the effects of experimentally induced hyperthyroidism in male and female SHHF rats on control of breathing and cardiac function. Gender-matched Wistar-Kyoto (WKY) rats were used as normotensive, euthryoid controls. We hypothesized that the combined effects of hyperthyroidism and hypertension would ...

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“…Respiratory function. Immediately after awakening, pulmonary function tests were performed as previously described [22], with subjects seated, and always in the same order allowing enough rest between each manoeuvre. All procedures were performed by the same technician, blinded to the results.…”

Section: Methodsmentioning

confidence: 99%

Inspiratory neural drive response to hypoxia adequately estimates peripheral chemosensitivity in OSAHS patients

García‐Río¹,

Pino²,

Ramı́rez³

et al. 2002

European Respiratory Journal

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The aim of the present study was to examine the relationships between the responses to progressive isocapnic hypoxia and hypoxic withdrawal test in patients with obstructive sleep apnoea-hypopnoea syndrome (OSAHS) and to analyse the determinants of carotid body sensitivity in OSAHS.Nineteen consecutive OSAHS patients and 13 healthy subjects were selected. Ventilatory (DV9I/Sa,O 2 /BSA) and inspiratory neural drive (DP0.1/Sa,O 2 ) responses to progressive isocapnic hypoxia were determined. Peripheral chemosensitivity was evaluated by the hypoxic withdrawal test, which measures the decrease in ventilation caused by two breaths of 100% oxygen (%DV9I).Withdrawal response and ventilatory and inspiratory neural drive responses to hypoxia were lower in OSAHS patients than in control subjects. In patients with OSAHS, %DV9I correlated significantly with DV9I/Sa,O 2 /BSA and with DP0.1/Sa,O 2 . On stepwise multiple linear regression analysis, a strong correlation between %DV9I and DP0.1/Sa,O 2 was found. Moreover, %DV9I, DV9I/Sa,O 2 /BSA and DP0.1/Sa,O 2 were significantly correlated with minimum arterial oxygen saturation and with arousal index.Obstructive sleep apnoea-hypopnoea syndrome patients have a strong relationship between peripheral chemosensitivity and respiratory response to hypoxia, suggesting that hypoxic stimulation of central chemoreceptors is minimally relevant in obstructive sleep apnoea-hypopnoea syndrome. Moreover, sensitivity of the carotid body in patients with obstructive sleep apnoea-hypopnoea syndrome is related to sleep disruption and to nocturnal hypoxia. Eur Respir J 2002; 20: 724-732 The study of peripheral chemosensitivity in patients with obstructive sleep apnoea-hypopnea syndrome (OSAHS) has been of considerable interest over several years [1][2][3][4][5][6][7]. The peripheral chemoreflexes are an important mechanism for regulation of both breathing and autonomic cardiovascular function [8]. In fact, abnormalities in chemoreflex mechanisms have been implicated in the increased cardiovascular stress in patients with OSAHS. The relationship between peripheral chemosensitivity and blood pressure profile suggests that recurrent obstructive apnoeas may reset the peripheral chemoreceptor output to a higher level, causing a chronic increase in sympathetic tone and initiating hypertension [9,10]. Intersubject variation of heart rate changes during sleep apnoea could also be due to variations in response to hypoxia [11].In spite of these pathophysiological implications, the role of peripheral chemoreception in OSAHS has not been adequately evaluated. The nature of the respiratory response to chemical stimuli in awake patients with OSAHS is still unclear. In these patients, depression of peripheral chemosensitivity has been reported [7]. In contrast, other investigators have concluded that response to hypoxia in OSAHS patients is normal [2][3][4][5][6] These discrepancies in findings concerning chemical sensitivity in OSAHS could be due in part to confounding factors, such as obesity, age, ...

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Regulation of breathing in hyperthyroidism: relationship to hormonal and metabolic changes

Cited by 28 publications

References 31 publications

Thyroid Gland in Chronic Obstructive Pulmonary Disease

Thyroid Gland in Chronic Obstructive Pulmonary Disease

Gender-specific effects of thyroid hormones on cardiopulmonary function in SHHF rats

Inspiratory neural drive response to hypoxia adequately estimates peripheral chemosensitivity in OSAHS patients

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