Impaired Water Handling in Chronic Airways Disease

White, Ronald J.; Woodings, D

doi:10.1136/bmj.2.5761.561

Cited by 22 publications

(6 citation statements)

References 9 publications

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“…The levels of ADH were insignificantly lower on the perindopril day ( fig 2). The levels of both these hormones whilst on perindopril were similar to values obtained in control patients with mild COPD (FEV, [1][2][3][4][5][6][7] (0 6) l and Pao2 9 7 (0 6) kPa) (figs 1 and 2). These controls excreted significantly greater amounts of sodium and water (p<005) (table 2).…”

Section: Methodssupporting

confidence: 53%

Effects of angiotensin converting enzyme inhibition on sodium excretion in patients with hypoxaemic chronic obstructive pulmonary disease.

Stewart

Waterhouse

Billings

et al. 1994

Thorax

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The development of oedema in patients with COPD is associated with stimulation of the renin-angiotensin-aldosterone axis and increased ADH release.68 The raised aldosterone levels may contribute to sodium retention and the increased ADH levels to hyponatraemia. However, rather than being the cause of the oedema in hypoxaemic COPD, these changes might reflect other aspects of the disease such as a further reduction in renal blood flow, altered intrarenal haemodynamics, the stress of the disease, or even the effects of treatment with drugs such as diuretics.If the activation of the renin-angiotensinaldosterone system with increased levels of angiotensin II and aldosterone was the major determinant of the sodium retention seen in hypoxaemic COPD, its blockade by an angiotensin converting enzyme (ACE) inhibitor should improve the ability of these oedematous patients to excrete a hypertonic saline load. MethodsNine patients with stable hypoxaemic COPD, with current or recent peripheral oedema and documented increase of the jugular venous pressure, were chosen from patients attending the chest clinic. Patients with other causes of oedema such as heart disease, liver disease, renal disease, and those with known hormonal disorders or diabetes mellitus were excluded.These nine patients underwent a hypertonic saline load test before and whilst taking perindopril, an ACE inhibitor, at a dose of 4 mg/ day (including the day of the test). The saline load protocol was almost identical to that used in other studies in COPD.79 Perindopril was started at a dose of 1 mg daily immediately after the first saline load test. The dose was increased to 2 mg/day and then 4 mg/day at fortnightly intervals. Pulse and blood pressure were monitored half hourly for two hours after the first and at each incremental dose. Patients remained on 4 mg/day for one month before the second saline load.

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Section: Methodssupporting

confidence: 53%

Effects of angiotensin converting enzyme inhibition on sodium excretion in patients with hypoxaemic chronic obstructive pulmonary disease.

Stewart

Waterhouse

Billings

et al. 1994

Thorax

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“…Secondly, the vasoconstrictor effect of hypercapnia-associated activation of the sympathetic nervous system predominates over the direct vasodilatation effect of hypercapnia (indirect vasoconstriction is absent when the vasomotor centre cannot respond to hypercapnia-induced sympathetic activation or when the vasomotor centre is disconnected from peripheral parts of the sympathetic nervous system) [268]. Thirdly, although most patients with COPD and fluid retention are hypercapnic [269,270], hypercapnia is not a necessary prerequisite for the development of fluid retention in these patients [257,259]. Lastly, the investigators [41] did not control for sodium intake, and all medications, including diuretics, were continued.…”

Section: Copd and Renin-angiotensin-aldosterone Systemmentioning

confidence: 99%

Endocrinological derangements in COPD

Laghi

Adıgüzel²,

Tobin³

2009

Eur Respir J

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Chronic obstructive pulmonary disease (COPD) is no longer considered to affect only the lungs and airways but also the rest of the body. The systemic manifestations of COPD include a number of endocrine disorders, such as those involving the pituitary, the thyroid, the gonads, the adrenals and the pancreas.The mechanisms by which COPD alters endocrine function are incompletely understood but likely involve hypoxaemia, hypercapnia, systemic inflammation and glucocorticoid administration. Altered endocrine function can worsen the clinical manifestations of COPD through several mechanisms, including decreased protein anabolism, increased protein catabolism, nonenzymatic glycosylation and activation of the rennin-angiotensin-aldosterone system.Systemic effects of endocrine disorders include abnormalities in control of breathing, decreases in respiratory and limb-muscle mass and function, worsening of respiratory mechanics, impairment of cardiac function and disorders of fluid balance.Research on endocrine manifestations of COPD embraces techniques of molecular biology, integrative physiology and controlled clinical trials. A sound understanding of the various disorders of endocrine function associated with COPD is prudent for every physician who practices pulmonary medicine.

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“…PATIENTS with respiratory failure frequently develop diminished renal function, including diminished renal plasma flow (Aber et al, 1963;Farber et al, 1977), diminished glomerular filtration rate (Daggett, 1977), diminished urinary sodium excretion (Kilburn and Dowell, 1971), and diminished free water excretion (White and Woodings, 1971). Although blood gas derangements are invariably present, their role in these renal abnormalities has remained unclear.…”

mentioning

confidence: 99%

Synergistic effects of acute hypoxemia and hypercapnic acidosis in conscious dogs. Renal dysfunction and activation of the renin-angiotensin system.

Rose¹,

Db²,

Godine³

et al. 1983

Circulation Research

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SUMMARY. The effects of acute hypoxemia and hypercapnic acidosis were examined in five unanesthetized dogs in which sodium intake was controlled at 80 mEq/24 hours for 4 days prior to study. Each animal was studied during combined acute hypoxemia and hypercapnic acidosis (Pac>2 = 36 ± 1 mm Hg, Paco? = 52 ± 1 mm Hg, pH = 7.18 ± 0.02), acute hypoxemia alone (Pac>2 = 32 ± 1 mm Hg, Pacch = 32 ± 1 mm Hg, pH = 7.34 ± 0.01), and acute hypercapnic acidosis alone (Paoj = 82 ± 2 mm Hg, Paco? = 51 ± 1 mm Hg, pH = 7.18 ± 0.02). Although mean arterial pressure, cardiac output, and heart rate increased during combined hypoxemia and hypercapnic acidosis, effective renal plasma flow and glomerular filtration rate decreased. In addition, filtered sodium load and urinary sodium excretion decreased during combined hypoxemia and hypercapnic acidosis. Either acute hypoxemia or hypercapnic acidosis alone resulted in increased mean arterial pressure, cardiac output, and heart rate. However, in contrast to their combined effects, renal hemodynamic function was unchanged and natriuresis was observed. Measurement of plasma renin activity and angiotensin II concentrations indicated that hypoxemia or hypercapnic acidosis alone resulted in moderate activation of the renin-angiotensin system. Moreover, combined hypoxemia and hypercapnic acidosis acted synergistically resulting in major renin-angiotensin activation. Systemic angiotensin II blockade using 1-sarcosine, 8-alanine, angiotensin II (2 Mg/kg per min) during combined acute hypoxemia and hypercapnic acidosis resulted in decreased renal hemodynamic function. We conclude that acute hypoxemia and hypercapnic acidosis act synergistically to increase mean arterial pressure, diminish renal hemodynamic function and activate the renin-angiotensin system. Systemic angiotensin inhibition studies suggest activation of the renin-angiotensin system maintains renal hemodynamic function during combined hypoxemia and hypercapnic acidosis, instead of mediating the renal vasoconsrriction. (Circ Res 53: 202-213, 1983)

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Impaired Water Handling in Chronic Airways Disease

Cited by 22 publications

References 9 publications

Effects of angiotensin converting enzyme inhibition on sodium excretion in patients with hypoxaemic chronic obstructive pulmonary disease.

Effects of angiotensin converting enzyme inhibition on sodium excretion in patients with hypoxaemic chronic obstructive pulmonary disease.

Endocrinological derangements in COPD

Synergistic effects of acute hypoxemia and hypercapnic acidosis in conscious dogs. Renal dysfunction and activation of the renin-angiotensin system.

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