pituitrin and Lung-Diseases--Obstructive

Disturbances in hormonal systems involved in sodium and water homeostasis are common during respiratory insufficiency. To investigate the role of hypercapnia, we designed a study to examine the hormonal response to acute hypercapnia induced at constant cardiac filling pressures and without hypoxemia. Seven sedated patients with COPD receiving mechanical ventilation were studied during five successive periods. Hemodynamics, arterial blood gases, and plasma hormone levels (atrial natriuretic peptide, renin, angiotensin II, aldosterone, vasopressin) were measured three times during 60 min of acute hypercapnia (52 +/- 5 mm Hg) and at control periods, before (36 +/- 4 mm Hg) and after (42 +/- 3 mm Hg) acute hypercapnia. During acute hypercapnia, mean pulmonary arterial pressure and cardiac output were increased without variation of other measured cardiorespiratory data and hormonal levels when compared with control values. After acute hypercapnia, cardiorespiratory variables returned to control values without variations of hormonal levels. Our results show that moderate acute hypercapnia does not significantly influence the hormonal levels when cardiac filling pressures and sympathetic tone remain stable. We suggest that changes in those plasma hormones involved in salt and water homeostasis during acute hypercapnia are secondary to hemodynamic changes induced by acute respiratory failure and not to acute hypercapnia per se.

Topics: Aged; Aldosterone; Angiotensin II; Atrial Natriuretic Factor; Hemodynamics; Homeostasis; Humans; Hypercapnia; Lung Diseases, Obstructive; Male; Middle Aged; Renin; Respiration, Artificial; Respiratory Dead Space; Vasopressins

Ten clinically stable, hypercapneic patients with advanced chronic obstructive pulmonary disease were studied to assess the effect of angiotensin-converting enzyme blockade on their inability to excrete a sodium load. Renal, hormonal, and cardiovascular responses to sodium loading were determined during two 5.5-h studies: control day, placebo; and experimental day, captopril. At baseline, compared with control subjects, patients displayed a decrease in urinary sodium associated with low effective renal plasma flow and high plasma level of aldosterone. Captopril, given before sodium loading, produced a significant increase in urinary sodium without increasing effective renal plasma flow and without suppressing plasma aldosterone more than sodium loading alone. Thus, the mechanism by which angiotensin-converting enzyme inhibition induces an acute sodium diuresis in these patients remains to be elucidated. The blockade of angiotensin with captopril also affected the osmotic regulation of vasopressin: for a given increase in plasma osmolality, the increase in plasma vasopressin was subnormal, a finding consistent with the hypothesis that angiotensin II contributes to the regulation of vasopressin secretion.

Topics: Angiotensin-Converting Enzyme Inhibitors; Captopril; Clinical Trials as Topic; Humans; Hypercapnia; Lung Diseases, Obstructive; Male; Natriuresis; Osmolar Concentration; Placebos; Random Allocation; Saline Solution, Hypertonic; Sodium; Time Factors; Vasopressins

Some patients with hypoxaemic chronic obstructive pulmonary disease (COPD) develop sodium and water retention and a subclinical autonomic neuropathy. The possibility that these might be associated has been investigated.. The ability of 24 patients with COPD to excrete a 6 ml/kg 2.7% intravenous saline or 15 ml/kg oral water load was studied and changes in plasma electrolyte levels, osmolality, plasma aldosterone and vasopressin levels, urinary volume and sodium content, glomerular filtration rate, renal blood flow, and cardiovascular autonomic nerve function were measured. Patients were divided into groups of eight: those in group A (controls) had mild COPD with a Pa02 of > 9 kPa and no oedema, patients in group B were more hypoxaemic but had never been oedematous, whilst those in group C were hypoxaemic and mildly oedematous at the time of the study.. Patients in groups B and C excreted less sodium and water during saline loading and a lesser proportion of the water load. Patients in group C had a reduction in renal blood flow and glomerular filtration rate and all had a subclinical autonomic neuropathy, which was also found in three patients in group B. Their plasma aldosterone level was raised but did suppress appropriately on saline loading. Vasopressin levels were abnormally raised for the osmolality in patients in group C and in those with autonomic dysfunction throughout the water load and at 240 minutes after the salt load. Sodium and urine excretion was highly correlated with autonomic dysfunction, aldosterone levels at time zero, and renal blood flow. The 11 patients with autonomic dysfunction were more likely to be oedematous, more hypoxaemic, excreted much less urine and sodium, had lower glomerular filtration rate and renal blood flow, and higher aldosterone and vasopressin levels than the remaining patients.. In patients with COPD the inability to excrete sodium and water is multifactorial. This is the first study to show that autonomic dysfunction is at least associated and might play an important part in the impaired sodium and water homeostasis seen in patients with severe COPD.

Topics: Aged; Aldosterone; Autonomic Nervous System Diseases; Glomerular Filtration Rate; Humans; Hypoxia; Lung Diseases, Obstructive; Middle Aged; Osmolar Concentration; Sodium; Vasopressins; Water

Topics: Adult; Aged; Aged, 80 and over; Body Water; Female; Humans; Kidney; Lung Diseases, Obstructive; Male; Middle Aged; Respiratory Insufficiency; Sodium; Vasopressins

The role of antidiuretic hormone (ADH) in the pathogenesis of renal impaired water excretion in acute respiratory failure has not been clearly delineated. Plasma sodium concentration and plasma ADH levels (radioimmunoassay) were therefore serially measured in 13 patients with acute respiratory failure (10 with acute exacerbations of chronic lung disease and three with acute lung disease) and eight "control" patients admitted ot the intensive care unit with suspected myocardial infarction. None of the patients had systemic hemodynamic, hepatic or renal dysfunction. ADH levels were significantly elevated in patients with acute respiratory failure (15.1 +/- 5.2 pg/ml versus 5.7 +/- 1.9 pg/ml, p less than 0.05) when compared with levels in control patients. The elevated ADH levels occurred despite significantly lower plasma sodium concentration (133 +/- 1 meq/liter versus 138 +/- 2 meq/liter, p less than 0.05) compared wit control values. Moreover, markedly increased ADH values (range 1.1 to 13.0 pg/ml) were often encountered in patients with acute respiratory failure despite significant hyposmolality (263 to 275 mOsm/kg H2O). This was not observed in any control patients. These results suggest that patients with acute respiratory failure are susceptible to water retention and hyposmolality due to nonosmotic release of antidiuretic hormone.

Topics: Acute Disease; Blood Gas Analysis; Body Water; Female; Humans; Kidney; Lung Diseases, Obstructive; Male; Osmolar Concentration; Prospective Studies; Respiratory Insufficiency; Sodium; Vasopressins

Topics: Aldosterone; Angiotensin II; Arginine Vasopressin; Carbon Dioxide; Chronic Disease; Humans; Kidney; Lung Diseases, Obstructive; Osmolar Concentration; Renin; Sodium; Vasopressins; Water

Impaired water excretion has been described in stable, nonedematous patients with chronic obstructive lung disease (COLD). To elucidate the mechanism involved, we measured basal glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and water, sodium, and solute excretion for 4 hours after water loading (20 ml. per kilogram orally or as D5W intravenously) in two groups of 10 age-matched, hypoxic, stable, nonedematous COLD normocapneic and hypercapneic patients (PCO2 less than or greater than 45 mm. Hg, respectively). In 5 patients of each group, additional measurements of plasma and urine osmolality and plasma vasopressin were made at 30-minute intervals after oral water loading and the results compared to those obtained in 10 normal control subjects. Hypoxic (PO2 61 plus or minus 2 mm. Hg), normocapneic (PCO2 39 plus or minus 1 mm. Hg) patients had normal GFR (114 plus or minus 5 ml. per minute) and ERPF (517 plus or minus 31 ml. per minute) and excreted the load normally (101 plus or minus 5 per cent of oral or intravenous water per 4-hours). This was associated with a normal rate of sodium excretion (34 plus or minus 5 mEq. per 4-hours) and low-normal plasma vasopressin (1.9 plus or minus 0.7 pg. per milliliter) which was suppressed appropriately with water loading. Hypercapneic (PCO2' 62 plus or minus 5), hypoxic (PCO2' 57 plus or minus 2) patients had normal GFR (106 plus or minus 7), low baseline vasopressin (1.1 plus or minus 0.2) which was suppressed appropriately, and decreased (p less than 0.05) 4-hour water excretion (63 plus or minus 8 per cent), 4-hour sodium excretion (15 plus or minus 9), and ERPF (394 plus or minus 31). A significant correlation was observed between impaired water and impaired sodium excretion (p less than 0.05). These studies indicate that in COLD patients: (1) hypercapnia but not hypoxemia is related to the abnormal water handling and to the increased reabsorption of sodium by the renal tubule; (2) the defect in water excretion is not related to abnormal vasopressin secretion or metabolism; (3) the alteration in sodium excretion may be due to hypercapneic-induced increase in renal bicarbonate reabsorption and/or abnormal renal blood flow.

Topics: Adult; Arginine; Chronic Disease; Glomerular Filtration Rate; Humans; Hypercapnia; Hypoxia; Kidney; Lung Diseases, Obstructive; Middle Aged; Osmolar Concentration; Radioimmunoassay; Regional Blood Flow; Regression Analysis; Sodium; Urine; Vasopressins; Water; Water-Electrolyte Balance

Topics: Aged; Chronic Disease; Humans; Lung Diseases, Obstructive; Male; Respiratory Insufficiency; Respiratory Tract Infections; Vasopressins