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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixteen male patients with stable chronic obstructive airways disease were separated into two groups of eight according to arterial carbon dioxide tensions. Hypercapnia was associated with lower arterial oxygen tensions, higher red cell volume, and increased weight, while normocapnic subjects were decidedly thin. The considerable difference in body weight between the two groups could not be explained by variation in caloric intake, and malabsorption was excluded as a cause of weight loss in the underweight subjects. Serum tri-iodothyronine, thyroxine, cortisol, and oestradiol concentrations were similar and normal in each group, but both groups had significantly low testosterone values as compared with controls, values in the hypercapnic being appreciably lower than in the normocapnic group. The adrenal androgen dehydroepiandrosterone was significantly high in the normocapnic group and low in the hypercapnic group compared with controls. Serum pituitary luteinising and follicle stimulating hormones were normal, but three hypercapnic individuals had high serum prolactin values. Early morning urinary aldosterone values were significantly higher in the hypercapnic than in the normocapnic group. Such hormone comparisons have not previously been made in subjects with chronic obstructive airways disease grouped according to arterial blood gas values, and it is concluded that major alterations in adrenal and testicular function may occur, possibly due to pituitary suppression from hypoxia. Such hormonal changes might in part account for the contrasting alterations in body habitus found in this condition.
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PMID:Diet, absorption, and hormone studies in relation to body weight in obstructive airways disease. 54 19

Experiments were conducted to test the hypothesis that one or more interrenal steroids are active in regulatory responses to respiratory acidosis in the toad, Bufo marinus. Toads were divided into four experimental groups. The first group received sham injections. The second group received 1-3 mg of aminoglutethimide (AG) every 8 hr. AG inhibits the conversion of cholesterol to pregnenolone, thus inhibiting all steroid hormone synthesis. The third group received AG + 5 micrograms of aldosterone on the same schedule. The fourth group received AG + 25 micrograms of corticosterone on the same schedule as the other groups. All four groups were subjected to hypercapnia using 5% CO2 to induce a respiratory acidosis. The sham-operated animals displayed the normal compensatory pattern of producing a metabolic alkalosis (elevated plasma HCO3-) after 24 hr. AG-treated toads failed to elevate plasma HCO3-. Administration of interrenal steroids produced compensation in varying degrees. Aldosterone produced a small compensation while corticosterone produced a compensation similar to that seen in sham-operated animals. Analysis of steroid titers in toad plasma during hypercapnia showed that Bufo marinus does not elevate aldosterone during respiratory acidosis, but that corticosterone is elevated. AG blocked the corticosterone elevation, however. AG also produced a hyponatremia that was corrected with aldosterone or corticosterone. Normocapnic controls showed that AG does not produce deleterious effects on pH or blood gases in toads in the absence of a respiratory acidosis. We conclude that corticosterone is important in acid-base regulatory responses to respiratory acidosis in this amphibian.
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PMID:Acid-base-electrolyte balance responses of Bufo marinus to aminoglutethimide, corticosterone, and aldosterone during hypercapnia. 150 25

Atrial natriuretic factor (ANF) is a peptide secreted by auricular cardiac cells and acts on the brain; it is a diuretic, a natriuretic and a vasodilator and inhibits the renin angiotensin aldosterone system at several levels. The lungs are rich in specific ANF receptors present both at a vascular cellular level and in the mesothelial cells. These receptors participate in the extraction of ANF during its pulmonary intravascular transit and also in its enzymatic degradation. Endogenous ANF (and exogenous) is a vasodilator of the pulmonary arterial bed, representing a regulatory system for right ventricular afterload and probably modifying pulmonary capillary permeability. Hypoxia and hypercapnia contribute by direct and indirect mechanisms to the stimulation of ANF secretion explaining their elevated levels in pulmonary arterial hypertension and chronic respiratory insufficiency. The lung can under certain conditions synthesise ANF itself as can neuro-endocrine bronchial tumours. ANF may be involved in the understanding of sodium retention during ventilation with PEEP and in the paraneoplastic hyponatraemia of certain bronchial tumours. Finally acute bronchial obstruction leads to hypersecretion of ANF which has some bronchodilator properties.
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PMID:[Atrial natriuretic factor and the lung]. 183 Mar 97

The renin response to hypoxia in late gestation fetal sheep has been well characterized. However, the renin response to asphyxia--the combination of hypoxia and hypercapnia--has not been extensively studied. The purpose of this study was to determine 1) the interaction of hypoxia and hypercapnia in the control of renin secretion in late gestation fetal sheep and 2) the role of peripheral arterial chemoreceptors therein. Chronically catheterized fetal sheep (intact or sinoaortic denervated) were exposed to hypoxia and/or hypercapnia for 30 minutes. Hypercapnia alone had no effect on plasma renin activity or aldosterone but did result in a significant increase in angiotensin II. Hypercapnia combined with hypoxia resulted in a significant increase in renin activity, angiotensin II, and aldosterone. Sinoaortic denervation attenuated the renin and angiotensin II responses to hypercapnia plus hypoxia. The increase in renin and angiotensin II in response to hypercapnia with or without concomitant hypoxia strongly correlated with the magnitude of the decrease in arterial pH in intact fetuses only. Hypoxia alone and in concert with hypercapnia increased mean arterial pressure and decreased heart rate in intact but not sinoaortic denervated fetuses. We conclude that 1) hypercapnia more potently increases plasma renin activity than does hypoxia in late gestation fetal sheep, 2) arterial pH may be the relevant signal perceived by the peripheral arterial chemoreceptors for the control of the renin-angiotensin system during asphyxia, and 3) the cardiovascular response to hypoxia is mediated, in part, by peripheral arterial chemoreceptors.
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PMID:Peripheral chemoreceptor control of fetal renin responses to hypoxia and hypercapnia. 211 38

In advanced chronic obstructive lung disease (COLD), sodium retention is common, associated with reduction in renal plasma flow (RPF) and stimulation of the renin-aldosterone (PRA-PA) system, two abnormalities due to or influenced by hypercapnia: the independent role of hypoxemia in perturbing sodium homeostasis is unknown. In five stable patients with COLD (FEV1 = 0.9 +/- 0.21, mean +/- SE) with mild edema, during two weeks of a low sodium diet (one week on room air: pH = 7.39 +/- 0.02; PaO2 = 55 +/- 4 mm Hg; PaCO2 = 49 +/- 4 mm Hg; and one week on O2: pH = 7.38 +/- 0.01; PaO2 = 72 +/- 6 mm Hg; PaCO2 = 52 +/- 4 mm Hg) we monitored sodium balance, systemic and renal hemodynamics, plasma sodium and potassium, PRA, PA, and atrial natriuretic hormone (ANH). During air breathing, patients uniformly showed a depression of RPF despite normal cardiac output; plasma hormone levels did not differ from controls but there was elevation (greater than 2 SD above the normal mean) of PRA in four patients, PA in two patients, and ANH in two of five patients. During O2 breathing, urinary sodium increased significantly from 67 +/- 7 to 102 +/- 10 mEq/24 h. Surprisingly, the patients experienced a small but significant weight gain (0.6 +/- 0.1 kg). None of the other variables was affected by O2 therapy. The following conclusions were reached: in advanced COLD, correction of hypoxemia results in sodium diuresis, indicating that hypoxemia (in the presence of hypercapnia) contributes to sodium retention. The mechanism for this beneficial effect of O2 will require further investigation.
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PMID:The effect of oxygen on sodium excretion in hypoxemic patients with chronic obstructive lung disease. 213 76

In 75 COPD patients with (group I) or without (group II) cor Pulmonale, we measured plasma renin activity (PRA), angiotensin I and II (ATI and ATII), and aldosterone (Ald) by RIA. We found that the levels of PRA, ATI, ATII, Ald in group I are all higher than those in 25 healthy subjects and in group II (P less than 0.05, P less than 0.001), The PRA, ATI, ATII, Ald also increased in patients with respiratory failure, especially accompanied by hypercapnia, and in patients with hyponatrium. In addition, the strong correlation was found between PaO2, PaCO2 and RAAS activation. These findings suggest that the activation of RAAS increased significantly in COPD patients with cor pulmonale or with respiratory failure, and the changes may involve in the pathophysiologic process in COPD patients.
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PMID:[The renin-angiotensin-aldosterone system changes in chronic obstructive pulmonary disease]. 263 30

The pathogenesis of edema in COPD patients is poorly understood. In 50 COPD patients without cor pulmonale, we measured water sodium and potassium excretion in 24 hours, concentration of sodium and potassium in plasma as well as PRA, ATII and aldosterone levels. We found that PRA, ATII, and aldosterone levels in COPD patients with edema are much higher than those in patients without edema and sodium and water excretion decreased significantly in edematous COPD patients. Elevation of PRA, ATII, and aldosterone correlated with inability to excrete sodium and water. These data suggest that, in conjunction with hypercapnia-hypoxia-mediated disturbance in renal function, stimulation of RAAS, especially the resulting increase of aldosterone may contribute to edema formation in COPD patients.
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PMID:[Role of the renin-angiotensin-aldosterone system in the pathogenesis of edema formation in chronic obstructive pulmonary disease]. 280 68

The control of aldosterone secretion may be altered during acute changes in arterial blood gases. We studied the blood gas, plasma electrolyte, renin (PRA), adrenocorticotropic hormone (ACTH), and aldosterone (ALDO) responses to acute hypercapnia (4 and 8% CO2), acute hypocapnic hypoxia (10% O2), acute severe normocapnic hypoxia (7% O2-4% CO2), and acute hypercapnic hypoxia (7% O2-8% CO2) in conscious, cannulated Long-Evans rats. Normoxia resulted in normal levels of PRA (6.9 +/- 2.0 ng.ml-1.h-1), ACTH (96 +/- 32 pg/ml), and ALDO (10 +/- 3 ng/dl). Hypercapnia had no effect on PRA but did lead to an increase in ACTH (to 298 +/- 69 pg/ml) and ALDO (to 33 +/- 7 ng/dl) during 8% CO2 exposure. Normocapnic hypoxia resulted in a significant increase in ACTH (to 196 +/- 14 pg/ml) and ALDO (to 30 +/- 3 ng/dl). Hypercapnic hypoxia resulted in the greatest increases in PRA (to 30 +/- 2 ng.ml-1.h-1), ACTH (to 397 +/- 114 pg/ml), and ALDO (to 41 +/- 5 ng/dl). We conclude that in conscious rats 1) hypercapnia (less than 80 Torr) had no significant effect on PRA, 2) isocapnic, severe hypoxia (Po2 approximately 34 Torr) increased ACTH, and 3) the combination of hypercapnia and hypoxia was a very potent stimulus to PRA, ACTH, and ALDO. The ALDO responses to increases in endogenous ACTH and angiotensin II appear to be normal in conscious rats during acute hypoxia and/or hypercapnia.
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PMID:Renin, ACTH, and aldosterone during acute hypercapnia and hypoxia in conscious rats. 283 42

The most common causes of hypoxic cor pulmonale are chronic bronchitis and emphysema. Although the clinical situation in some patients is characterized early by hypoxemia, oedema is rare in patients with an arterial pO2 above 60 mm Hg. The presence of oedema can be regarded as an unfavorable prognostic indicator. For many years, peripheral oedema had been considered an expression of congestive cardiac failure; it may be assumed, however, that neither right nor left ventricular failure is prerequisite to the development of oedema. Oedema formation can be attributed to excessive retention of salt and water or a redistribution of body water into the extracellular compartment. Hypercapnia and acidosis affect direct stimulation of renal hydrogen ion secretion. The resulting electrochemical imbalance is compensated by reabsorption of sodium. Hypercapnia and, in acute phases possibly, hypoxia lead to a fall in renal blood flow mediated by alpha-adrenergic stimulation through activation of the renin-angiotensin-aldosterone system. An increase in plasma ADH may also contribute to development of oedema. The development of cor pulmonale or respiratory insufficiency can be enhanced by nocturnal hypoventilation and hypoxia during sleep as well as by sleep apnoea. Nocturnal hypoxia, smoking and reduced oxygen tension in the relevant kidney cells responsible for erythropoietin release promote the occurrence of secondary polycythaemia. For treatment of acute exacerbations in cor pulmonale associated with infections bronchitis antibiotics such as amoxycillin and cotrimoxacol are drugs of first choice. While the use of digoxin is of doubtful value, the cautious administration of diuretics may bring symptomatic relief. In addition to physiotherapy, beta-2-selective bronchodilators and nebulized bronchodilator therapy can be useful; theophyllines dilate airways and increase cardiac output but they can cause arrhythmias and a deterioration of arterial blood gases in hypoxic patients. If the patient has been treated chronically with corticosteroids, the dosage will have to be incremented; if asthma is suspected, corticosteroid treatment is essential. Controlled oxygen therapy is the most important single therapy aimed at relief of severe arterial hypoxaemia. Oxygen should be titrated initially (for the first one or two days) to achieve an arterial tension of at least 48 mm Hg. Thereafter, the oxygen flow should be increased to yield an arterial tension in excess of 60 mm Hg during continued treatment for two to three weeks.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypoxic cor pulmonale: a review. 294 54

The mechanisms of oedema in cor pulmonale remain unexplained. On the basis of a small number of studies, cor pulmonale is not caused by cardiac muscle failure, at least in early oedematous phases. Progressive and persistent elevation of pulmonary vascular resistance may exceed the pumping capacity of the right ventricle in later stages. Alternative explanations for the sharp fall in renal blood flow as oedema appears should be sought. The renin-angiotensin-aldosterone system seems causally related to oedema. The curious position of hypercapnia remains an enigma. Surprisingly few studies of hypercapnia, renal blood flow and renal hormones are reported. Redistribution of body water from intracellular to the extracellular space may be in part due to the need to buffer extracellular respiratory acidosis caused by hypercapnia. It provides an explanation for one form of hypercapnic oedema. Cyclical loss and gain of tissue mass seems more evident in cor pulmonale than ischaemic or valvular heart failure.
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PMID:Oedema in cor pulmonale. 703 67


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