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

Water balance is tightly regulated within a tolerance of less than 1 percent by a physiologic control system located in the hypothalamus. Body water homeostasis is achieved by balancing renal and nonrenal water losses with appropriate water intake. The major stimulus to thirst is increased osmolality of body fluids as perceived by osmoreceptors in the anteroventral hypothalamus. Hypovolemia also has an important effect on thirst which is mediated by arterial baroreceptors and by the renin-angiotensin system. Renal water loss is determined by the circulating level of the antidiuretic hormone, arginine vasopressin (AVP). AVP is synthesized in specialized neurosecretory cells located in the supraoptic and paraventricular nuclei in the hypothalamus and is transported in neurosecretory granules down elongated axons to the posterior pituitary. Depolarization of the neurosecretory neurons results in the exocytosis of the granules and the release of AVP and its carrier protein (neurophysin) into the circulation. AVP is secreted in response to a wide variety of stimuli. Change in body fluid osmolality is the most potent factor affecting AVP secretion, but hypovolemia, the renin-angiotensin system, hypoxia, hypercapnia, hyperthermia and pain also have important effects. Many drugs have been shown to stimulate the release of AVP as well. Small changes in plasma AVP concentration of from 0.5 to 4 muU per ml have major effects on urine osmolality and renal water handling.
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PMID:The clinical physiology of water metabolism. Part I: The physiologic regulation of arginine vasopressin secretion and thirst. 39 80

The influence of the prevailing PaCO2 on the water-retaining effects of sustained elevations in ADH was assessed by administering vasopressin (5 U in oil, twice daily) and a fixed water intake to dogs with eucapnia (n, 7), chronic hypercapnia (n, 6), and chronic hypocapnia (n, 8). Although water excretion initially fell to a similar extent in all three groups, cumulative water retention by day 4 of vasopressin administration was 77 mg/kg in the hypocapnic group, 46 ml/kg in the eucapnic group, and only 14 ml/kg in the hypercapnic group. These differences were reflected in a marked disparity in the degree of hyposmolality of body fluids, plasma osmolality falling by day 4 to an average value of 223, 237, and 268 mosmol/kg in the hypocapnic, eucapnic, and hypercapnic animals, respectively. In a separate group of dogs, water deprivation and water loading studies revealed that sustained hypercapnia does not affect the maximal concentrating or diluting ability of the kidney. We conclude, therefore, that the striking influence of the prevailing PaCO2 on the water-retaining effects of administered vasopressin cannot be ascribed to an altered responsiveness of the nephron per se, but that this influence reflects an alteration in the ease with which the kidney can escape from the antidiuretic effects of this substance.
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PMID:Influence of steady-state PaCO2 on escape from ADH-induced water retention in the dog. 64 65

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.
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PMID:Impaired water handling in chronic obstructive lung disease. 114 29

Elevated plasma antidiuretic hormone (ADH) levels were noted in seven patients with status asthmaticus during the acute illness. These values returned to normal with resolution of the disease. The mechanism of this release is not completely understood but is consistent with the hypothesis that bronchospasm leads to decreased pulmonary blood flow, decreased volume return to the left atrium, and stimulation of the atrial volume receptors regulating ADH release. Planning for fluid therapy in patients with status asthmaticus should take into account a high probability of increased plasma ADH concentration during the acute illness. Water intoxication as well as hypoxia and hypercarbia should be considered as a possible cause of an altered state of consciousness associated with status asthmaticus.
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PMID:Elevated plasma antidiuretic hormone levels in status asthmaticus. 124 95

Extracellular recordings were made from 127 neurons, identified by antidromic activation from the supraoptic nucleus, in the A1 area of urethan-anesthetized rabbits. The median axonal conduction velocity was 0.7 m/s, and the median discharge rate was 3.9 spikes/s. Raising arterial pressure decreased the discharge rate in 94 of 101 neurons tested. Lowering arterial pressure increased the discharge rate in 50 of 64 neurons tested. Of 70 neurons inhibited by baroreceptor activation, 40 were excited and 25 inhibited by hypercapnic hypoxia. Of 23 neurons excited by hypercapnic hypoxia, all were excited by hypoxia but only 2 were affected by hypercapnia. Of 16 neurons inhibited by hypercapnic hypoxia, 15 were inhibited by hypoxia and 1 was inhibited by hypercapnia. Of 14 neurons excited by hypoxia, 13 were excited by injection of sodium cyanide into the common carotid artery. Of five neurons inhibited by hypoxia, four were inhibited by sodium cyanide. Our results provide electrophysiological evidence that neurons projecting from the A1 area to the supraoptic nucleus increase their discharge rate in response to baroreceptor unloading and decrease their discharge rate in response to baroreceptor activation. These neurons may form part of the central pathway mediating secretion of vasopressin in response to hemorrhage. A high proportion of the neurons also receive peripheral chemoreceptor inputs, and these A1 cells may also be part of the central pathway whereby chemoreceptor stimulation modifies the secretion of vasopressin.
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PMID:Chemoreceptor and baroreceptor responses of A1 area neurons projecting to supraoptic nucleus. 132 16

The association between infections with respiratory syncytial virus and plasma concentrations of antidiuretic hormone was assessed in 48 patients who had been admitted to hospital. The mean (SEM) concentration of antidiuretic hormone was significantly raised in patients with bronchiolitis (9.3 (1.4) ng/l) compared with non-pulmonary respiratory syncytial virus infections that cause apnoea or upper respiratory tract symptoms (6.1 (1.7) ng/l). The highest concentrations of antidiuretic hormone were seen in patients receiving mechanical ventilation (18.0 (6.7) ng/l). There were no differences in mean serum sodium concentrations among the subgroups. Hypertranslucency on chest radiograph or an arterial carbon dioxide tension above 6.67 kPa were associated with a significantly higher concentration of antidiuretic hormone. Increased or normal maintenance fluid intake in children with pulmonary respiratory syncytial virus infections may cause the same symptoms of fluid overload as the syndrome of inappropriate secretion of antidiuretic hormone. Patients with pulmonary respiratory syncytial virus infection, hypertranslucency in chest radiograph, hypercapnia, or mechanical ventilation are at risk for raised concentrations of antidiuretic hormone. Restricted fluid intake and careful monitoring of fluid balance and plasma electrolyte concentrations are therefore necessary in these patients.
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PMID:Excessive secretion of antidiuretic hormone in infections with respiratory syncytial virus. 212 82

During the winter of 1986-1987, 64 children with respiratory syncytial virus (RSV) infection were admitted to our hospital. The diagnosis was made by direct immunofluorescent antibody technique. Twenty-three children (36%) needed intensive care treatment. Nearly 11 (52%) had a preexisting disease state, identified as a risk factor i.e., prematurity (n = 8), bronchopulmonary dysplasia (n = 2), congenital heart disease (n = 1). Twelve patients (50%) were intubated and ventilated. Conditions for intubation and ventilation were repetitive apnea with or without bradycardia (n = 4), clinical deterioration (n = 3) or hypercarbia (n = 5). Seventy-five percent of the patients who needed intensive care management were under three months of age compared to 34% of the children who were admitted to the clinical ward. The mean age for ventilated patients was 7.9 weeks. The mean duration of ventilation was 5.5 days. Volume controlled ventilation was initially applied to all patients. Pulmonary complications (atelectasis, pneumonia, pneumothorax or adult respiratory distress syndrome) were present in 15 (65%) IC patients. Nine (39%) of them also had symptoms of inappropriate antidiuretic hormone secretion (IADHS). Only two patients had symptoms of IADHS and two others had convulsions. Three children (5%) died as a result of respiratory insufficiency. Two of these infants belonged to the risk group.
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PMID:Respiratory syncytial virus infections in children admitted to the intensive care unit. 281 76

To test the influence of an opioid on vasopressin (AVP) secretion, plasma AVP concentration was measured in five semirecumbent unmedicated volunteers before and during two continuous i.v. infusions of fentanyl. Infusion rates were adjusted to produce steady-state plasma fentanyl concentrations of 2.0 +/- 0.4 and 4.1 +/- 0.6 ng/ml; mild to moderate hypercarbia was induced during the control and infusion periods. Fentanyl increased plasma AVP concentration in a dose-dependent manner to 559 +/- 215 and 929 +/- 199% of the basal level of 1.9 +/- 0.7 pg/ml. Neither mild hypercarbia (PCO2 = 50 +/- 1 mm Hg) in the absence of fentanyl nor moderate hypercarbia (PCO2 = 66 +/- 3 mm Hg) in the presence of fentanyl changed plasma AVP concentration. Neither fentanyl nor hypercarbia, nor the combination of the two, altered plasma renin activity.
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PMID:Effects of fentanyl on vasopressin secretion in human subjects. 311 1

We examined the interaction of graded hypoxia and hypercapnia on stimulation of vasopressin (AVP), ACTH, and corticosteroids in nonsurgically stressed, pentobarbital-anesthetized, gallamine-paralyzed ventilated dogs. Partial pressure of O2 in arterial blood (PaO2) levels of approximately 26-29, 38-41, 54-57, and 83-88 Torr were achieved by altering the fractional concentration of O2 in dry inspired gas with a normocapnic (PaCO2, 35 Torr) and hypercapnic (PaCO2, 59 Torr) background. Normocapnic hypoxia produced a PaO2-dependent increase in AVP, ACTH, and corticosteroids. The threshold PaO2 for AVP was lower (approximately 35 Torr) than for ACTH (approximately 45 Torr). AVP, ACTH, and corticosteroids at all PaO2 levels were higher during hypercapnia. In addition, an ACTH and corticosteroid dose-response correlation estimated the threshhold ACTH to be 20-30 pg/ml. The PaO2-dependent hormone increases and the augmentation of these relationships by hypercapnia are consistent with a peripheral chemoreceptor-mediated reflex. In addition, hypoxia and hypercapnia did not seem to alter the high sensitivity of the adrenal cortex for ACTH.
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PMID:Vasopressin, ACTH, and corticosteroids during hypercapnia and graded hypoxia in dogs. 630 30

Hypoxia and hypercapnia have been shown to cause an increase in the concentration of vasopressin in plasma, but their effects on vasopressin in cerebrospinal fluid (CSF) are not known. In addition, the effect of metabolic acidosis on plasma and CSF vasopressin has not been reported. In this study, plasma and CSF vasopressin levels were measured in anesthetized dogs subjected to either hypoxia, hypercapnia, or metabolic acidosis. Rate and depth of respiration were closely regulated with the aid of muscle paralysis and mechanical ventilation. Vasopressin increased markedly in both plasma and CSF during severe hypoxia (10% O2) and during hypercapnia (10% CO2) but did not change during either mild (15% O2) or moderate (12.5% O2) hypoxia. Although mild hypoxia by itself did not affect either plasma or CSF vasopressin, it did potentiate the increase in plasma and CSF vasopressin that was induced by severe hypercapnia, thus suggesting that hypoxia and hypercapnia may exert synergistic effects on vasopressin secretion. Metabolic acidosis produced by slow intravenous infusion of 1 N hydrochloric acid decreased arterial pH to values comparable to those induced by hypercapnia and increased vasopressin in plasma; CSF vasopressin was unchanged. These results are consistent with the concept that the source of vasopressin secreted into plasma may be different from that secreted into CSF.
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PMID:Vasopressin in plasma and cerebrospinal fluid of dogs during hypoxia or acidosis. 649 66


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