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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

1. In chronically catheterized sheep fetuses, during normal pregnancy, the concentration of PGE in the fetal femoral arterial plasma is invariably greater than that of PGF, and increases during the 12 to 24 hr preceding delivery. The concentration of both PGE and PGF decreases repidly after birth. 2. These changes in fetal prostaglandin levels contrast with the marked increase in PGF, but negligible increase in PGE, in the maternal uteroovarian vein before parturition. 3. The changes in prostaglandin concentrations in fetal plasma at term are associated with only small changes in the concentrations of PGE and PGF in tracheal fluid. In amniotic fluid the concentrations of PGE and PGF increase during the last 4 days in utero. At birth the concentrations of PGE and PGF in fetal urine are similar to the concentrations in amniotic fluid. 4. The concentration of PGE in fetal plasma and in tracheal fluid is significantly elevated for up to 3 days after surgery. The concentration of PGF is significantly elevated in fetal plasma nad tracheal fluid for at least 24 hr after surgery. 5. Three fetuses which were chronically hypoxemic had elevated plasma PGE concentrations in utero. However, acute (1 hr) hypoxia or hypercapnia induced in the fetal lamb by making the ewe breathe appropriate gas mixtures did not produce consistent changes in fetal plasma prostaglandin concentrations. 6. During late pregnancy (day 128) exogenous PGE2 infused at about 1.6 microgram/min for 60 min into the fetal carotid artery achieved concentrations in the fetal femoral artery which were within the physiological range seen at term. At this infusion rate, there was no effect on fetal arterial Po2, Pco2, pH, or hematocrit, and no consistent effect on fetal blood pressure or heart rate. PGE2 infusion had no significant effect on the concentration of growth hormone or prolactin in fetal plasma. Within 30 min after beginning the infusion, however, there was a significant increase in the cortisol concentration in fetal plasma. This effect was seen even at times in pregnancy when the fetal adrenal gland responds only poorly to exogenous or endogenous ACTH.
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PMID:Prostaglandins in the sheep fetus: implications for fetal function. 64 1

Previous studies have suggested that the hypoxia and/or hypercapnia associated with chronic lung diseases may lead to pituitary and gonadal dysfunction, with destruction of the sella turcica. It is unclear, however, whether these abnormalities were due to lung disease or to confounding factors. We studied the relationships between hormonal levels (triiodothyronine, thyroxine, T3 resin uptake, thyrotropin, prolactin, cortisol, and testosterone) and PaO2, PaCO2, pH, and alveolar-arterial gradient in 25 patients with chronic lung disease. These patients were highly homogeneous for diagnosis, age, sex, ambulatory status, lack of other illnesses, and minimal use of medications unrelated to lung disease, but did have various degrees of hypoxia and hypercarbia at the time of study. We found no relationship between hormonal levels and lung function, or evidence of major pituitary involvement on lateral roentgenograms of the skull, CT of the sella turcica, or stimulation of the pituitary. An inverse correlation did occur between serum levels of thyroxine and the daily dose of oral prednisone. We conclude that most of the endocrine dysfunction ascribed to chronic lung diseases is probably due to factors other than hypoxia or hypercarbia.
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PMID:Hypoxia and hypercarbia of chronic lung disease: minimal effects on anterior pituitary function. 210 79

The level of pituitary prolactin reserve (PPR) was studied in 56 patients with chronic respiratory failure (CRF) in the acute stage after injections of metoclopramide and Thyrotropin Releasing Hormone (TRH). PPR was low in 90% of the subjects in both groups so that the pathogenic mechanism is more likely to be hypophyseal than hypothalamic and due to the reduced synthesis of PRL by the pituitary gland as a result of inadequate ATP synthesis and/or functional alterations to the receptors or pituitary cells following hypoxaemia and hypercapnia.
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PMID:[Pituitary prolactin reserve in acute exacerbation of chronic respiratory insufficiency]. 358 22

Somatolactin is a putative pituitary hormone of the growth hormone/prolactin family in fish. Its function is still unknown. The effects of environmental hypercapnia and hypoxia, acid (HCl) infusion and exhaustive exercise on plasma somatolactin levels were examined in the chronically cannulated rainbow trout to study the possible physiological roles of somatolactin. Respiratory acidosis induced by hypercapnia (2% CO2) did not affect plasma somatolactin level. In contrast, metabolic acidosis induced by acid infusion and exercise increased plasma somatolactin level. Blood pH was depressed to a similar extent by both types of acidosis, whereas plasma [HCO3-] was elevated by respiratory acidosis but reduced by metabolic acidosis. A moderate hypoxia (water PO2 9.3kPa) affected neither acid­base status nor plasma somatolactin level. A more severe hypoxia (water PO2 6.1kPa) resulted in metabolic acidosis accompanied by an apparent rise in plasma somatolactin level, although the difference in somatolactin level from the control value was not statistically significant. Somatolactin immunoneutralization retarded recovery of plasma [HCO3-] following acid infusion. These results indicate that somatolactin is involved in the retention of HCO3- during metabolic acidosis but not in the active accumulation of HCO3- for acid­base compensation of respiratory acidosis in rainbow trout Oncorhynchus mykiss.
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PMID:Possible involvement of somatolactin in the regulation of plasma bicarbonate for the compensation of acidosis in rainbow trout 932 95

Responses of plasma prolactin (PRL) concentration to alterations in carbon dioxide pressure ( pCO(2)) induced by 4 min of rebreathing out of a bag with 6 l gas initially containing a concentration of 93% O(2) and 7% CO(2) (hypercapnia hyperoxia; HH) and 4 min of voluntary hyperventilation (VH) at a respiratory rate of 28 - 32 per minute were investigated in ten males. During rebreathing in HH, an augmentation of pCO(2) from 40.2 +/- 2.1 to 63.7 +/- 5.4 mmHg and a decrease of pH from 7.4 +/- 0.02 to 7.32 +/- 0.04 were found in capillary blood (p < 0.01). Neither breathing frequency (BF) nor plasma PRL changed during this period. After two minutes of post-rebreathing, pCO(2) and pH returned to basal values. BF increased from 2 min of rebreathing (12.4 +/- 1.9 breath/min) until 11 min of recovery period (18.1 +/- 4.9 breath/min) (p < 0.01), while plasma PRL increased from end of rebreathing (11.59 +/- 1.49 ng/dl) to 11 min of recovery period (13.63 +/- 1.97 ng/dl) (p < 0.01). In VH, hyperventilation decreased pCO (2) from 39.91 +/- 2.62 to 21.73 +/- 2.59 mmHg (p < 0.01) and increased pH from 7.39 +/- 0.04 to 7.58 +/- 0.04 (p < 0.01) in capillary blood. After four minutes of recovery from hyperventilation, pH and pCO(2) were back to their basal values. No changes in plasma PRL were found throughout VH. This present pilot study's new finding is that plasma PRL increases after hypercapnia acidosis. This indicates that acidosis-induced central chemoreflex function increases phrenic nerve activity based on serotonergic modulation, leading to an augmentation of BF. As serotonin is also the main PRL-releasing factor, this might have had the collateral effect of causing PRL release and delayed appearance in the peripheral circulation.
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PMID:Plasma prolactin concentration increases after hypercapnia acidosis. 1460 94

Acute hypercapnia was studied to assess its potential as a noninvasive and simple test for evoking neuroendocrine, cardiovascular and psychological responses to stress in man. A single breath of four concentrations of carbon dioxide (CO(2)), 5%, 25%, 35% and 50%, was administered to nine healthy volunteers in a randomized, single-blind fashion. Although no adverse effects occurred, most subjects were unable to take a full inspired vital capacity breath of 50% CO(2). In response to the remaining exposures, subjective and somatic symptoms of anxiety increased in a dose-dependent manner. Unlike 5% and 25% CO(2), 35% CO(2) stimulated significant adrenocorticotropic hormone and noradrenaline release at 2 min and cortisol and prolactin release at 15 min following inhalation. This same dose also provoked a significant bradycardia that was followed by an acute pressor response. No significant habituation of psychological, hypothalamic-pituitary-adrenal (HPA) or cardiovascular responses following 35% CO(2) was seen when this dose was repeated after 1 week. A single breath of 35% CO(2) safely and reliably produced sympathetic and HPA axis activation and should prove a useful addition to currently available laboratory tests of the human stress response.
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PMID:Acute carbon dioxide exposure in healthy adults: evaluation of a novel means of investigating the stress response. 1504 56

Panic disorder patients are exquisitely and specifically sensitive to hypercapnia. The demonstration that carbon dioxide provokes panic in fear-unresponsive amygdala-calcified Urbach-Wiethe patients emphasizes that panic is not fear nor does it require the activation of the amygdala. This is consonant with increasing evidence suggesting that panic is mediated caudally at midbrain's dorsal periaqueductal gray matter (DPAG). Another startling feature of the apparently spontaneous clinical panic is the counterintuitive lack of increments in corticotropin, cortisol and prolactin, generally considered 'stress hormones'. Here we show that the stress hormones are not changed during DPAG-evoked panic when escape is prevented by stimulating the rat in a small compartment. Neither did the corticotropin increase when physical exertion was statistically adjusted to the same degree as non-stimulated controls, as measured by lactate plasma levels. Conversely, neuroendocrine responses to foot-shocks were independent from muscular effort. Data are consonant with DPAG mediation of panic attacks.
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PMID:In a rat model of panic, corticotropin responses to dorsal periaqueductal gray stimulation depend on physical exertion. 2561 92