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

The effects of induced hypo- and hypercapnia upon the rate of hydroxylation of tryptophan and tyrosine in the rat brain were studied by measuring the accumulation of 5-HTP and DOPA following administration of the aromatic L-aminoacid decarboxylase inhibitor 3-hydroxybenzylhydrazine HCl (NSD 1015). The results suggest that the hydroxylation of tryptophan varies directly with the tissue Po2. On the other hand, the hydroxylation of tyrosine did not show a simple relationship to Po2 but appeared to be influenced by pH changes.
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PMID:Effect of hypercapnia and hypocapnia on tryptophan and tyrosine hydroxylation in rat brain. 1 38

The response of single chemoafferent fibres to hypoxic and hypercapnic stimulation was studied in vitro under different experimental conditions: 1. control, 2. 24 h after reserpinization (5 mg/kg iv) and 3. 18 h after iv injection of alpha-methyl-p-tyrosine (100 mg/kg in the rabbit, and 1. control and 2. 24 h after reserpinization (5 mg/kg ip) in the cat. The spontaneous activity was decreased by monoamine depletion. The amplitude of the response to hypoxia and to hypercapnia was decreased by reserpinization in the rabbit and in the cat, the change being less marked in the latter species. Similarly, treatment with alpha-methyl-p-tyrosine decreased the ability of chemoreceptors to respond to hypoxia and hypercapnia and, in a few instances, these receptors could only be excited by superfusion of nitrogen-equilibrated medium. These results emphasize to possible role of monoamine, and particularly dopamine, in modifying the sensitivity of arterial chemoreceptors to their natural stimuli.
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PMID:Chemoreceptor response to hypoxia and hypercapnia in catecholamine depleted rabbit and cat carotid bodies in vitro. 371 44

One-day-old rats were exposed to a gas mixture of 15% CO2-21% O2-64% N2 for a 30-min period. Monoamine synthesis in whole brain was measured during, and at various intervals after, hypercapnia by estimating the accumulation of dihydroxyphenylalanine (DOPA) and 5-hydroxytryptophan (5-HTP) after inhibition of aromatic L-amino-acid decarboxylase with NSD 1015. Endogenous concentrations of tyrosine, dopamine (DA), noradrenaline (NA), tryptophan, 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were measured at the same intervals. Exposure to CO2 induced an increased synthesis of catecholamines and 5-HT. Further, an increase in DA concentration was seen during hypercapnia, while NA and 5-HT were unchanged. After the CO2 exposure the increased in vivo synthesis rates of catecholamines and 5-HT were rapidly normalized, as was the endogenous DA concentration. A slight increase in 5-HT and 5-HIAA concentrations was seen immediately after CO2 exposure. These results indicate that in neonatal animals, hypercapnia induces changes in central monoamine neurons, primarily an increased synthesis. These alterations may be relevant to some physiological changes seen during CO2 exposure, such as the alteration in central respiratory performance.
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PMID:Monoamine synthesis and concentration in neonatal rat brain during hypercapnia and recovery. 612 54

Cells of the fetal carotid body have been obtained by enzymatic digestion and maintained in culture both as single cells and as clusters for up to 2 mo. The glomus cells in culture synthesize catecholamines and adenine nucleotides, as determined by histochemical methods, and contain characteristic dense-core vesicles. Their growth requirements are different from other cells of neural crest origin in that they do not depend on nerve growth factor (as do sympathetic neurons) or corticosteroids (as do SIF cells) for survival. Neither hypoxia nor hypercarbia affects survival or relative preponderance of glomus cells in culture. Tyrosine-free medium, which selects for cells containing tyrosine hydroxylase, eliminates most of the nonadrenergic cells, thereby providing a culture dramatically enhanced in glomus cells.
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PMID:Carotid body cell culture and selective growth of glomus cells. 669 53

Intravenous infusion of arginine vasopressin (AVP) depresses the slope of the ventilatory response to CO2 during acute hypercapnia. We therefore tested the hypothesis that AVP V1-receptor blockade would increase the slope of the ventilatory response to CO2. After a 20-min control period, an AVP V1-receptor antagonist (d(CH2)5[Tyr(Me)2]AVP) was injected into six conscious resting dogs. Thirty minutes after AVP V1-receptor blockade, dogs were exposed to sequential 20-min periods of 5 and 6.5% inspired CO2 in air. A second protocol (no AVP V1-receptor blockade) was conducted as a control. As predicted, AVP V1-receptor blockade enhanced ventilation during inhalation of 6.5% CO2 in association with an increased metabolic rate and increased plasma angiotensin II (ANG II). In eupneic dogs, stimulation of respiration by AVP V1-receptor blockade is mediated by ANG II. A third protocol with ANG II-receptor blockade (intravenous infusion of saralasin) combined with AVP V1-receptor blockade indicated that ANG II mediated the increase in metabolism and the augmented ventilation during inhalation of 6.5% CO2. We conclude that during acute hypercapnia of sufficient magnitude, and perhaps duration, AVP inhibits an ANG II-mediated stimulation of metabolism and respiration.
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PMID:During acute hypercapnia vasopressin inhibits an angiotensin drive to ventilation in conscious dogs. 856 18

Recently we have found that hypercapnia induces nuclear protein (FOS) expression in the brainstem chemosensitive neurons, including catecholamine-containing cells. In the present studies we examined the role of protein kinase C (PKC) pathway in CO2-induced c-fos expression. Because of the complexity of the CNS system, experiments were performed in pheochromocytoma cells (PC12 cells). These cells originate from neuronal crest and express catecholaminergic traits. We depleted PKC from PC12 cells by prolonged (48 h) exposure to high concentration of phorbol 12-myristate, 13-acetate (PMA, 100 nM), and then determined the expression of: (1) c-fos mRNA by Northern blot (2) PKC isoforms, tyrosine phosphorylated and unphosphorylated MAP (mitogen activated protein) kinases by Western blot. Depletion of PKC abolished the effect of CO2 on c-fos mRNA expression, inhibited MAP kinases tyrosine phosphorylation and suppressed the expression of PKC(alpha) and PKC(zeta). These results suggest that MAP kinases, PKC(alpha) and/or PKC(beta) might be involved in CO2-induced c-fos mRNA expression.
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PMID:A possible role for protein kinase C in CO2/H+-induced c-fos mRNA expression in PC12 cells. 957 65

Evidence suggests both opioid mu and delta receptors may participate in the regulation of respiration at different central nervous system sites. In the past, the overlapping receptor specificity of various opioid drugs has made it difficult to dissect the receptor subtype-specific activities involved in respiratory regulation. The new family of delta receptor selective agents such as cyclic[D-Pen2, 5]enkephalin, deltorphins, (+)-4-((alpha-R)-alpha-((2S,5R)-4-allyl-2, 5-dimethyl-1-piperazinyl)-3-hydroxybenzyl)-N,N-diethylbenzamide, naltrindole and H-Tyr-Tic(psi)[CH2NH]Phe-Phe-OH have now made it feasible to more clearly define the role of delta receptors in respiratory control. In a series of experiments we observed that systemic infusion of rats with the highly mu receptor-specific opioid alfentanil induced antinociception and hypercapnia, and both of these effects were antagonized by the mu antagonist D-Phe-Cys-Tyr-Orn-Thr-Pen-Thr-NH2. However, peripheral administration of the delta receptor antagonist naltrindole reverses the hypercapnia but not the antinociceptive activity of alfentanil. This differential effect of naltrindole on antinociception and hypercapnia could also be produced with the delta agonist (+)-4-((alpha-R)-alpha-((2S,5R)-4-allyl-2, 5-dimethyl-1-piperazinyl)-3-hydroxybenzyl)-N,N-diethylbenzamide. In addition, intracerebroventricular delivery of a number of peptide delta ligands cyclic[D-Pen2,5]enkephalin, deltorpnin II and H-Tyr-Tic(psi)[CH2NH]Phe-Phe-OH also produced the same differential reversal of hypercapnia without affecting antinociception. Thus, both the traditional delta agonists and antagonists are able to reverse the alfentanil-induced hypercapnia without affecting antinociception. The reversal of alfentanil-induced hypercapnia by these delta ligands was antagonized by a novel synthetic delta antagonist cis-4-(alpha-(4-((Z)-2-butenyl)-3, 5-dimethyl-1-piperazinyl)-3-hydroxybenzyl)-N,N-diethylbenzamide. We propose that in this experimental respiration model, the delta antagonists naltrindole and H-Tyr-Tic(psi)[CH2NH]Phe-Phe-OH behave like delta agonists with low but sufficient intrinsic activities to reverse alfentanil-induced hypercapnia in rats. The results suggest that a function of the delta receptor is to modulate or counteract the respiratory depression induced by the mu receptor.
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PMID:Delta-opioid ligands reverse alfentanil-induced respiratory depression but not antinociception. 986 59

Malnutrition, hypoxia and energy deficit may affect protein metabolism. We wanted to evaluate the cross-sectional association between serum amino acids and fat-free mass in a group of hypoxic patients. We also wanted to explore, in the same group of patients, whether the blood amino-acid pattern could possibly be influenced by differences in lung function and energy intake. Serum amino acids were measured in 71 hypoxic underweight and normal-weight patients with advanced pulmonary disease and related to the fat-free-mass index, arterial oxygen (PaO2) and carbon dioxide tension (PaCO2), forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1) and energy intake. Only one amino acid (aspartic acid) remained significantly correlated to the fat-free-mass index after adjustments for age and sex (beta = -0.30, P=0.011). None of the amino acids were significantly correlated to PaO2 but alanine was significantly negatively correlated to PaCO2 (beta = -0.46, P<0.001), phenylalanine to FVC1 (beta = 0.52, P=0.001) and tyrosine to FVC (beta = 0.36, P=0.008). Citrulline and tryptophan were significantly correlated to energy intake (beta = 0.32, P=0.008; beta=0.37, P=0.009 respectively). In conclusion, there was no convincing association between fat free mass and serum amino acids. The negative effect of hypercapnia and reduced lung function on some serum amino acids was suggested and some amino acids were sensitive to reduced energy intake.
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PMID:Serum amino acids in relation to nutritional status, lung function and energy intake in patients with advanced pulmonary disease. 1100 Oct 78

The c-ret proto-oncogene encodes a tyrosine-kinase receptor involved in survival and differentiation of neural crest cell lineages. Previous studies have shown that homozygous c-ret-/- mice die soon after birth and have impaired ventilatory responses to hypercapnia. Heterozygous c-ret +/- mice develop normally, but their respiratory phenotype has not been described in detail. We used whole-body flow plethysmography to compare baseline breathing and ventilatory and arousal responses to chemical stimuli in unrestrained heterozygous c-ret +/- newborn mice and their wild-type c-ret +/+ littermates at 10-12 h of postnatal age. The hyperpnoeic and arousal responses to hypoxia and hypercapnia were not significantly different in these two groups. However, the number and total duration of apnoeas and periodic breathing episodes were significantly higher in c-ret +/- than in c-ret +/+ pups during hypoxia and post-hypoxic normoxia. These results are further evidence that respiratory control at birth is heavily dependent on genes involved in the neural determination of neural crest cells.
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PMID:Ventilatory responses to hypercapnia and hypoxia in heterozygous c-ret newborn mice. 1212 22

Hyperglycemia and hypercapnia aggravate intra-ischemic acidosis and subsequent brain damage. However, hyperglycemia causes more extensive post-ischemic damage than hypercapnia, particularly in the cingulate cortex. We investigated the changes in the subcellular distribution of protein kinase Cgamma (PKCgamma) and the Ca2+/calmodulin-dependent protein kinase II (CaMKII), as well as changes in protein tyrosine phosphorylation during and following 10 min normoglycemic, hyperglycemic (plasma glucose approximately 20 mM) and hypercapnic (paCO2) approximately 300 mm Hg) global cerebral ischemia. During reperfusion period, the translocation to cell membranes of PKCgamma, but not CaMKII, was prolonged by intra-ischemic hyperglycemia, while it was only marginally affected by hypercapnia. The tyrosine-phosphorylation of proteins in the synaptosomal membranes, as well as the extracellular signal-regulated kinase (ERK) in the cytosol, markedly increased during reperfusion following hyperglycemic ischemia, but to a lesser degree following hypercapnic ischemia. Our data suggest that PKCgamma, tyrosine kinase and ERK systems are involved in the process of ischemic damage in the cingulate cortex, where hyperglycemia may affect these kinases through an additional mechanism other than exaggerated acidosis.
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PMID:Hyperglycemia and hypercapnia differently affect post-ischemic changes in protein kinases and protein phosphorylation in the rat cingulate cortex. 1467 11


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