Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

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

The role of the skeleton in electrolyte equilibrium, well known for various diseases, remains difficult to understand during chronic hypercapnia. An experimental study of normoxic (O2:21%) hypercapnia (CO2:8 +/- 1%) was carried out for two, four and six weeks, followed by a systematic quantitative determination, in thigh-bone samples of Na+, K+, Ca++, PO4--, N2 and CO2 in 72 rats, and of total H2O and extracellular H2O (H2Oe) in 129 rats. Considering the mean values of groups (from 16 to 42 subjects for each group), at various times of hypercapnia, bone K+ was increased during hypercapnia (+3 to 4 X 10(-3) mEq/g fresh tissue), Ca++ diminished (--12.5 to 15.4 mEq). PO4-- and Na+ temporarily decreased at two and four weeks of hypercapnia. On account of the scatter of individual results, only the variation of K+ was statistically significant (at two weeks). This increase in bone K+, accompanying a partially compensated acidaemia, is to compare with the significant hyperkaliemia observed at two and four weeks, whereas this period is characterized by a decrease in K+ in skeletal muscle, as shown in a previous work. In a group of 72 rats, the analysis of correspondances and correlations points out the bone CO2 as a very significant variable, opposite to the variable H2Oe. PO4--is positively correlated to Na+. The complexity of the results does not permit a decisive interpretation of the phenomenon. On the other hand, this study corroborates the bone calcium loss and reveals the gain in bone potassium during hypercapnia.
...
PMID:[Bone electrolytes in experimental chronic hypercapnia (author's transl)]. 101 78

Fourteen young men (on the average 25 years), well trained (maximal oxygen consumption, VO2 max., between 2.7 to 3.5 1) have been studied at two different levels of exercise: 90 and 140 watts (about 40 and 70% of VO2 max.) in chamber, where the atmosphere was regulated. The subjects performed the exercise after a sojourn of six hours in the chamber, at the same level, either in air or in hypercapnic conditions (FICO2: 0.04; FIO2: 0.21); the order of the exercise tests was determined at random. The rise of total ventilation (VE) during exercise in CO2 atmosphere was particularly related to the increased tidal volume (VT). In spite of the larger increase of VE in hypercapnia, CO2 output (VCO2) and respiratory quotient (R) were lower while PaCO2 was elevated (48 at rest and 54 mmHg during exercise). Oxygen consumption during exercise was the same in both conditions. Values of arterial lactic acid concentration were not different at 90 watts level. On the contrary, at the level of 140 watts, the lactic acid concentration was significantly lower in CO2 atmosphere. The well known changes during exercise of other electrolytes (rise of Na+, K+ and total Ca) was similar in air and in CO2. Only the inorganic phosphorus was higher in CO2 atmosphere at 140 watts.
...
PMID:[Metabolism during exercise in young men breathing 4% CO2 (author's transl)]. 101 74

The bile acid-base parameters are analyzed in 42 male Wistar rats under pentobarbital anaesthesia, in normal conditions of blood acid-base equilibrium. The reproducibility of the results is emphasized. In acute hypercapnia (FICO2 : 0.12 for 15 min) without hypoxia, and for the same increase in PCO2, and pH variation is lesser in bile than in blood, thus showing an high buffer capacity. In vitro and in vivo comparative studies show that bile buffer capacity is about five times higher in vivo, independently of a possible increase in choleresis. Comparative studies of bile-acid-base equilibrium are effected during perfusions of dehydrocholate, sodium taurocholate, secretin and acetazolamide. Sodium and chlorine remain stable during hypercapnia both in blood and in bile ; potassium concentration is increased in the two media. To explain these results, the role of the liver is still to specify.
...
PMID:[Acute hypercapnia and bile. Experimental studies in the rat (author's transl)]. 101 82

The effect of sympathetic stimulation (stellate ganglion) on dog cerebral and cephalic blood flows was studied via a cervical or a thoracic approach to the stellate ganglion under sodium pentobarbital or chloralose anesthesia. Two different stimulation voltages (3v and 5v) of monophasic pulses were applied for 1 minute. Venous outflow was measured at the confluence of the sagittal, straight and lateral sinuses with the lateral sinuses occluded and with them patent. When the lateral sinuses were occluded, stellate ganglion stimulation resulted in a marked decrease in common carotid blood flow to 38 plus or minus 2.5% (SE) of control and dilation of the ipsilateral pupil, but cerebral blood flow did not change. Similar effects were observed with each of the anatomic approaches, anesthetics, and voltages used and in dogs with low cerebral vascular tone induced by hypercapnia. When the lateral sinuses were kept patent, sympathetic nerve stimulation decreased the venous outflow to 89 plus or minus 2.9% of control and clamping both of the external jugular veins increased venous outflow to 120 plus or minus 2.7% of control. When the lateral sinuses were kept patent and the extracranial venous pressure was increased by clamping both of the external jugular veins, the decrease in venous outflow in response to sympathetic stimulation was even larger: venous outflow was only 65 plus or minus 4.9% of control. We conclude that stimulation of the stellate ganglion has no effect on the cerebral vasculature. Sympathetic stimulation significantly decreases venous blood flow measured at the confluence of the sinuses only when communications between the intracranial and extracranial venous vasculatures are present.
...
PMID:Effect of sympathetic nerve stimulation on cerebral and cephalic blood flow in dogs. 112 72

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

Digoxin-like immunoreactive factor (DLIF) is an endogenous substance with natriuretic and diuretic activity. Elevated plasma levels of DLIF are found in various clinical states characterized by water and sodium retention. Chronic respiratory failure, particularly of an advanced stage, also is frequently associated with water and sodium retention. In order to determine whether elevated plasma levels of DLIF are present in chronic respiratory failure, we measured plasma DLIF levels in seven patients (four with COPD [two of whom had associated sleep apnea disturbance] and three with kyphoscoliosis) suffering from advanced chronic respiratory failure with severe hypoxemia and hypercapnia. We found that in these patients plasma levels of DLIF were significantly higher than in healthy control subjects. We conclude that patients with advanced chronic respiratory failure respond with increased levels of DLIF. This may represent an attempt at homeostasis of water and sodium metabolism which is frequently deranged in this clinical condition.
...
PMID:Endogenous digoxin-like immunoreactive factor is elevated in advanced chronic respiratory failure. 130 96

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.
...
PMID:Chemoreceptor and baroreceptor responses of A1 area neurons projecting to supraoptic nucleus. 132 16

We tested the hypothesis that differential sympathetic innervation explains the attenuated cerebral blood flow (CBF) response to hypercapnia (hyper) in fore-brain (fb) compared with brain stem in 1- to 2-wk-old piglets. In pentobarbital sodium-anesthetized piglets, CBF (microspheres) was measured during hypocapnia, normocapnia (normo), and hypercapnia [arterial CO2 partial pressure (PaCO2) of 25, 40, and 65 mmHg, respectively] in random sequence. After pretreatment values were obtained, piglets were randomized to undergo sham treatment (n = 5), high cervical spinal cord transection (n = 6), or pharmacological alpha-adrenergic blockade (prazosin 1 mg/kg + yohimbine 1 mg/kg, n = 6). After each experimental treatment, CO2 reactivity was again measured. Before experimental manipulation, hypercapnic reactivity [(CBFhyper - CBFnormo)/(PaCO2hyper - PaCO2normo)] in brain stem was approximately three times greater than in forebrain (e.g., sham; 3.6 +/- 0.8 vs. 1.2 +/- 0.3 ml.min-1.100 g-1.mmHg-1). Hypercapnic reactivity in forebrain was not increased by cord transection (1.4 +/- 0.3 vs. 1.1 +/- 0.2 ml.min-1.100 g-1.mmHg-1) or alpha-blockade (1.6 +/- 0.6 vs. 1.2 +/- 0.4 ml.min-1.100 g-1.mmHg-1). Likewise, hypercapnic cerebral vascular resistance (CVR) was unchanged by experimental treatment (e.g., CVRfb; cord transection 1.1 +/- 0.1 vs. 1.0 +/- 0.1; alpha-blockade 1.1 +/- 0.2 vs. 1.0 +/- 0.1 mmHg.ml-1.min-1.100 g-1). Hypocapnic vasoconstriction, however, was attenuated by both cord transection and alpha-blockade in forebrain and brain stem. We conclude that physiological stimulation of the noradrenergic component of the sympathetic nervous system does not explain regional differences in CBF reactivity during hypercapnia in 1- to 2-wk-old piglets.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Hypercapnic blood flow reactivity not increased by alpha-blockade or cordotomy in piglets. 135 31

Hyperammonemia increases brain glutamine levels, causes astrocytic swelling, and depresses cerebral blood flow (CBF) responsivity to CO2. Methionine sulfoximine (MSO) inhibition of glutamine synthetase activity, known to be enriched in astrocytes, prevents ammonia-induced increases in brain glutamine and water content. We tested the hypothesis that inhibition of glutamine accumulation restores CBF responsivity to CO2 during acute hyperammonemia. Pentobarbital-anesthetized rats treated with either vehicle or MSO (150 mg/kg i.p.) received a 6-hour intravenous infusion of either sodium or ammonium acetate. With subsequent induction of hypercapnia, CBF increased from 113 +/- 14 (mean +/- SEM) to 194 +/- 9 ml/min per 100 g in control rats but was unchanged from 107 +/- 13 to 79 +/- 10 ml/min per 100 g in hyperammonemic rats. Treatment with MSO in hyperammonemic rats restored the CBF response to hypercapnia (from 73 +/- 8 to 141 +/- 14 ml/min per 100 g). With induction of hypocapnia, CBF decreased from 114 +/- 11 to 88 +/- 11 ml/min per 100 g in control rats but increased from 112 +/- 13 to 142 +/- 19 ml/min per 100 g in hyperammonemic rats. Treatment with MSO in hyperammonemic rats did not fully restore the response to hypocapnia but prevented the paradoxical increase in CBF (from 80 +/- 8 to 80 +/- 8 ml/min per 100 g). In control rats, MSO did not affect CO2 responsivity. Treatment with MSO prevented ammonia-induced increases in intracranial pressure. Hyposmotic-induced increases in brain water content and intracranial pressure attenuated the CBF response to hypercapnia but, unlike hyperammonemia, did not attenuate the response to hypocapnia. In contrast to hypercapnia, vasodilation in response to arterial hypotension was intact in hyperammonemic rats. We conclude that the grossly abnormal CBF responsivity to CO2 alterations during hyperammonemia is linked to glutamine accumulation rather than ammonia per se. Cerebral edema secondary to glutamine accumulation may contribute in part to abnormal CBF responses, although other aspects of astrocyte dysfunction are likely to be important.
...
PMID:Restoration of cerebrovascular CO2 responsivity by glutamine synthesis inhibition in hyperammonemic rats. 139 82

1. The effects of two anaesthetics, sodium pentobarbital and urethane, and the effects of anaesthesia-associated hypothermia on acid-base status and blood gases were studied in rats without assisted ventilation. 2. Manipulation of conscious rats produces a progressive increase in arterial lactate associated with slight hyperventilation. 3. Sodium pentobarbital anaesthesia produces mild respiratory acidosis accompanied by increase in lactate arterial values. Urethane anaesthesia leads to partially compensated metabolic acidosis. 4. Hypothermia reduces metabolic acidosis and hypercapnia induced by sodium pentobarbital anaesthesia. No difference between hypothermic and normothermic values was observed in urethane anaesthesia.
...
PMID:Differential effects of hypothermia upon blood acid-base state and blood gases in sodium pentobarbital and urethane anaesthetised rats. 139 74


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---