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

Resting level of ventilation is affected by change in hydrogen ion [H+] and by certain amino acid neurotransmitters in the brain and cerebral fluids. Hypercapnia alters both [H+] and amino acid content. Therefore, the effect of 90 min of hypercapnia on blood and cerebrospinal fluid (CSF) contents of selected amino acids and ammonia was studied in anesthetized mongrel dogs using 13N-labeled ammonia. Metabolic turnover of CSF ammonia was not significantly altered by hypercapnia, but CSF equilibrium concentration of metabolized ammonia, i.e., glutamine, a precursor of the neurotransmitters glutamic acid and gamma amino butyric acid, varied linearly with CSF bicarbonate and hydrogen ion concentration. The percentage of CSF glutamine derived from tracer-labeled ammonia metabolized in the central nervous system (CNS) rose from 30% at normocapnia to 60% after 90 min of hypercapnia, whereas at the same time, the CSF transfer rate of glutamine increased by a factor of 2. These observations show that there is a significant correlation between CNS transfer of glutamine and CNS hydrogen ion regulation during hypercapnia.
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PMID:Relationship between central nervous system hydrogen ion regulation and amino acid metabolism in hypercapnia. 687 69

A technique is described for measuring regional blood flow concomitantly in the brain and in extracranial tissues of the cat. Hydrogen clearance using the tissue polarographic electrode appears to be a useful technique for intermittent measurements of cerebral blood flow (CBF) in relatively small areas. H2 was administered by inhalation for 10 min. Both chronic and acutely implanted electrodes were placed at different depths in the cat brain, on the surface of the cortex, and in extracranial tissues. Clearance rates in gray matter of 75 to 119 ml/min/100 g tissue have been obtained and of 11 to 14 ml/min/100 g tissue in white matter. Clearance curves have invariably been monoexponential in character in white matter and biexponential in gray matter. Successful recordings of H2 clearance curves were obtained from both chronically (up to 5 months) and acutely implanted electrodes. A new type of electrode is described. The "paperclip" electrode is placed at the surface of the cortex, has a reactive surface much greater than that of needle electrodes, thus limiting the possible variations due to vascularization differences from one local area to the next, and induces no damage to the brain tissue. To test the reliability of the technique, blood flow was measured during hypercapnia and progressive exsanguination. All electrodes indicated increased rCBF following 5-7% CO2 inhalation. A marked decrease in blood flow was seen with peripheral electrodes during exsanguination, whereas it was necessary to lower arterial blood pressure by more than 60% of the baseline value to record decreased flow in brain tissues. The constancy of response from electrodes and the lack of obvious tissue damage on dissection of the brain renders the method an adequate one. It provides highly focal recording of both CBF and extracranial flow in chronically implanted animals.
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PMID:Regional cerebral and extracranial blood flow measurements in acutely and chronically implanted cats: hydrogen clearance technique. 731 64

Sulfonylureas reduce cerebral blood flow (CBF) during hypoxia but not during hypercapnia, whereas blockers of nitric oxide (NO) synthesis reduce hypercapnic CBF. However, the effect of NO blockers on hypoxic CBF is uncertain. CBF was measured in the cortex of 51 enflurane-anesthetized rats by the hydrogen clearance technique during eucapnia, hypercapnia (arterial PCO2 65 Torr), and hypoxia (arterial PO2 40 Torr). CBF increased twofold in both hypercapnia and hypoxia from eucapnia. Intracortical (ic) NG-monomethyl-L-arginine (L-NMMA, 100 microM-5 mM) attenuated both the hypercapnic and hypoxic dilations by 60-70%, and L-arginine (300 mg/kg iv) partially reversed these effects. Glibenclamide (10 microM ic) and L-NMMA gave no further attenuation of the hypoxic dilation than L-NMMA alone. Cromakalim (10 microM, ic) increased CBF in eucapnia, but this was not seen in the presence of glibenclamide. The adenosine antagonist 8-phenyl-theophylline did not attenuate the hypoxic dilation. This suggests that NO synthesis plays a major role in the regulation of CBF in hypercapnia and hypoxia. But the combined effects of glibenclamide and L-NMMA do not further attenuate CBF in hypoxia.
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PMID:Effect of L-NMMA, cromakalim, and glibenclamide on cerebral blood flow in hypercapnia and hypoxia. 757 35

Hypoglycemia increases the vulnerability of the perinatal brain to asphyxia, but it is not known if hypoglycemia-induced changes in cerebral hemodynamics and vascular reactivity underlie this vulnerability. This study tested the hypothesis that hypoglycemia exacerbates postischemic hypoperfusion, and impairs postischemic CO2 reactivity. The authors also examined the hypothesis that postischemic hypoperfusion is associated with a reduction in the interstitial concentration of the vasodilator metabolite adenosine. Global cerebral ischemia of 10 minutes duration was induced in newborn pigs anesthetized with isoflurane by occlusion of subclavian and brachiocephalic arteries; cortical cerebral blood flow (CBF) and interstitial adenosine concentration were evaluated simultaneously using the combined hydrogen clearance/microdialysis technique. Hypoglycemia (blood glucose < 25 mg/dl) was induced by regular insulin (25 IU/kg) administered intravenously 2 hours prior to induction of ischemia. In the eight normoglycemic animals, baseline CBF was 38 +/- 4 ml/min/100 gm and baseline adenosine concentration was 1.2 +/- 0.1 microM; in the eight hypoglycemic animals, these values were 39% (p < 0.05) and 62% (p < 0.05) greater, respectively, under baseline conditions. At 1 hour of postischemic reperfusion in normoglycemic animals, CBF was reduced 39% relative to the preischemic baseline (p < 0.01), concomitant with a 27% reduction (p < 0.05) in adenosine concentration, suggesting that this lowered concentration may underlie delayed hypoperfusion. These postischemic reductions in CBF and interstitial adenosine concentration were significantly greater in hypoglycemic animals, with CBF and adenosine concentration reduced 70% (p < 0.001) and 71% (p < 0.01), respectively, relative to baseline. In nine animals preischemic reactivity to hypercapnia was unaffected by hypoglycemia. Postischemic hypercapnic reactivity was retained in the eight normoglycemic animals, but was attenuated 73% (p < 0.05) in hypoglycemic animals. Thus, in the newborn pig, hypoglycemia exacerbates postischemic cortical hypoperfusion and impairs postischemic cerebrovascular reactivity to hypercapnia.
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PMID:Effect of hypoglycemia on postischemic cortical blood flow, hypercapnic reactivity, and interstitial adenosine concentration. 796 18

The increase in blood flow in the cerebral cortex of the anaesthetized rat during hypoxia and hypercapnia was investigated. Cerebral blood flow (CBF) was measured using the hydrogen clearance method with acutely implanted platinum electrodes. Hypoxia (PaO2 35.3 +/- 2.4 Torr) and hypercapnia (PaCO2 68.1 +/- 5.1 Torr) increased basal CBF from 76.3 +/- 9.0 ml/100g/min to 168.1 +/- 20.1 ml/100g/min and 162.4 +/- 31.9 ml/100g/min respectively. The sulphonylurea tolbutamide (1mM in 1%DMSO) had no significant effect on CBF in hyperoxia or in hypercapnia. However, it attenuated the increase of CBF during hypoxia by 66 +/- 11% (p < 0.01). This suggests that opening of tolbutamide-sensitive potassium channels may be involved in the process of hypoxic vasodilation in the rat cerebral cortex.
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PMID:The effect of tolbutamide on cerebral blood flow during hypoxia and hypercapnia in the anaesthetized rat. 830 97

These studies were conducted in neurosurgical patients to determine brain tissue nonbicarbonate buffering of pH changes during hypercapnia. Following a craniotomy, a sensor which continuously measures oxygen pressure, carbon dioxide pressure, pH and temperature was inserted into cortex tissue of nine subjects. Bicarbonate concentration was calculated from the Henderson-Hasselbach equation. Following baseline measures, PaCO2 was increased 10mmHg for 10 min. Tissue pCO2 increased 9 mmHg (p < 0.05) without a change in tissue pO2. In six patients, tissue bicarbonate concentration increased from 18 to 20 meq L-1 (p < 0.05), indicating a 40-50% attenuation of the increase in hydrogen ion (H+) by nonbicarbonate buffering mechanisms. Three patients showed no increase in tissue bicarbonate during hypercapnia; 2 had baseline tissue pH less than 6.5 and one displayed signs of tissue hypoxia during the CO2 challenge. In all patients, increases in tissue H+ during hypercapnia were related to baseline tissue bicarbonate concentration. Marked increases in H+ were seen when baseline bicarbonate decreased below 10 meq L-1. These results suggest that when tissue bicarbonate is depleted, the risk of H+ induced injury during hypercapnia is increased.
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PMID:Brain tissue acid-base response to hypercapnia in neurosurgical patients. 862 93

Previous studies found that regular confinement of dogs in an experimental environment preceding onset of an avoidance task was associated with increases in blood pressure and decreases in heart rate and respiration rate that were not prevented by adrenergic antagonists. The present study investigated a) whether divergent changes in blood pressure and heart rate also occur in micropigs preceding onset of an avoidance task, and b) the nature of changes in blood gases, plasma pH, plasma bicarbonate, hematocrit, and plasma electrolytes observed under these conditions. Blood pressure increased and heart rate decreased during 2-h preavoidance periods, whereas both blood pressure and heart rate were elevated during 20-min avoidance periods. During preavoidance periods, pO2, plasma pH, and plasma potassium pCO2 were decreased below home kennel levels during early preavoidance, whereas pCO2 and plasma bicarbonate were persistently increased and hematocrit was persistently decreased for the duration of the preavoidance periods. Each of these changes was reversed during the avoidance sessions. These findings suggest that behaviorally induced hypercapnia might participate in blood pressure regulation via increased renal sodium/hydrogen exchange and renal sodium retention.
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PMID:Preavoidance hypercapnia and decreased hematocrit in micropigs. 877 77

Acutely tightening a snare around one pulmonary artery previously was shown to trigger a reversible ventilation-perfusion (V/Q) mismatch in broilers, as reflected by decreases in the partial pressure of oxygen in arterial blood (hypoxemia), accompanied by increases in the hydrogen ion concentration (acidosis) and partial pressure of carbon dioxide (hypercapnia). In the present study, snares were loosely implanted around the right pulmonary artery and the right extrapulmonary primary bronchus in anesthetized male broilers. These snares were tightened and released independently and then simultaneously to evaluate the possibility that directing the entire respiratory minute volume toward the left lung might attenuate the V/Q mismatch caused by forcing the entire cardiac output (CO) through the left lung. Fully reversible arterial blood hypoxemia, acidosis, and hypercapnia occurred when either snare was tightened independently. Presumably, tightening the bronchial snare restricted ventilation but not blood flow to the right lung, thereby permitting blood to perfuse poorly ventilated gas exchange surfaces. Simultaneously tightening both snares triggered arterial blood hypoxemia, acidosis, and hypercapnia similar to or greater in magnitude than the responses obtained by tightening the pulmonary artery snare independently. Tightening either snare independently or both snares simultaneously caused pulmonary arterial pressure to increase (pulmonary hypertension), and permanent obstruction of one bronchus in a separate experiment caused an increase in the right:total ventricular weight ratio, which is indicative of chronic pulmonary hypertension. The mean systemic arterial pressure decreased when the pulmonary artery snare was tightened independently or in combination with the bronchial snare, but not when the bronchial snare was tightened independently. The respiratory rate increased and the heart rate decreased when the pulmonary artery snare was tightened independently, but not when the bronchial snare was tightened independently or in combination with the pulmonary artery snare. These results demonstrate that the V/Q mismatch caused by forcing all the CO to perfuse one lung cannot be attenuated by simultaneously directing the entire respiratory minute volume toward the same lung.
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PMID:Independent and simultaneous unilateral occlusion of the pulmonary artery and extra-pulmonary primary bronchus in broilers. 893 96

To assess the responsiveness of cerebral blood flow to arterial carbon dioxide tension (Pa,CO2), arterial oxygen tension (Pa,O2), and pH modifications, in chronic hypercapnia, we measured middle cerebral blood flow velocity (CBFV) by transcranial Doppler ultrasound in 13 chronically hypercapnic, long-term ventilated patients with chronic obstructive pulmonary disease (COPD), in the following conditions: 1) breathing room air; 2) with oxygen supplementation; 3) during mechanical noninvasive intermittent positive pressure ventilation (nIPPV) with O2 enrichment. Under baseline conditions (room air), the CBFV was within the normal range. During oxygen administration, a statistically significant increase was obtained in Pa,O2 (6.5 +/- 0.6 vs 11.2 +/- 1.9 kPa (49.1 +/- 4.3 vs 84.3 +/- 14.6 mmHg)), without relevant variations in: CBFV (54.2 +/- 9.1 cm.s-1), Pa,CO2 (8.6 +/- 1.0 kPa (64.7 +/- 7.7 mmHg)) and hydrogen ion concentration [H+] (42.9 +/- 2.9 nM), compared to baseline values (CBFV = 52.8 +/- 10.7 cm.s-1; Pa,CO2 = (8.4 +/- 0.9 kPa (63.1 +/- 7.1 mmHg; [H+] = 41.8 +/- 2.8 nM). After nIPPV, Pa,O2 did not increase any further (10.6 +/- 1.7 kPa (79.2 +/- 12.7 mmHg)), while CBFV (40.9 +/- 12.6 cm.s-1), Pa,CO2 (7.5 +/- 1.3 kPa (56.2 +/- 9.4 mmHg)) and [H+] (39.1 +/- 4.6 nM) showed a significant reduction compared to oxygen therapy (p < 0.01). We therefore conclude that in chronically hypercapnic long-term ventilated patients cerebral blood flow depends mainly on changes in Pa,CO2 and [H+], whilst oxygen does not seem to interfere with cerebral flow velocity. The reduction of Pa,CO2, due to mechanical ventilation, may determine cerebral blood vessel constriction, with possible impairment of cerebral functions.
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PMID:Correction of hypoxia and hypercapnia in COPD patients: effects on cerebrovascular flow. 915 13

We report a case of acute head injury with severe diffuse brain swelling in which early global cerebral ischemia was followed by brain death. Global cerebral ischemia was detected by cerebral arteriovenous lactate content difference, cerebral arteriovenous carbon dioxide tension (PCO2) difference, and cerebral arteriovenous hydrogen ion content difference. Physiopathological aspects of cerebrovenous hypercarbia are discussed.
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PMID:Cerebral arteriovenous PCO2 difference and early global cerebral ischemia in a patient with acute severe head injury. 923 89


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