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

The ability of children with cyanotic breath-holding spells to respond to anger or frustration by voluntary breath-holding for prolonged periods (often to the point of precipitating hypoxic seizure activity) suggested the hypothesis that such children may have a less powerful urge to breathe in the presence of hypoxia and/or hypercapnia than children who do not have breath-holding spells. Because ventilatory chemosensitivity is difficult to measure in infants and young children, this hypothesis was tested indirectly by measuring the ventilatory responses to hyperoxic progressive hypercapnia and to isocapnic progressive hypoxia of seven individuals who had a history of cyanotic breath-holding spells in infancy and 17 control subjects. The mean values for sensitivity to hypoxia and to hypercapnia were not significantly different between the two groups, and the responses of the majority of the subjects with cyanotic breath-holding spells were clearly within the normal range. There were fewer individuals with high-normal ventilatory responses among the subjects with cyanotic breath-holding spells. Although children with cyanotic breath-holding spells may have decreased ventilatory chemosensitivity transiently during infancy or may differ from other children in some other aspect of the control of breathing, the pathogenesis of infantile cyanotic breath-holding spells does not involve a permanently blunted sensitivity to hypercapnia or hypoxia.
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PMID:Ventilatory chemosensitivity in subjects with a history of childhood cyanotic breath-holding spells. 396 48

The effect of asphyxia on seizures was determined in neonatal dogs. In normoxic (paralyzed and ventilated) neonatal dogs, bicuculline-induced seizures produced significant elevations of arterial blood pressure, PO2, glucose, lactate, and epinephrine. Cerebral blood flow increased severalfold; brain glucose, adenosine triphosphate (ATP), and phosphocreatine (PCr) did not decrease significantly. In contrast, seizures during asphyxia were associated with hypoxia, hypotension, hypercarbia, and acidosis. Significant cerebral ischemia developed. Brain glucose, ATP, and PCr were significantly depleted. Complete oxygen deprivation during neonatal seizures exhausts brain energy stores, which leads to cessation of seizure activity.
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PMID:Physiologic and metabolic alterations associated with seizures in normoxic and asphyxiated neonatal dogs. 647 9

Reactive hyperemia has been characterized in many vascular beds, but little is known about quantitative characteristics of reactive hyperemia in the cerebral circulation. We measured velocity of blood flow and pial artery diameter to characterize the time course of reactive hyperemia and used microspheres to study regional blood flow in the brain. Cerebral ischemia was produced by raising intracranial pressure or by arterial occlusion with a cuff around the neck. Five seconds of ischemia produced virtually maximal peak reactive hyperemia, and 30 s of ischemia produced maximal peak reactive hyperemia. During reactive hyperemia after 30 s of cerebral ischemia, there was a three- to fourfold increase in cerebral blood flow. The magnitude of reactive hyperemia was greater in gray matter than in white matter. Minimal resistance during reactive hyperemia, after ischemia produced by arterial occlusion, is similar to minimal resistance during seizures or hypercapnia, which suggests that reactive hyperemia produces maximal vasodilatation. Oxygen saturation of cerebral venous blood increased almost twofold during reactive hyperemia, which indicates that factors in addition to venous (and presumably tissue) oxygen are important determinants of reactive hyperemia. In summary, 1) we have characterized the time course of reactive hyperemia in the cerebral circulation; 2) reactive hyperemia after arterial occlusion produces maximal cerebral vasodilatation; and 3) there is marked heterogeneity of the response, with much larger increases in flow in cortical gray matter than white matter.
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PMID:Characteristics of reactive hyperemia in the cerebral circulation. 669 88

Epileptogenic foci were created by topical application of penicillin to the cerebral cortex in 40 paralyzed and artificially ventilated cats receiving halothane anesthesia. The animals were divided into two equal groups to compare primary and secondary foci. The following variables were recorded at normocapnia, hypocapnia, and hypercapnia prior to and during seizure activity: cerebral blood flow (CBF), determined by clearance of xenon 133; cortical redox states, measured by the fluorescence of reduced pyridine nucleotides (PN); brain pH, measured using a lipid-soluble, pH-sensitive fluorescent indicator; and electroencephalograms (EEG). Mean arterial blood pressure, arterial pH, arterial carbon dioxide tension (PaCO2), and arterial oxygen tension (PaO2) were monitored in each animal. All animals had a normal PaCO2-CBF response prior to the creation of a seizure focus, assuring the presence of autoregulation and normal metabolic function. CBF increased equally with seizures in the primary and secondary hemispheres. The relative increase was related to the PaCO2 but approximated 68% at normocapnia. There was an alteration in the PaCO2-CBF response with seizures, but the ability of the cerebral vasculature to constrict and dilate with hypocapnia and hypercapnia was retained. There was no significant difference in the reduced PN signal with variations in PaCO2 prior to seizures, but there was an apparent 10 to 15% fall with seizures. The "equivalent" intracellular pH fell to 6.94 at normocapnia in the primary focus but remained essentially unchanged from the control value of 7.10 in the secondary focus. These differences in pH were consistent with the greater degree of seizure activity observed in the primary focus. We conclude that a nonhypoxic acidosis existed in the primary focus and that changes in CBF were not related to it because the CBF changed equally in both hemispheres.
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PMID:Correlation of intracellular redox states and pH with blood flow in primary and secondary seizure foci. 678 36

Brain glucose metabolism was studied in paralyzed, ventilated rats given electroconvulsive shock (ECS) under normocapnic and hypercapnic conditions. Brains were obtained with a freeze-blowing apparatus. Rates of glucose utilization were determined with [2-14C]glucose and [3H]deoxyglucose as tracers. In normocapnic rats, ECS caused a large increase in the rate of glycolysis to 5--6 mumol/g/min. Brain lactate levels increased three- to fourfold. The stimulation of glucose metabolism was reflected in decreased brain glucose 6-phosphate concentration as early as 2--3 s after ECS. There were significant decreases in brain glucose and glycogen levels at 20 and 30 s after ECS. The decreases in endogenous brain glucose accounted for most of the increases in glucose utilization measured isotopically, implying that influx of glucose from blood into brain did not increase greatly over these time periods. Animals made hypercapnic by respiration with 10% CO2 for 2 min prior to ECS were different in their metabolic responses to ECS in several ways. The increases in glycolytic rate and lactate content of brain were half of those found in normocapnic rats. Brain glycogen and glucose concentrations did not change significantly in the hypercapnic rats during seizure activity. Thus, hypercapnia lessened the stimulation of glycolysis caused by ECS, but increased net influx of glucose from blood to brain. The mechanisms of these effects of hypercapnia are uncertain, but it is postulated that the effect on glycolytic activity is due to the acidosis and that the effect on glucose transport is due to an increase in capillary surface area.
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PMID:Cerebral metabolic responses to electroconvulsive shock and their modification by hypercapnia. 680 Dec 6

The effects of intravenously administered lidocaine on the cerebral cortical energy state and glycolytic metabolism were studied in rats. In one series, rats were divided into five groups according to EEG patterns, i.e., control, desynchronized, synchronized, seizure (1-min duration) and recovery groups. With lidocaine infusion (0.75 mg/min), there were no significant changes from the control group in the cerebral energy state except for a modest increase in phosphocreatine (PCr) in the seizure group and a small decrease in ADP in the non-seizure groups. The cerebral energy charge remained unchanged. Lactate and pyruvate significantly decreased in the non-seizure groups. In a second series, rats were divided into five groups, i.e., control, lidocaine seizure groups (5-min duration, 1.5 mg/min) at hypocapnia, normocapnia and hypercapnia, and a bicuculline (1.2 mg/kg) seizure group. The metabolic changes during lidocaine seizure were essentially the same as those observed in the seizure group in the first series. However, the increase in PCr during lidocaine seizure was significant only in the hypocapnic and the normocapnic groups. Bicuculline-induced seizures were accompanied by a significant decrease in high energy phosphates. In summary, neither a non-seizure nor-seizure dose of lidocaine caused any reduction in the cerebral energy charge nor was there any evidence of increased anaerobic metabolism in the cerebral cortex during lidocaine-induced seizures.
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PMID:Cerebral energy state and glycolytic metabolism during lidocaine infusion in the rat. 721 27

The purpose of this study was to measure changes in local cerebral blood flow (1-CBF) during generalized seizures, and to study whether or not formation of prostaglandins or related substances contributes to the increased flow rates. Seizures were induced in ventilated rats maintained on 70% N2O and 30% O2 by the i.v. injection of the GABA receptor blocker bicuculline (1.2 mg . kg-1). Formation of prostaglandins was inhibited by the administration of the fatty acid cyclo-oxygenase inhibitor indomethacin (10 mg . kg-1). Local CBF in 21 defined brain structures was measured autoradiographically with 14C-iodoantipyrine as the diffusible tracer. After 20 min of continuous seizure activity 1-CBF increased 1.5--5-fold, the smallest increases (less than 200% of control) being observed in frontal and auditory cortex and in the caudoputamen, and the largest (greater than 400% of control) in substantia nigra, thalamus, visual cortex, lateral geniculate and hypothalamus. In general, the largest increases in 1-CBF occurred in sensory and limbic systems (and hypothalamus) while motor systems showed a pronounced variability. In the majority of structures examined indomethacin failed to modify the CBF response during seizures. Although this result suggests that seizures, in contrast to hypercapnia, lead to an increased CBF by other mechanisms than those related to prostaglandin formation, some structures (nucleus ruber, cerebellum, and superior colliculus) showed a clearly reduced 1-CBF in indomethacin-treated animals.
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PMID:Local cerebral blood flow in the brain during bicuculline-induced seizures and the modulating influence of inhibition of prostaglandin synthesis. 728 97

Although preischemic hyperglycemia is known to aggravate damage due to transient ischemia, it is a matter of controversy whether or not this is a result of the exaggerated acidosis. It has recently been reported that although tissue acidosis of a comparable severity could be induced in normoglycemic dogs by an excessive rise in arterial CO2 tension, short-term functional recovery was improved, rather than compromised. In the present experiments we induced excessive hypercapnia (PaCO2, approximately 300 mm Hg) in normoglycemic rats before inducing forebrain ischemia of 10-min duration. This reduced the brain extracellular pH to values normally encountered in hyperglycemic rats subjected to ischemia. The events induced by hypercapnia clearly enhanced ischemic brain damage, as assessed histologically after 7 days of recovery. We hypothesize that the decisive event was an exaggerated decrease in extra- and intracellular pH and that the results thus demonstrate an adverse effect of acidosis. However, since postischemic seizures did not occur in the hypercapnic ischemic rats, the results also demonstrate that changes in intra-extracellular pH and bicarbonate concentrations modulated ischemic damage in an unexpected way.
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PMID:Acidosis induced by hypercapnia exaggerates ischemic brain damage. 811 21

After occlusion of an artery to the brain, hypercarbia and seizures may produce a paradoxical reduction in cerebral blood flow to the region supplied by collateral vessels. We measured pressure in an occluded branch of the middle cerebral artery and measured regional cerebral blood flow (rCBF) to collateral-dependent cerebrum in dogs (n = 25) to examine hemodynamic mechanisms that account for the reduction in flow. During hypercarbia (arterial PCO2 = 70 +/- 5 mmHg), rCBF to collateral-dependent cerebrum, measured with microspheres and identified using the shadow flow technique, decreased from 95 +/- 6 (mean +/- SE) to 71 +/- 9 ml.100 g-1.min-1 (P < 0.05), while flow to normal brain increased from 105 +/- 9 to 281 +/- 15 ml.100 g-1.min-1 (P < 0.05). Pressure in a branch of the middle cerebral artery decreased during hypercarbia from 50 +/- 6 to 25 +/- 3 mmHg (P < 0.05), concurrent with a significant increase in resistance of collateral vessels. Small vessel resistance was the same in collateral-dependent and normal brain. During bicuculline-induced seizures, with blood pressure maintained at control levels by withdrawal of blood, rCBF decreased in collateral-dependent cerebrum from 128 +/- 16 to 67 +/- 11 ml.100 g-1.min-1 (P < 0.05), and flow to normal brain increased from 169 +/- 14 to 418 +/- 17 ml.100 g-1.min-1 (P < 0.05). Small vessel resistance decreased in both regions, but the decrease was much greater in normal cerebrum. Changes in cerebral artery pressure and resistance of collateral vessels during seizure were similar to those during hypercarbia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of redistribution of cerebral blood flow during hypercarbia and seizures. 820 5

Hypoventilation in children with hypertrophied tonsils can cause hypoxemia, hypercarbia, acidosis and pulmonary vasoconstriction resulting in cardiac arrhythmias or cor pulmonale. In addition, cerebral symptoms such as day-time hypersomnia or even seizures may be present. Early recognition of hypertrophied tonsils is necessary to avoid development of severe cardiac symptoms. If cardiac incompensation is present, medical treatment is advocated prior to tonsillectomy. Anaesthesia for tonsillectomy in these children is associated with special considerations. Preoperative sedation should be excluded, and inhalational induction with O2 and Halothane is recommended. On induction a difficult intubation should be expected.
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PMID:[Hypertrophic tonsils, upper airway obstruction and cardiac complications. A combined otological, medical and anesthesiological problem]. 825 5


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