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

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

Five Merino sheep were dosed 3 g/kg of dry, finely-milled Homeria glauca (Natal yellow tulp) plant material. An electrocardiogram was recorded and the arterial and central venous blood pressure, blood gases, haematological variables, plasma electrolytes (Na+, K+, Ca2+, Mg2+, Cl- and PO4(2-) ) and a variety of serum enzymes and chemical constituents were measured hourly until death (3 sheep) or until sheep were in extremis (2 sheep). Heart rate rose progressively as a result of sinus and, later, ventricular tachycardia. Systolic blood pressure rose, but there was little change in the mean and diastolic arterial pressures and central venous pressure. There was progressive hypoxaemia, hypercarbia and acidaemia with depletion of plasma bicarbonate. Haemoconcentration, hyperkalaemia and hypochloraemia were found along with rising serum creatinine and plasma glucose. Rises in serum enzymes indicated widespread tissue damage. Electrocardiographic recordings were being made at the moment of death in 3 of the 5 sheep. In these 3 sheep the cause of death was ventricular fibrillation.
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PMID:Some physiopathological features of experimental Homeria glauca (Wood & Evans) N. E. Br. poisoning in Merino sheep. 664 61

The effects of enflurane anesthesia on the cerebral cortical energy state and glycolytic metabolism were studied in rats. Twenty-four rats were divided into four groups with increasing concentrations of enflurane in the arterial blood, i.e. control (1.9 +/- 0.3 mg/dl, means +/- s.e.mean), level I (16.1 +/- 1.1 mg/dl), level II (26.0 +/- 1.6 mg/dl), and level III (32.9 +/- 0.9 mg/dl). At level I, high voltage 1-3 Hz slow waves superimposed on low voltage 10-12 Hz waves were predominant, and at levels II and III, spiking activity and burst suppression were recorded in the EEG. The duration of suppression at level III was significantly longer than that at level II. During enflurane anesthesia, there were no significant differences compared with the control group in the cerebral energy state or energy charge. Glycolytic metabolism remained unchanged except for an increase in glucose at levels II and III. Effects of hypocapnia and hypercapnia were examined in an additional 12 rats with an enflurane concentration in the blood similar to that at level II. Irrespective of PaCO2 levels, there were no significant changes in cerebral energy charge and glycolytic metabolites except for a decrease in glucose and an increase in lactate at hypocapnia. It was concluded that there was neither evidence of derangement of energy state nor increased anaerobic metabolism in the cerebral cortex during enflurane anesthesia.
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PMID:Cerebral energy state and glycolytic metabolism during enflurane anesthesia in the rat. 673 Aug 86

Acute respiratory failure developed in three patients needing ventilatory support within hours after total parenteral nutrition was started. We postulate that the high carbohydrate load provided in the parenteral solution resulted in the use of glucose as the primary energy source, with the development of substantial increases in the carbon dioxide production and the respiratory quotient. Because these patients had a relatively fixed ventilatory response, hypercapnia ensued. Excessive carbohydrate loading may precipitate respiratory acidosis in patients unable to adequately improve their alveolar ventilation when compensating for increased carbon dioxide production.
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PMID:Respiratory failure precipitated by high carbohydrate loads. 679 9

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

Local cerebral blood flow (LCBF) was measured autoradiographically in newborn puppies by an indicator fractionation technique using 4-iodo-[14C]antipyrine as the diffusible indicator. Measurements were obtained in unanesthetized, normotensive animals, and the sensitivity of blood flow to hypercapnia and acute hypoxia was determined in 32 brain structures. LCBF in normal and hypoxic puppies was correlated with local cerebral glucose utilization (LCGU) obtained under the same experimental conditions (Duffy et al, 1982). In normocapnic (PaCO2 33 mm Hg) control animals, highest rates of blood flow were found in gray matter nuclei of the brainstem, in the medulla oblongata, and in the posterolateral nucleus of the thalamus (50 to 77 ml/100 gm/min); far lower flows were recorded among white matter structures (5 to 11 ml/100 gm/min). The vasodilatory response to both hypercapnia and hypoxia was greatest among brainstem gray matter structures, intermediate among cortical and diencephalic gray matter structures, and least in white matter. When LCBF was plotted as a function of LCGU for control animals, a positive linear correlation was obtained for all structures (p less than 0.001), implying that in newborns, as in adults, cerebral blood flow and metabolism are physiologically coupled. In hypoxic puppies, no consistent relationship between LCGU and LCBF could be demonstrated; however, there was suggestion that the two measurements correlated inversely, presumably reflecting enhanced anaerobic glycolysis in structures (e.g., hemispheric white matter) that were not adequately protected by compensatory hyperemia. White matter damage, a frequent complication of perinatal hypoxia-asphyxia, may be a consequence in part of the limited capacity of white matter to vasodilate in response to te chemical "signals" of hypercapnia and lactic acidosis.
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PMID:Regulation of local cerebral blood flow in normal and hypoxic newborn dogs. 680 92

Fetal and maternal blood gas tensions, pH, packed cell volume and glucose, fructose and lactic acid concentrations were monitored during the last two days of gestation, during parturition and and the first hour after birth. Blood samples were taken by means of indwelling catheters (implanted seven to 14 days before parturition) from 12 fetuses in seven sows. All fetuses were liveborn at a mean gestational age of 113.1 days. The significant finding was that all variables in fetal blood were stable during labour and, although mild hypercapnia was present during the last three hours, no significant changes in mean values were seen until those of samples taken within 15 minutes of birth. In some fetuses, no changes were seen until after birth, while in others pH and pO2 values declined during the last hour of fetal life. Immediately after birth a rapid increase in pO2 and decrease in pCO2 followed the onset of respiration. Blood pH fell during the first 30 minutes after birth and this fall was accompanied by increasing blood lactic acid concentrations. Blood glucose concentrations rose rapidly in the first 15 minutes after birth and were maintained during the first hour despite separation of the piglets from the sow. There was a transient, but significant, increase in packed cell volume during the period from 15 minutes before to 15 minutes after birth. Maternal values for all variables measured remained virtually unchanged during delivery.
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PMID:Changes in fetal and maternal blood at the end of pregnancy and during parturition in the pig. 680 20

The objective of the present study was to explore whether the systemic consequences of sympathoadrenal activation influence the cerebral circulatory and metabolic effects of hypercapnia in the rat. To that end, a bilateral blockade of the sympathetic chain was performed at the low thoracic level by paravertebral injection of local anaesthetic. The injection was followed by a reduction in blood pressure and, in comparison to animals injected with local anaesthetic intramuscularly, those with paravertebral blockade showed lower blood and tissue concentrations of glucose and lactate. Overall ("cortical") CBF and CMRO2 were measured with a 133xenon modification of the Kety-Schmidt technique, and local CBF was estimated autoradiographically with 14C-iodoantipyrine as the diffusible tracer. Paravertebral blockade failed to modify the circulatory response to hypercapnia, nor did it prevent the increase in CMRO2d previously noted in this preparation. In animals maintained ventilated on 70% N2O, paravertebral blockade reduced overall CBF by 30% and local CBF by 30-40%, with a suggested but statistically nonsignificant reduction in CMRO2. In unparalysed, awake animals the blockade failed to affect local CBF. It is concluded, therefore, that blockade of the sympathetic chain causes a reduction of CBF only in the stressful conditions prevailing in paralysed and ventilated animals.
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PMID:Cerebral blood flow and oxygen consumption in normocapnia and hypercapnia: modulating influence of paravertebral sympathetic blockade at the low thoracic level. 681 Jun 41

Brain glucose metabolism was studied in developing rats at ages 10 and 20 days postnatal under normal and hypercapnic conditions. Brains were removed and frozen within 1 s with a freeze-blowing apparatus. Glucose utilization was measured with [2-14C]glucose and [3H]deoxyglucose as tracers. Metabolites were determined by standard enzymatic techniques. Data from [3H]deoxyglucose phosphorylation indicated that normal brain glucose utilization increased almost threefold between the 10th and 20th postnatal days. From the relative rates of utilization of the two isotopes in the 20-day-old control group, it appeared that about 25% of 14C label derived from metabolism of [2-14C]glucose was lost from brain (probably as lactate) rather than entering the Krebs cycle. Under hypercapnic conditions (20% CO2-21% O2-59% N2), rates of glucose utilization by brain were decreased by one-half at both ages and there were progressive decreases in the concentrations of many intermediary metabolites. The bases for concluding that these metabolites were used to supplement glucose as a fuel for respiration, rather than being lost by leakage into blood, are discussed. Despite the differences in brain glucose metabolism between 10-day-old and 20-day-old rats, their responses to hypercapnia are remarkably similar: Rates of glucose utilization are reduced to approximately the same proportion of the original rate by 20% CO2, and endogenous metabolites (particularly glutamate and lactate) appear to be oxidized as replacement fuels.
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PMID:Brain carbohydrate metabolism in developing rats during hypercapnia. 720 66

Hypoxia impairs brain function by incompletely defined mechanisms. Mild hypoxia, which impairs memory and judgment, decreases acetylcholine (ACh) synthesis, but not the levels of ATP or the adenylate energy charge. However, the effects of mild hypoxia on the synthesis of the glucose-derived amino acids [alanine, aspartate, gamma-amino butyric acid (GABA), glutamate, glutamine, and serine] have not been characterized. Thus, we examined the incorporation of [U-14C]glucose into these amino acids and ACh during anemic hypoxia (injection of NaNO2), hypoxic hypoxia (15 or 10% O2), and hypoxic hypoxia plus hypercarbia (15 or 10% O2 with 5% CO2). In general, the synthesis of the amino acids and of ACh declined in parallel with each type of hypoxia we studied. For example, anemic hypoxia (75 mg/kg of NaNO2) decreased the incorporation of [U-14C]glucose into the amino acids and into ACh similarly. [Percent inhibition: ACh (57.4), alanine (34.4), aspartate (49.2), GABA (61.9), glutamine (59.2), glutamate (51.0), and serine (36.7)]. A comparison of several levels (37.5, 75, 150, 225 mg/kg of NaNO2) of anemic hypoxia showed a parallel decreased in the flux of glucose into ACh and into the amino acids whose synthesis depends on mitochondrial oxidation: GABA (r = 0.98), glutamate (r = 0.99), aspartate (r = 0.96), and glutamine (r = 0.97). The synthesis of the amino acids not dependent on mitochondrial oxidation did not correlate as well with changes in ACh metabolism: serine (r = 0.68) and alanine (r = 0.76). The decreases in glucose incorporation into ACh and into the amino acids with hypoxic hypoxia (15% or 10% O2) or hypoxic hypoxia with 5% CO2 were very similar to those with the two lowest levels of anemic hypoxic. Thus, and explanation of the brain's sensitivity to a decrease in oxygen availability must include the alterations in the metabolism of the amino acid neurotransmitters as well as ACh.
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PMID:Decreases in amino acids and acetylcholine metabolism during hypoxia. 725 4


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