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

The interconnections between EEG, intermediary and energy metabolism of the brain cortex and CSF potassium level are studied during severe hypercapnia in anaesthetized, artificially ventilated cats. Hypercapnic animals were ventilated with 40 to 50% to CO2 in oxygen. During severe hypercapnia the EEG becomes isoelectric. The CSF potassium concentration is raised and the changes in metabolism suggest an acidosis-induced inhibition of phosphofructokinase and, probably, of hexokinase. The energy charge potential remains unchanged whereas the cortical ATP concentration increases slightly. It is assumed that the changes in P-creatine and creatine levels are related to the pH-dependency of creatine phosphokinase. Recovery animals were ventilated with 40% CO2 in O2 and subsequently with room air. After termination of CO2 inhalation the EEG reappears, the CSF potassium concentration normalizes, and the inhibition of the glycolytic enzymes disappears. The energy charge potential shows a small decrease. It is not possible to trace back the disappearance of the EEG to only one of the recorded parameters. Cortical P-creatine levels, CSF potassium concentration, changes in membrane permeability and cortical amino acid concentrations are considered in this context.
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PMID:Influence of severe hypercapnia upon cerebral cortical metabolism, CSF electrolyte concentrations and EEG in the cat. 13 59

The study of electrocardiogram and opercular movement records, from eels exposed for prolonged periods to hypercarbic water (saturation by the gaseous mixture 2% CO2, 98% air) shows that 1) heart rate is not significantly changed; 2) the duration of spontaneous apnea phases and the magnitude of opercular movements during ventilatory phases are increased under hypercapnic conditions. Because the integrated records of opercular movements only give an arbitrary estimate of changes in ventilation rate, direct measurements of the ventilation volume were performed in order to state the way of the dominant action of CO2. This method allows us to conclude that exogenous hypercapnia significantly decreases the ventilatory rate in eels.
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PMID:[Cardiorespiratory effects of exogenous hypercapnia in eels]. 13 81

Arterial blood-gas changes were studied in 21 healthy women undergoing laparoscopic sterilization with local anesthesia and supplemental IV sedation, employing CO2 as the inflating gas. No significant hypercarbia was noted. Two patients became transiently apneic following IV medication and 2 became extremely agitated during the procedure. This constituted a major nonsurgical complication rate of 19 percent. Safety requirements for patients undergoing this procedure is suggested.
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PMID:Laparoscopic sterilization with local anesthesia: complications and blood-gas changes. 14 Dec 28

We examined ventilatory and waking responses to hyperoxic hypercapnia in 3 dogs during natural sleep. Progressive hypercapnia was induced by a rebreathing technique, and sleep was determined by electroencephalographic and behavioral criteria. In non-rapid eye movement sleep (high-voltage, slow-frequency electroencephalography) rebreathing continued for 0.99 +/- 0.05 min (mean +/- SE) before arousal occurred, and the alveolar PCO2, at arousal was 54.2 +/- 3.4 mm Hg. In contrast, during rapid eye movement sleep, rebreathing lasted for 1.71 +/- 0.27 min (P less than 0.05) before arousal occurred and the alveolar PCO2 at arousal was 60.3 +/- 4.2 mm Hg (P less than 0.05). Linear regression analysis of breath-by-breath instantaneous minute volume of ventilation, tidal volume, and respiratory frequency against alveolar PCO2 revealed regression coefficients in rapid eye movements sleep that were 14 to 33 per cent of those found in non-rapid eye movement sleep, and correlation coefficients of 0.26 to 0.46, compared to 0.71 to 0.91 in non-rapid eye movement sleep. Thus, the link between CO2 and ventilation appeared to be strong in non-rapid eye movement sleep but considerably disrupted during rapid eye movement sleep. We conclude that centers involved in both waking and ventilatory responses to hypercapnia behave as if they are less aware of or responsive to CO2 in rapid eye movement sleep than in non-rapid eye movement sleep.
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PMID:Ventilatory and waking responses to CO2 in sleeping dogs. 19 Sep 27

Extracellular recordings were made of 52 respiratory neurons in the brainstem of cats, anesthetized (chloralose-urethane), vagotomized and artificially ventilated. Phrenic nerve activity was recorded and quantified as an index of the output of the respiratory neuronal organization in the brainstem. The unit activity was quantified by using the modal spike frequency as a possible indication of the activating effect of one unit on other respiratory neurons (Smolders and Folgering, 1979). Inspiratory neurons showed the strongest reaction to changes in PA,CO2 and/or PA,O2. Expiratory neurons and frequency modulated neurons responded less to changes in chemical drive. Phase spanning neurons did not show any consistent response. Four out of ten continuously firing neurons without any respiratory rhytmicity increased their firing frequency when PA,CO2 was increased. Apart from the increase in modal spike frequency, the respiratory neuronal organization also reacted with an increase in active units (recruitment) when the chemical drive was increased. The relationship between quantified phrenic nerve activity and spike frequency was independent of the stimulus (hypercapnia or hypoxia). A model was developed in which the increase in modal frequency of a unit arouses other units: when the chemical drive increases, progressively more units tend to be recruited into the respiratory neuronal organization in the brainstem.
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PMID:The steady state response of brainstem respiratory neuron activity to various levels of PA,CO2 and PA,O2. 23 Apr 56

Ventilatory responses to CO2 and to lung inflation were compared in four dogs during tonic and phasic segments of rapid-eye-movement (REM) sleep. Phasic REM sleep (P-REM) was identified by the presence of bursts of rapid eye movements, visible muscle twitchings, and frequent phasic discharges in the nuchal electromyogram. These features were absent during tonic REM sleep (T-REM). During P-REM the response of minute volume of ventilation (VI) to progressive hypercapnia (0.58 +/- 0.19 (l/min)/Torr, mean +/- SE) was significantly less than in slow-wave sleep (SWS) (1.40 +/- 0.14; P less than 0.05). In contrast, during T-REM the response (1.48 +/- 0.19) was similar to that in SWS. Similarly, during P-REM the duration of apnea (5.9 +/- 1.5 s) elicited by sustained inflation of the lungs with 1.0 liter of air, was significantly shorter than in SWS (25.8 +/- 0.8); in contrast, during T-REM the duration of apnea (17.8 +/- 3.6) was similar to that in SWS. The results indicate that previously described decreases in VI responses to CO2 and apneic responses to lung inflation during P-REM, compared to SWS, are related to the phasic phenomena of REM sleep, rather than to the REM sleep state per se.
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PMID:Ventilatory responses to CO2 and lung inflation in tonic versus phasic REM sleep. 23 2

Tissue (gas pocket) oxygen levels and erythropoietic activity were monitored in groups of rats chronically exposed to hypoxia (70 Torr PIO2), hypercapnia (60 Torr PICO2), or a combination of the two conditions. Arterial gas tensions and pH were also measured. Overall condition of the animals was assessed by comparison of growth rates with pair-fed controls. Hypoxic-hypercapnic pocket PO2 values (24-40 Torr) were similar to normoxic-normocapnic values (28-37 Torr), but greater than in hypoxia-normocapnia, and less than in normoxia-hypercapnia. Erythropoietic activity during hypoxia-hypercapnia ceased and the rats had a growth rate significantly below that of other groups. While chronic CO2 does increase tissue (pocket) oxygenation to near normal levels, probably due to increased ventilation and subsequently PaO2, the hypoxic-hypercapnic rats evidenced greater detrimental effects than did rats in hypoxic or hypercapnic environments.
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PMID:Tissue oxygenation and splenic erythropoiesis during chronic hypoxia and hypercapnia. 23 6

Guinea pigs and rats exposed to 15% CO2 for 7 days showed a parallel time course of changes in pH, body temperature (TB), and oxygen consumption (VO2). Between 1 and 6 h of exposure the maximal drop in actual pH occurred in guinea pigs simultaneously with the maximal fall in TB and VO2. During the subsequent period pH TB, VO2 rose again. Skin blood content (heat loss) also exhibited a biphasic pH-dependent time course. Animals showing no partial compensation of respiratory acidosis during 3 days exposure also failed in raising their TB back to normal in this time. The behavior of TB was found to be a good indicator of the acid-base status and adaptive potential of the animals to hypercapnia. Similar results were obtained in rats. Thermo-regulatory processes in the hypothalamus were affected during exposure to 15% CO2. Both guinea pigs and rats showed a decrease in norepinephrine content of the hypothalamus during the first part of exposure reaching a maximal fall at the end of 24 h. The serotonin content increased slightly during this period. During prolonged exposure to 3% CO2 for 7 days, TB showed a transient rise, and VO2 was slightly elevated.
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PMID:Effect of chronic hypercapnia on body temperature regulation. 23 76

Increased CO2 flow to the lung produced by increasing cardiac output (with constant PVCO2) results in hyperpnea with arterial PCO2 maintained at its control value (J. Appl. Physiol. 36: 457, 1974). To study if arterial PCO2 could be similarly regulated when CO2 flow was elevated by increasing PVCO2 (without changing cardiac output), we produced graded increases in PVCO2 (up to a mean of 69 mmHg) using an extracorporeal gas exchanger in five chloralose-urethan-anesthetized dogs. CO2 output increased up to fourfold. Ventilation increased in proportion to the additional CO2 flow to the lung with consequent regulation of arterial PCO2 at its control value. Comparable increases in VE produced by "conventional" airway loading resulted in arterial hypercapnia. The resulting CO2 response curve was similar to that found in unanesthetized dogs. We conclude that intravenous delivery of CO2 to the lung results in infinite "sensitivity" when computed as Delta VE/Delta paco2. These results provide evidence for a CO2-linked hyperpnea which is not mediated by measurable increases in mean arterial PCO2.
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PMID:Regulation of arterial PCO2 during intravenous CO2 loading. 23 64

1. The acid-base state of arterial blood and cerebrospinal fluid, and the ventilatory response to CO2, were measured in twelve patients with liver disease. The CO2 response was also measured in eight goats before and after the experimental production of liver failure. Arterial PCO2 and pH, cerebral blood flow and the cerebral metabolic rate for oxygen were also measured in four of the goats while they breathed air and various CO2-enriched gas mixtures. 2. Liver failure was accompanied by a respiratory alkalosis in both the patients and in the goats. Decreased PCO2 and increased pH occurred in the cerebrospinal fluid and in the arterial blood of the patients. 3. The slope of the ventilatory response to CO2 was reduced when liver failure was severe, in patients and goats alike. In addition there was a reduction in the extrapolated PCO2 at zero ventilation, even when liver failure was mild. 4. Cerebral blood flow and metabolic rate were consistently reduced in the goats during liver failure. There was also less cerebral vasodilatation and a greater reduction in cerebral metabolism during experimental hypercapnia when these animals were in liver failure. 5. The decreases in the ventilatory and cerebral circulatory responsiveness to CO2 indicate that the brain is less well defended against hypercapnia in liver failure, and these changes are especially unfavourable as cerebral function deteriorates when the PCO2 is increased.
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PMID:Effect of liver failure on the response of ventilation and cerebral criculation to carbon dioxide in man and in the goat. 23 83


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