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

In order to test the relationship between changes in plasma potassium concentration and pH changes of respiratory origin, we produced hypercapnia (mean PaCO2 71 mmHg = 9.5 kPa) in a group of 17 patients and hypocapnia (mean PaCO2 21 mmHg = 2.8 kPa) in another 20 patients during neurolept analgesia and intraabdominal operations. A control group of 19 patients was studied under normocapnia but otherwise identical conditions. During hypercapnia, serum potassium rose, deltaK/deltapH amounting to -0.82, -1.05 and -1.34 after 30, 60 and 90 min, respectively. During hypocapnia, serum potassium decreased, deltaK/deltapH being a little more negative than during hypercapnia (mean values -1.62, -2.44 and -1.60). Red cell potassium concentration decreased in all three groups to a similar extent. Blood lactate levels during hypercapnia decreased to 75% of control and during hypocapnia rose to a maximum of 186% of control. In order to obtain reasonable values for base excess in primarily respiratory acid-base disorders, it is necessary to use nomograms based on in vivo ECF-CO2-titration curves. With this premise, hypercapnia or hypocapnia in our patients was not associated with significant changes in base excess.
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PMID:Effects of acute hypercapnia and hypocapnia on plasma and red cell potassium, blood lactate and base excess in man during anesthesia. 3 56

Continuous tissue pH and intermittent central arterial pH were measured in six rabbits during 10-min exposures to a mixture of 10% CO2 and 90% O2. In control and recovery situations tissue pH was more acidic than arterial pH by a mean value of 0.07 pH units. During periods of rapidly increasing pCO2, the steady state relationship was inverted with tissue pH being more alkaline than arterial pH. After a second exposure to CO2, mean tissue pH values did not recover to baseline. It is concluded that in the rabbit during acute hypercarbia, the relationship of tissue to central pH is variable. The possible implications of these results in human fetuses during labor are discussed.
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PMID:The relationship between tissue and arterial pH in hypercarbic rabbits. 3 19

In 29 cats, the extent and time-course of the pial arterial reactions to hypo- and hypercapnia were studied by means of the skull-window technique. The typical, well-known dilatations and constrictions during hyper- and hypocapnia were seen. The latent period for dilatation after the beginning of CO2-inhalation was ca. 20 sec. There was no stable relation observable between vessel diameter and arterial carbon dioxide tension (paCO2). Diameter changes lagged behind CO2-changes, indicating that CO2 acts via metabolic regulation, probably extracellular pH.
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PMID:Pial arterial reactions to hyper- and hypocapnia: a dynamic experimental study in cats. 3 9

The cerebral blood flow (CBF) and cerebral oxygen consumption (CMRO2) in the rat during normocapnia and hypercapnia were investigated by means of the intraarterial 133Xenon injection technique; measurements were performed during normocapnia and hypercapnia and the effect of propranolol upon CBF and CMRO2 was studied. The CBF technique applied to rat yield reliable results even in high flow situations. A steady state period of only 10--15 s is all that is necessary to obtain the initial slope of the 133Xenon clearance curve from which CBF is calculated and measurements may be repeated within minutes. Hypercapnia caused an increase in CMRO2 of 35% which confirms the findings of other investigators. The beta-adrenergic receptor blocker propranolol (2 mg per kg i.v.) prevented this increase and could eliminate an increase in CMRO2 already induced; this indicates that CO2 affects adrenergic mechanisms. Although propranolol eliminated the CMRO2 response to hypercapnia, it only reduced the CBF response; this dissociation of CBF and CMRO2 response occurred probably because the beta-receptor blockage only eliminated a CBF increase mediated through an increased CMRO2 (cellular response) whereas a direct CO2 effect upon the arterioles (vascular response) persisted.
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PMID:The effect of propranolol on cerebral oxygen consumption and blood flow in the rat: measurements during normocapnia and hypercapnia. 3 22

During various time periods lasting 3--28 days rats were continuously exposed to FICO2 = 0.08 or 0.16 in normoxic conditions, pHi was measured by the 3H-inulin and 14C-DMO method in the erythrocyte, the gastrocnemius and in the whole body. The erythrocyte acid base disturbances were linked to the extracellular acidosis. The muscle and the mean body pHi developments were the same during 9 or 14 days depending on the FICO2. They diverged after 28 days at FICO2 = 0.08 (Tables and Fig. 2). This could be explained as an acid base reaction of the "non-muscular" part of the whole body intracellular compartment which may be different from the acid base development of the muscular mass. A short term (1 h) acute hypercapnia (FICO2 - 0.20--0.22) was superimposed on the sustained hypercapnia (FICO2 = 0.16). Acid base disturbance was greater when the acute hypercapnia was added at the beginning (3rd day) of the CO2 exposure (Fig.1).
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PMID:Intracellular pH changes during experimental sustained hypercapnia. 3 89

It is a clinical impression that less fentanyl is needed for anesthesia during hyperventilation and hypocarbia. If true, it might be due to both increased penetration of fentanyl, a highly lipid-soluble agent, into the brain and increased brain tissue binding. Serum and brain concentrations of fentanyl were determined in dogs anesthetized with halothane during normocarbia, hypocarbia by hyperventilation, and hypercarbia by addition of CO2 to the inspired mixture. Fentanyl, 12.5 micrograms/kg, was injected iv, and serum and brain samples were taken for fentanyl analysis by radioimmunoassay. Brain fentanyl values peaked latest (15--20 min) and were highest during hypocarbia; brain fentanyl values peaked earliest (0--5 min) and were lowest during hypercarbia; values during normocarbia were intermediate in time to peak (10--15 min) and concentration. Thereafter, brain levels declined, but during hypocarbia were significantly higher and during hypercarbia were significantly lower than during normocarbia. Interestingly, serum fentanyl levels were also significantly higher during hypocarbia. The brain--blood fentanyl ratios for each of the three CO2 levels increased for 30 min and thereafter stayed relatively constant. The brain--blood ratios were highest with hypocarbia and lowest with hypercarbia. At 35 min, when clinical analgesia may be considered terminated, hypocarbic brain levels were double those of normocarbia. The authors feel this reflects, to a large extent, higher serum fentanyl concentrations and delayed cerebral wash-out because of decreased blood flow. To a small but unknown extent the higher brain fentanyl levels result from increased brain--blood penetration due to increased lipid solubility, and increased brain tissue binding of fentanyl during respiratory alkalosis.
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PMID:Fentanyl concentrations in brain and serum during respiratory acid--base changes in the dog. 3 75

The carotid bodies appear to be the only peripheral chemoreceptors mediating ventilatory control during exercise in man. While little is known about the mechanism of stimulation, much is known about the effects of carotid body stimulation upon pulmonary ventilation (VE). These effects have been produced by hypercapnia, hypoxia, metabolic acidosis, arterial blood pressure, temperature, and catecholamines. A signal from CO2 flow is attractive because of the strong correlation between CO2 output and VE during exercise. The carotid body's role in the hyperpnea depends on the intensity of exercise. During heavy exercise, pH falls and hyperventilation ensues. The carotid bodies appear to be the exclusive mediators of the ventilatory compensation for the acidosis at this exercise intensity. For moderate exercise, mean arterial PCO2 does not change. Therefore, how is the CO2 signal transmitted to the respiratory center? Two current theories are: (1) since arterial PCO2 and pH oscillate with each breath, the amplitude and period of these oscillations may change during exercise and may be of sufficient magnitude to stimulate the carotid bodies, and (2) there exists a disequilibrium between hydrogen ion activity within the red blood cell and in the plasma because carbonic anhydrase is found in the former but not the latter. This theory assumes that the enzyme is not accessible to the plasma.
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PMID:Peripheral chemoreceptors and exercise hyperpnea. 4 92

The metabolic effects of 60-min exposure to 250-2000 mg gamma-hydroxybutyrate (GHB) per kilogram or 150-1200 mg gamma-butyrolactone (GBL) per kilogram were studied in rats by measurement of the cerebral hemisphere contents of energy phosphates and glycolytic-Krebs' cycle metabolites. A general pattern of increased glycogen and glucose with decreased pyruvate, lactate, alpha-ketoglutarate, and malate was observed. This pattern in association with unchanged adenylates and decreased energy phosphate utilization was consistent with a metabolic adaptation to a state of cerebral depression. The major qualitative difference between the two drugs was that higher doses of GBL were associated with additional decreases of citrate and glutamate. Since these doses of GBL were also associated with acute increases of arterial CO2 tension, it is proposed that these differences were secondary to hypercapnia and not due to a distinctive primary action of GBL. Derivation of the cytoplasmic NAD(P)H:NAD(P)+ ratios indicated that GHB and GBL were not associated with consistent alterations of the cytoplasmic redox state.
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PMID:A comparison of the effects of gamma-hydroxybutyrate and gamma-butyrolactone on cerebral carbohydrate metabolism. 4 Jun 77

Progressive hypercapnia in the normal chick embryo late in incubation (14-19 days) is temporally associated with a gradual decline in motor activity and the corresponding frequency of polyneuronal (burst) activity in the spinal cord. We have studied the possible correlation between the increasing hypercapnia and the declining frequency of burst activity seen during these later stages of incubation by systematic manipulation of CO2 levels. Burst frequency was seen to decrease as a result of a 5-min exposure to different carbon dioxide environments at all ages studied. The magnitude of this inhibition and the ability to recover from consecutive bouts of hypercapnia (pulses) is pulse and age dependent. These short-term (less than 5.0 min) changes differ qualitatively from the long-term (greater than 2.5 h) effects of subsequent hypercapnic episodes. This evidence suggests a role for metabolic factors in the normal developmental changes in motility and electrophysiological activity in the chicken embryo spinal cord.
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PMID:A neurophysiological analysis of the effects of hypercapnia on the embryonic spinal cord. 4 Jul 85

Cerebral blood flow (CBF) and oxygen consumption (CMRO2) were measured during acute and long-term ethanol intoxication in the rat. The purpose was to investigate whether the adaptive changes (development of tolerance) occurring in the CNS during ethanol intoxication were associated with changes in CBF and/or CMRO2. Consistent with other studies we found that acute severe ethanol intoxication (median blood alcohol concentration (BAC = 5.4 mg/ml)) caused a significant decrease in CBF and CMRO2. After 3-4 days of severe intoxication (BAC of 6.6 mg/ml) these physiological variables were less affected indicating that functional tolerance had developed: CMRO2 and CBF during acute ethanol intoxication were 9.3 ml/100 g/min and 60 ml/100 g/min respectively; after the long term intoxication period these variables reached 11.2 ml/100 g/min and 78 ml/100 g/min respectively, i.e. values not significantly lower than those of the control group. After induction of hypercapnia (PaCO2 about 80 mmHg) CBF increased by 360% in the control group; in the acutely intoxicated group CBF increased by only 127% and in the long term intoxicated group by 203% indicating that the cerebrovascular CO2-reactivity had also adapted to the ethanol intoxication. It is concluded that adaptive changes of the CNS to chronic ethanol intoxication comprise alterations in CMRO2, CBF and cerebrovascular reactivity.
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PMID:Adaptive changes in cerebral blood flow and oxygen consumption during ethanol intoxication in the rat.. 4 9


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