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

Some renal parameters have been studied in newborns with respiratory distress syndrome (RDS). During the first 24 h, the serum creatinine level of the severe cases of RDS are significantly increased, decreasing gradually with improvement of the RDS and reaching normal values within 10 days. Blood urea nitrogen remained unchanged. In the milder cases of RDS, the serum creatinine also showed a slighter increase, which became normal within 4 days after birth. During the acute phase of RDS, there is a reversible impairment in the renal function, which correlates with the degree of hypoxia, hypercapnia and acidosis determined by the primary disease.
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PMID:Alterations in creatinine clearance during respiratory distress syndrome. 3 62

8 term fetal pigs (110-112 days gestation) and one 97-day fetus were asphyxiated in utero by occlusion of the umbilical cord. Mean times to last gasp and last heart beat were 5.1 and 22.4 for term and 5.4 and 30.4 min for the 97-day fetus. Cord occlusion was followed by profound bradycardia and an increase in blood pressure which was maintained until gasping ceased. Profound acidemia, hypercapnia and hyperlactacidemia developed in all animals and values following asphyxiation were comparable with those seen in stillborn piglets. Liver and cardiac glycogen levels were lower in asphyxiated fetuses than in littermates but muscle glycogen levels were similar in both groups.
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PMID:Studies on the effect of acute asphyxia on the fetal pig in utero. 3 63

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

In 660 supine, intubated and anaesthetized, healthy patients scheduled for various elective surgical procedures, the distribution of arterial carbon dioxide tension (PaCO2) was investigated during manual non-monitored ventilation. The study comprised six equal groups: group 1: ventilation with a circle circuit absorber system; group 2: ventilation with the Hafnia A circuit using a total fresh gas flow (FGF) of 100 ml . kg-1 . min-1; groups 3-6: ventilation with a Hafnia D circuit with fresh gas flows of 100, 80, 70 and 60 ml . kg-1 . min-1, respectively. The mean PaCO2's of the first three groups were situated in the lower range of normocapnia (the observations in the first group having the greatest total range), whereas the rebreathing (Hafnia A and D) circuits resulted in a clustering of observed data. Employing the rebreathing circuits, protection against hypocapnia can be achieved by lowering the fresh gas flow. The most satisfying result was obtained with the Hafnia D circuit with a fresh gas flow of 70 ml . kg-1 . min-1 resulting in normocapnia with a modest and limited spread towards hypo- and hypercapnia. FGF in excess of this level must be considered as wasted. The study indicates that corrections of fresh gas flows for age are superfluous. Use of relaxants and type of surgery had no influence on the observations.
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PMID:Arterial carbon dioxide tensions during anaesthesia with manual ventilation. A descriptive study of the effects of various non-polluting circuits. 3 15

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

The myocardial cell pH (pHi) observed during breathing of 0, 7.5, or 10% CO2 in air for 3 h was studied in rats with myocardial hypertrophy due to aortic stenosis and in sham-operated rats. The change in pHi during hypercapnia was significantly smaller in the rats with myocardial hypertrophy, with the apparent nonbicarbonate buffer value (delta [HCO3-]i/delta pHi) being almost three times that of the sham-operated rats. In vitro CO2 equilibrium of myocardial tissue homogenates showed no difference in nonbicarbonate buffer value between homogenates obtained from normal rats and from rats with myocardial hypertrophy. Therefore, it appears that the increased ability of the myocardial cell to regulate its pH during hypertrophy is not due to an increase in the cellular level of nonbicarbonate buffers, but seems to be related to a larger bicarbonate uptake by the myocardial cell during hypercapnia.
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PMID:Intracellular pH regulation of normal and hypertrophic rat myocardium. 4 27


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