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

Experiments were conducted on cats under nembutal anesthesia; a study was made of pulse activity of bulbar respiratory neurons, electrical activity of the diaphragm and of the intercostal muscles; pO2, pCO2, pH, arterial blood oxygen saturation were determined in combined action of hypoxia and hypercapnia. When hypoxic gaseous mixture was given for respiration the developing hypocapnia disturbed the discharge rhythmic activity of the respiratory neurons, the respiration acquiring a pathological character of the Cheyne--Stokes type. After addition to the hypoxic gaseous mixture of 2% CO2 the gaseous composition of the arterial blood approached the initial values; this addition prevented the development of hypercapnia and disturbances of rhythmic discharge activity of the respiratory neurons. Addition of 5% CO2 to the hypoxic gaseous mixture produced a negative effect: at first it intensified and then depressed the pulse activity of the respiratory neurons, caused metabolic and respiratory acidosis, and promoted asphyxia.
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PMID:[Combined effects of hypoxia and hypercapnia on the functional state of the respiratory center]. 0 Jan 3

The effect of oxygen saturation and PCO2 on brain uptake of glucose analogues was studied in rabbits. Using a modified Oldendorf technique, 14C-labeled glucose analogues with a 3H2O reference standard were introduced into the cerebral circulation via the common carotid artery, and the radioactivity of the ipsilateral cerebral cortex was counted and expressed in terms of a brain uptake index (BUI). Severe hypoxia (oxygen saturation less than or equal to 18%) resulted in approximately a 40% decrease in the BUI of 2-deoxy-D-glucose and a 45% decrease in the BUI of 3-0-methyl-D-glucose. Severe hypercapnia (PCO2 = 100 mm Hg) caused a 45% decrease in the BUI of both of these glucose analogues. Hypercapnia superimposed on severe hypoxia had no additional effect. Hypocapnia (PCO2 = 15 mm Hg) increased the BUI of 3-0-methyl-D-glucose by 35% of the control value, and this increase was extremely sensitive to competitive inhibition. When BUI values were plotted against pH rather than PCO2 for the same experiments, there was a good correlation with the calculated linear regression. These results are compared with previous findings on pathologically induced changes in brain uptake of glucose analogues, and the possible role of blood flow is considered in detail.
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PMID:Effects of oxygen saturation and pCO2 on brain uptake of glucose analogues in rabbits. 0 Aug 21

The combined effect upon cerebral blood flow (CBF) of an elevation of cerebrospinal fluid pressure (CSFP) and changes in respiratory CO2 was studied in nine baboons under chloralose anesthesia. The animals were mildly hyperventilated and provided with increasing amounts of CO2 in O2-air. Arterial CO2 tensions (PaCO2) increased from 17 to 58 mm Hg. Internal carotid blood flow (ICBF) was measured at normal CSFP and at hydrostatically maintained 50 mm Hg CSFP. It was found that: 1) end-tidal CO2 may be used as a substitute for arterial PaCO2 determinations; 2) this elevation of CSFP has little effect on ICBF during hypercapnia and normocapnia; however, 3) during hypocapnia the ICBF is reduced an additional 20% when CSFP is elevated; that is, ICBF is reduced 50% from normal when end-tidal CO2 is reduced to 2% at this elevated level of CSFP. Caution should be exercised during hyperventilation therapy particularly if the elevated CSFP or intracranial pressure (ICP) is not reduced to approach normal levels; in these conditions, the combination of decreasing PaCO2 and elevated ICP may reduce CBF below critical levels and thus lead to cerebral hypoxia.
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PMID:Effects of hyperventilation, CO2, and CSF pressure on internal carotid blood flow in the baboon. 0 53

The physiology of respiratory control of acid-base balance is reviewed. The pathophysiological mechanisms during hypercapnia and hypocapnia are discussed in the light of the causes and clinical manifestations of these disturbances. In addition to the role of the kidney in the compensatory processes of these disturbances, renal functional changes during acute and chronic pulmonary acid-base derangement is discussed. Some of the difficulties encountered in the patient with chronic renal disease in whom respiratory abnormalities may be present are also discussed.
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PMID:Respiratory acidosis and alkalosis. 1 97

1. The regulation of cerebrospinal fluid (c.s.f.) bicarbonate concentration was studied using the cat choroid plexus isolated in a chamber in situ. 2. Decreases in plasma bicarbonate concentration caused relatively small changes in the c.s.f. bicarbonate concentration. 3. Alterations in c.s.f. bicarbonate concentration (c.s.f. HCO3-=9 or 28 m-equiv/l.) were countered by changes in the bicarbonate concentration of the fluid produced by the plexus or in the rate of bicarbonate transport which returned c.s.f. bicarbonate towards normal. 4. There was significant regulation of pH in the choroid plexus fluid during hypocapnia and hypercapnia. 5. Alterations of plasma acid-base status did not significantly alter the potential difference across the choroid plexus. However, the potential difference increased when c.s.f. bicarbonate was increased and decreased when c.s.f. bicarbonate was decreased. 6. The data indicate that the bicarbonate concentration in the c.s.f. is actively regulated by the choroid plexus during acid-base disturbances occurring either systemically or in the c.s.f.
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PMID:Regulation of cerebrospinal fluid bicarbonate by the cat choroid plexus. 1 33

The acid-base values of 13 patients with stable carbon dioxide tensions under controlled ventilation have been used to define the response to chronic hypocapnia in man. These patients had a respiratory paralysis and no apparent complicating disorders. Over a range of carbon dioxide tensions from 24 to 40 millimetres of mercury, the arterial blood hydrogen ion concentration decreased linearly by 0.32 nanomole per litre per millimetre of mercury decrement in carbon dioxide tension. Of primary interest was the finding that the slope of the regression line in chronic hypocapnia is close to that already reported for chronic hypercapnia. The physiological response to chronic hypocapnia in man is defined by a band that is approximately 10 nanomoles per litre (0.09 pH unit) wide for hydrogen ion concentration and 6 millimoles per litre wide for bicarbonate concentration. These significance bands may be used to differentiate additional acid-base disorders in patients with chronic hypocapnia over a clinically useful range of carbon dioxide tensions.
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PMID:Acid-base response to chronic hypocapnia in man. 2 Jan 87

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

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

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

Responses of aortic chemoreceptor afferents to a range of arterial carbon dioxide tension (Paco2) changes at various levels of arterial oxygen tension (Pao2) were investigated in 18 cats anesthetized with alpha-chloralose and maintained at 38 degrees C. Aortic chemoreceptor activity, end-tidal oxygen pressure, end-tidal carbon dioxide pressure, and arterial blood pressure were continuously monitored. Arterial blood gases were measured in steady states. Single or a few clearly identifiable afferents were studied during changes and steady states of Pao2 and Paco2. All the aortic chemoreceptor afferent discharge rates increased with Paco2 increases from hypercapnia (10-15 Torr) to normocapnia and moderate hypercapnia (30-50 Torr) and with Pao2 decreases from above 400 to 30 Torr. Hypoxia augmented the response to Paco2 most effectively in the range of 10-40 Torr. At any Pao2, the discharge rate reached a plateau with sufficient intensity of hypercapnia. The Paco2 stimulus threshold at a Pao2 of 440 Torr was about 15 Torr, and at a Pao2 of 60 Torr it was 10 Torr. In the transition from hypocapnia to hypercapnia, responses increased gradually, usually without an overshoot. The steady-state responses to Paco2 of the majority of aortic chemoreceptors resembled those of carotid chemoreceptors. The responses of both receptors can be attributed to the same basic type of mechanism.
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PMID:Aortic body chemoreceptor responses to changes in PCO2 and PO2 in the cat. 4 29


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