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

Continuous monitoring of the cerebral blood flow, oxyhemoglobin, deoxyhemoglobin, total hemoglobin, oxidized cytochrome a, a3, and tissue pH during prolonged CO2 or N2 loading in 2-week-old rabbits was performed by near-infrared spectroscopy, the thermocouple method, and a tissue pH meter. Near-infrared spectroscopy demonstrated decreases in oxyhemoglobin and oxidized cytochrome a, a3 and increases in deoxyhemoglobin and total hemoglobin in the early stage within 5 min, which gradually lessened with time on both 10% concentration of inspired O2 with CO2 and N2. CBF increased with venous retention in the early stage and then slowly decreased in parallel with blood pressure and oxidized cytochrome a, a3 on abolition of autoregulation. These changes were more remarkable during the 10% concentration of inspired O2 with CO2 than N2 which may be caused by marked acidosis and hypotension associated with hypercarbia. Oxidized cytochrome a, a3, however, demonstrated a gradual decrease in 10% concentration of inspired O2 with N2 rather than CO2; therefore, the continuous monitorings demonstrated hemodynamic and oxygenation changes despite the same extent of prolonged hypoxic loading. These changes in prolonged hypoxic conditions may occur in human intrapartum asphyxia which develops into postnatal hypoxic-ischemic encephalopathy.
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PMID:Monitoring of immature rabbit brain during hypoxia with near-infrared spectroscopy. 155 75

Trout were exposed to hypercapnia, two levels of aerobic exercise, or three successive periods of supramaximal exercise to evaluate the effects on erythrocyte and plasma K+. During aerobic exercise, plasma K+ increased slightly with the intensity of work, while no change was found in the erythrocyte K+ content. In contrast, both hypercapnia and supramaximal exercise induced a net erythrocyte K+ uptake. This uptake changed to a net loss of K+ as arterial pH and hemoglobin-bound oxygen saturation returned to control values during recovery. The maximal rates of net K+ uptake found during hypercapnia and supramaximal exercise corresponded to 195 and 350 mumol.kg fish-1.h-1, respectively, and the maximal rates of net K+ loss found during recovery corresponded in both cases to approximately 130 mumol.kg fish-1.h-1. Hypercapnia had only a minor effect on plasma K+, but return to normocapnic conditions induced a 0.8 mM rise in plasma K+. Of this increase, approximately 70% could be accounted for by the simultaneous net release of erythrocyte K+. Each period of supramaximal exercise induced an elevated plasma K+ level, resulting in accumulation of plasma K+ despite slight decreases in plasma K+ in between the exercise periods. At the same time the net erythrocyte K+ uptake caused an estimated reduction in plasma K+ of 1.5 mM. It is concluded that both hypercapnia and supramaximal exercise cause profound net changes in the erythrocyte K+ content with significant effects on plasma K+.
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PMID:Changes in plasma and erythrocyte K+ during hypercapnia and different grades of exercise in trout. 159 16

Neuronal activity causes local changes in cerebral blood flow, blood volume, and blood oxygenation. Magnetic resonance imaging (MRI) techniques sensitive to changes in cerebral blood flow and blood oxygenation were developed by high-speed echo planar imaging. These techniques were used to obtain completely noninvasive tomographic maps of human brain activity, by using visual and motor stimulus paradigms. Changes in blood oxygenation were detected by using a gradient echo (GE) imaging sequence sensitive to the paramagnetic state of deoxygenated hemoglobin. Blood flow changes were evaluated by a spin-echo inversion recovery (IR), tissue relaxation parameter T1-sensitive pulse sequence. A series of images were acquired continuously with the same imaging pulse sequence (either GE or IR) during task activation. Cine display of subtraction images (activated minus baseline) directly demonstrates activity-induced changes in brain MR signal observed at a temporal resolution of seconds. During 8-Hz patterned-flash photic stimulation, a significant increase in signal intensity (paired t test; P less than 0.001) of 1.8% +/- 0.8% (GE) and 1.8% +/- 0.9% (IR) was observed in the primary visual cortex (V1) of seven normal volunteers. The mean rise-time constant of the signal change was 4.4 +/- 2.2 s for the GE images and 8.9 +/- 2.8 s for the IR images. The stimulation frequency dependence of visual activation agrees with previous positron emission tomography observations, with the largest MR signal response occurring at 8 Hz. Similar signal changes were observed within the human primary motor cortex (M1) during a hand squeezing task and in animal models of increased blood flow by hypercapnia. By using intrinsic blood-tissue contrast, functional MRI opens a spatial-temporal window onto individual brain physiology.
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PMID:Dynamic magnetic resonance imaging of human brain activity during primary sensory stimulation. 160 78

According to conventional wisdom the difference between alveolar and arterial O2 tensions, the AaPO2, should distinguish between hypoxemia caused by alveolar hypoventilation and hypoxemia caused by alveolar hypoventilation complicated by other abnormalities of gas exchange. To test this concept we have calculated the AaPO2 from arterial blood gas measurements, breathing air, in 23 patients with hypercapnia, hypoxemia, and advanced obstructive lung disease (mean FEV1 = 0.88 L). We found that AaPO2 varied inversely with PaCO2 (r = -0.83, p less than 0.001). In five of these patients with the most severely elevated PaCO2 (range, 59 to 81 mm Hg) the AaPO2 was within normal limits. We also calculated the difference between the O2 contents of "ideal" pulmonary capillary blood and arterial blood and expressed this as the venous admixture (QVA/QT) based on an assumed arteriovenous content difference of 4.5 ml/dl. In contrast to the AaPO2, the QVA/QT, was abnormal in all patients (mean = 41 +/- 8%). We conclude that the AaPO2 may be an unreliable indicator of abnormal gas exchange in the presence of alveolar hypoventilation. This finding can be explained by substantial changes in the position of the alveolar and arterial points on the oxygen dissociation curve for hemoglobin in the presence of alveolar hypoxia secondary to hypoventilation.
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PMID:Interpretation of the alveolar-arterial oxygen difference in patients with hypercapnia. 189 45

In order to study the effect of the decrease in P-Pi caused by low pH on hemoglobin-oxygen affinity, we measured P-Pi,2,3-diphosphoglycerate (2,3-DPG), and oxygen tension at 50% saturation (P50) in 36 cases with acute exacerbation of chronic respiratory failure with hypercapnia. The cases were classified into two groups by arterial blood pH values obtained on the day of admission. Group A: pH less than or equal to 7.35 and Group B: pH greater than or equal to 7.36. P50 was calculated by a modification of Severinghaus' equation developed by Yusa and Kohsaka, and it was corrected by applying the carboxy-hemoglobin (COHb) coefficient. On the day of admission (stage I), 2,3-DPG and P50 in both groups were slightly higher than in the control group. In Group A, a week after admission (stage II), these values decreased and became significantly lower than they had been at stage I. Especially 2,3-DPG in stage II was even lower than those of the control group. Approximately 14 days after admission, in stage III, it was found that these values had risen to the initial level at stage I. In Group A, similar changes were also observed for P-Pi. The value of P-Pi was low in stage II and recovered to the initial value in stage III. On the other hand, we found that the urinary excretion of phosphorus (U-Pi) increased at stage I in Group A. It was supposed that the increase in U-Pi at stage I caused a decrease in P-Pi, which caused the decrease in 2,3-DPG, in stage II.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemoglobin-oxygen affinity in acute exacerbation of chronic respiratory failure]. 207

Endothelial modulation of norepinephrine (NE)-induced constriction of the isolated rat aorta was studied at normal (PCO2, 41 +/- 0 mmHg) and high CO2 tensions (PCO2, 91 +/- 1 mmHg). In preparations with intact endothelium, increased CO2 tension resulted in rightward shift of the NE dose-response curve with attenuation of maximal contraction. This effect of CO2 was not modified by indomethacin. Treatment with hemoglobin or rubbing of the endothelium meant that increased CO2 tension still resulted in rightward shift of the NE dose-response curve but without altering the maximal contractile response. The basal guanosine 3',5'-cyclic monophosphate (cGMP) levels in control and NE-treated aortic preparations were not affected by increasing the CO2 tension. Thus the inhibitory action of CO2 on NE-induced contraction in the presence of endothelium may not be derived from facilitation of endothelium-derived relaxation factor (EDRF)-induced cGMP synthesis. Increasing the CO2 tension attenuated the sustained contraction induced by the addition of NE and Ca2+ (2.5 mM) to intact endothelium preparations previously bathed in Ca2(+)-free solution. Further addition of Ca2+ (total 5.0 mM) did not increase the contraction. These findings suggest that the intrinsic activity of NE is greatly modified by endothelium at a high CO2 tension. Vasodilation during hypercapnia may be induced at least in part by synergistic actions of EDRF and CO2 on smooth muscle cells.
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PMID:Endothelial modulation of norepinephrine-induced constriction of rat aorta at normal and high CO2 tensions. 210 38

Cerebral blood oxyhemoglobin (HbO2), deoxyhemoglobin (HbR) and total hemoglobin (Hb) were examined in N2 and CO2 induced hypoxemia by near-infrared spectroscopy and compared with CBF examined by the H2 clearance method. HbO2 and HbR changed more sensitively than total Hb, reflecting the blood volume. Low CO2-loading showed marked increase in CBF with little change of blood volume, and higher CO2-induced hypoxemia was less increased and followed by a crossed after-reaction, probably because of persistent arterial dilatation due to the marked hypercarbia and acidosis. Neck venous compression showed a specific pattern of increased total Hb and HbR with little change in CBF. Thus, for near-infrared spectroscopy the intracranial blood volume may be affected mainly by arterial dilatation with an increase in CBF and venous dilatation with congestion. And Hb fractions of HbO2 and HbR may be influenced by cerebral blood oxygenation as well as the arteriovenous blood volume.
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PMID:Response on near-infrared spectroscopy and of cerebral blood flow to hypoxemia induced by N2 and CO2 in young rabbits. 212 62

Infants with myelomeningocele have abnormalities in ventilatory control. To determine whether these persist into later life, we studied 14 patients with myelomeningocele and Arnold-Chiari malformation (age 18.0 +/- 0.8 (SE) years), and compared them with 14 control subjects (age 24.0 +/- 0.9 years). Pulmonary function and ventilatory muscle strength did not differ between patients with myelomeningocele and control subjects. Hypercapnic ventilatory responses were significantly lower in the group with myelomeningocele (1.98 L/min/mm Hg) compared with control values (3.33 L/min/mm Hg; p less than 0.01). Hypoxic ventilatory responses (-1.4 L/min/%oxygen saturation of hemoglobin in arterial blood) were not significantly different from control values (-2.14 L/min/%oxygen saturation). In control subjects the hypercapnic and hypoxic ventilatory responses were highly correlated with each other within subjects (r = 0.84; p less than 0.002) but not in those with myelomeningocele (r = 0.34; not significant). We concluded that adolescents and young adults with myelomeningocele have abnormalities in control of ventilation during sleep and wakefulness. We speculate that the Arnold-Chiari malformation interferes with central chemosensitivity (hypercapnic ventilatory response) and central integration of chemoreceptor output.
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PMID:Abnormal control of ventilation in adolescents with myelodysplasia. 258 25

The effects of acute, progressive isocapnic hypoxia and hyperoxic hypercapnia on heart rate (HR) were determined in 13 normal individuals. In all subjects there was an inverse linear relationship between hemoglobin oxygen saturation and HR. For the group, the HR (mean +/- SE) increased from 72 +/- 2 to 89.5 +/- 3 beats/min representing a 25% increase. During progressive hypercapnia, the HR increased from 72 +/- 2 to 75 +/- 2 beats/min, representing only a 4% increase. In contrast to the HR response to hypoxia, there was a heterogeneous HR response to hypercapnia, with most subjects having a mild increase in HR, but some showing no response and a few exhibiting a decrease in HR. We conclude that although there is a significant tachycardic response to isocapnic hypoxia, the tachycardic response to hyperoxic hypercapnia is small and clinically insignificant. In addition, while there is uniformly a tachycardic response to isocapnic hypoxia, there is a considerable interindividual variability of the HR response to hyperoxic hypercapnia.
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PMID:Chronotropic effects of progressive hypoxia and hypercapnia. 274 Jun 37

Respiratory acid-base disorders elicit physiological responses that alter O2 delivery to various tissues. We have used a near infrared (NIR) optical technique to monitor cytochrome a,a3 oxidation state, tissue O2 store (relative hemoglobin plus myoglobin oxygenation), and regional blood volume in intact resting skeletal muscle during respiratory acid-base disturbances in anesthetized cats. Hypercapnic acidosis and hypocapnic alkalosis were produced in separate groups of animals by ventilation with increasing concentrations of CO2 (n = 13) or hyperventilation (n = 8). Respiratory acidosis decreased oxygen availability to hindlimb muscle while respiratory alkalosis did not change tissue oxygenation. Inspired CO2 progressively decreased muscle blood volume, cytochrome a,a3 oxidation level, and muscle oxygen store. These optical responses were greatly attenuated both by pre-treatment with bretylium and by hemorrhagic hypotension, suggesting mediation through sympathetic vasoconstriction. Metabolic acidosis, produced by intravenous HCl infusion (n = 8), did not reproduce the hindlimb optical responses mediated by CO2. These experiments demonstrate that hypercapnic acidosis significantly decreases oxygen supply to resting skeletal muscle in the anesthetized cat, probably via neuroregulatory responses to CO2 which do not depend on changes in arterial [H+] in the tested pH range.
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PMID:Skeletal muscle oxygen availability during respiratory acid-base disturbances in cats. 282 60


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