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

The effects of hypercapnia and hypocapnia on respiratory resistance were studied in 15 healthy subjects and 30 asthmatic subjects. Respiratory resistance (impedance) was measured with the pseudo-random noise forced oscillation technique while the subjects rebreathed from a wet spirometer in a closed respiratory circuit in which end tidal carbon dioxide tension (PCO2) could be controlled. Hypercapnia was induced by partially short circuiting the carbon dioxide absorber, and hypocapnia by voluntary hyperventilation. The circulating air was saturated with water vapour and kept at body temperature and ambient pressure. A rise of end tidal PCO2 of 1 kPa caused a significant fall in respiratory resistance in both normal and asthmatic subjects (15% and 9% respectively). A fall of PCO2 of 1 kPa did not cause any significant change in impedance in the control group. In the asthmatic patients resistance increased by 13%, reactance fell by 45%, and the frequency dependence of resistance rose 240%. These findings confirm that hypocapnia may contribute to airway obstruction in asthmatic patients, even when water and heat loss are prevented.
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PMID:Effects of hypercapnia and hypocapnia on respiratory resistance in normal and asthmatic subjects. 190 37

In an unpaired study, in vivo measurements of pH in vitreous were performed on normal pig eyes and pig eyes treated with retinal xenon photocoagulation. In one group (n = 7) the mean vitreal pH was 7.29 at a mean arterial pH of 7.41. In the other group (n = 8) two to three weeks after retinal xenon photocoagulation, a significant increase in mean vitreal pH of 0.06 to 7.35 (P less than 0.01) was observed at a similar arterial pH. Induced hypercapnia resulted in a decrease in pH vitr. and induced hypocapnia in an increase, with similar changes in pH art. The respiratory pH changes were similar in the two groups. These findings allow one to assume that, as a result of retinal photocoagulation, a change in the retinal metabolism is induced, either by a change in the relationship between aerobic and anaerobic metabolism or as a result of a general reduction of the metabolic activity.
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PMID:Changes in the vitreous body pH of pigs after retinal xenon photocoagulation. 190 70

Deviations of the alveolar ventilation rate from normality induce respiratory acid-base disturbances. Alveolar hyperventilation leads to hypocapnia and thus respiratory alkalosis whereas alveolar hypoventilation induces hypercapnia leading to respiratory acidosis. The changes in CO2 induce compensatory alterations of renal bicarbonate transport: Hypercapnia stimulates renal reabsorption of bicarbonate whereas hypocapnia enhances urinary bicarbonates. The plasma bicarbonate concentration rises in response to hypercapnia and falls following hypocapnia. Renal regulation of plasma bicarbonate results in a characteristic dependence on systemic PCO2 permitting the formation of diagnostic criteria for respiratory imbalance of acid-base homeostasis. In chronic respiratory acidosis plasma bicarbonate should rise by 0.35 mmol/l per mmHg increase in PCO2. In chronic respiratory alkalosis, on the other hand, plasma bicarbonate should fall by 0.4 mmol/l for every mmHg decrease in PCO2. If the measured bicarbonate values do not fall into this expected range, acute respiratory or mixed (respiratory and metabolic) acid-base disturbances should be suspected. The clinical significance and application of these diagnostic criteria are illustrated by examples.
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PMID:[Hypo- and hyperventilation: consequences for acid-base balance]. 192 34

In the intact rat kidney, bicarbonate reabsorption in the early proximal tubule (EP) is strongly dependent on delivery. Independent of delivery, metabolic acidosis stimulates EP bicarbonate reabsorption. In this study, we investigated whether systemic pH changes induced by acute or chronic respiratory acid-base disorders also affect EP HCO3- reabsorption, independent of delivery (FLHCO3, filtered load of bicarbonate). Hypercapnia was induced in rats acutely (1-3 h) and chronically (4-5 d) by increasing inspired PCO2. Hypocapnia was induced acutely (1-3 h) by mechanical hyperventilation, and chronically (4-5 d) using hypoxemia to stimulate ventilation. When compared with normocapneic rats with similar FLHCO3, no stimulation of EP or overall proximal HCO3 reabsorption was found with either acute hypercapnia (PaCO2 = 74 mmHg, pH = 7.23) or chronic hypercapnia (PaCO2 = 84 mmHg, pH = 7.31). Acute hypocapnia (PaCO2 = 29 mmHg, pH = 7.56) did not suppress EP or overall HCO3 reabsorption. Chronic hypocapnia (PaCO2 = 26 mmHg, pH = 7.54) reduced proximal HCO3 reabsorption, but this effect was reversed when FLHCO3 was increased to levels comparable to euvolemic normocapneic rats. Thus, when delivery is accounted for, we could find no additional stimulation of proximal bicarbonate reabsorption in respiratory acidosis and, except at low delivery rates, no reduction in bicarbonate reabsorption in respiratory alkalosis.
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PMID:Delivery dependence of early proximal bicarbonate reabsorption in the rat in respiratory acidosis and alkalosis. 199 47

We performed Fourier analysis of the middle cerebral artery blood flow velocity waveform envelope in 14 normal subjects (group A) and 15 patients, of whom five had arteriovenous malformations (group B), five had cerebral vasospasm (group C), and five had arterial hypertension (group D). Measurements were obtained under conditions of normocapnia, hypercapnia, and hypocapnia. The Fourier coefficients measured in the first five harmonics of the Doppler waveforms of group A were used as the reference baseline and were compared with the coefficients found in the other three groups. Group B showed significantly lower Fourier coefficients, while groups C and D showed higher coefficients (p less than 0.05). The elevation of the Fourier coefficients occurred in an alternating pattern in group C and a decremental pattern in group D. This distinction was attributed to possible differences in the underlying pathophysiological processes. The degree of vascular distensibility of the cerebral arterioles, inferred from the shape of the Fourier analysis curves, was compared in all four groups. Vascular distensibility was characterized as abnormal in arteriovenous malformations, vasospasm, and arterial hypertension. Fourier coefficients may be better indicators of cerebrovascular abnormalities than mean blood flow velocity in hypertension and pulsatility index in arteriovenous malformations, vasospasm, and hypertension.
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PMID:Fourier analysis of the cerebrovascular system. 205 69

We studied the relationship between contractile function and intracellular pH (pHi) in the isolated rat diaphragm when superfusate PCO2 was changed during hyperoxia or hypoxia. Superfused diaphragm strips were field stimulated at 0.5 Herz, and twitch tension (TT) was recorded. The pHi was calculated from the volume distribution of a weak acid, dimethyl-oxazolidinedione. In hyperoxia, hypercapnic acidosis (pH 7.06-6.63) depressed diaphragm pHi and TT, whereas hypocapnic alkalosis (pH 7.82-8.15) increased pHi but did not significantly affect TT. TT was maximum at physiological pHi (7.06), but in hyperoxic hypercapnic muscles substantial force was still generated at pHi values as low as 6.44. Hypoxia (PO2 30-38 mm Hg) markedly reduced TT; this effect was slightly exacerbated by hypercapnia and attenuated by hypocapnia. Hypoxia lowered pHi by about 0.2 units, which was insufficient to account for the hypoxic contractile failure. Knowledge of the hyperoxic muscle TT/pHi relationship suggests that, in other contexts, caution should be exercised in attributing severe muscle fatigue or force loss to modest falls in pHi.
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PMID:The effect of pH and hypoxia on function and intracellular pH of the rat diaphragm. 210 18

To investigate the effect of carbon dioxide on the myocardial oxygenation during hemorrhagic shock, myocardial oxygen tension and coronary flow were measured during normocapnia, hypocapnia and hypercapnia. Eight adult mongrel dogs were anesthetized with pentobarbital, intubated and ventilated mechanically with 100% oxygen to maintain normocapnia. Then their chest was opened. An electromagnetic blood flow probe was applied on the left anterior descending artery. Two pairs of combined polarographic needle electrodes were carefully inserted, one pair in the epicardial layer, and the other in the endocardial layer of the heart. The animals were progressively bled in increments of 35-40ml.kg-1 (body weight). Hypocapnia was produced by increasing respiratory rate, and then normocapnia and hypercapnia were induced by adding the exogenous carbon dioxide. Hypocapnia decreased the coronary flow, and myocardial oxygen tension in outer and inner layer. On the contrary, hypercapnia increased them. It is possible that hypocapnia may compromise the oxygenation of the myocardium during hemorrhagic shock.
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PMID:[The effect of hypocapnia and hypercapnia on myocardial oxygen tension in hemorrhaged dogs]. 211 63

Cerebral capillaries in cats subjected to variations in carbon dioxide tensions were studied using carbon black perfusion fixation. Five animals each were grouped into hypocapnia, normocapnia, and hypercapnia and 500 cortical, 250 white matter and 250 caudate nucleus capillaries per group were analyzed at 400 x magnification. Capillary diameters were found to change significantly in the cortex (6.1-10.0 microns), white matter (6.5-9.6 microns) and caudate nucleus (6.3-8.8 microns) from hypocapnia to hypercapnia, respectively. These findings suggest that capillary vasomotion occurs and that capillaries are not rigid tubes as previously portrayed.
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PMID:The effect of carbon dioxide on the diameter of brain capillaries. 211 12

1. The purpose was to evaluate the hypothesis that neural expiration is composed of two phases: I, a post inspiratory period; and II, the period at which expiratory activities of spinal nerves reach peak values. We hypothesized that the discharge of pulmonary stretch receptors might differentially alter neural activities during these two phases. 2. Activities of the phrenic nerve, intercostal nerve and nerves innervating the thyroarytenoid muscle of the larynx and triangularis sterni muscle of the chest wall were recorded in decerebrate and paralysed cats. 3. The experimental animals were ventilated with a servo-respirator which produced changes in tracheal pressure, and lung volume, in parallel with alterations in integrated activity of the phrenic nerve. 4. In order to assess the influence of the discharge of slowly adapting pulmonary stretch receptors upon neural activities during expiration, lung volume was held at end-expiratory or end-inspiratory levels for individual respiratory cycles. 5. When pulmonary inflation was prevented, phrenic activity increased, as did activity of the thyroarytenoid nerve during early expiration. In contrast, activities of the triangularis sterni and intercostal nerves during mid- to late expiration declined. 6. Holding the lungs at end-inspiratory levels caused a reduction of thyroarytenoid activity and increases in peak triangularis sterni and intercostal activities. Neural expiration typically continued as long as the lungs were maintained at the end-inspiratory level. 7. Responses were qualitatively similar in hypocapnia, normocapnia and hypercapnia, but the magnitude of changes in neural activities was typically augmented with elevations in end-tidal fractional concentrations of CO2. 8. We conclude that the discharge of slowly adapting pulmonary stretch receptors inhibits neural activities during early expiration and augments activities during mid-to late expiration. Hence, our data support the concept that neural expiration is composed of two stages in which neural activities may be differentially controlled.
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PMID:Discharge of vagal pulmonary receptors differentially alters neural activities during various stages of expiration in the cat. 211 78

The effects of hyper- and hypocapnia on oxidative metabolism were evaluated by near-infrared (NIR) multiwavelength spectroscopy in intact brain and skeletal muscle tissues of the anesthetized cat. A 3-wavelength NIR algorithm was used to monitor cytochrome a,a3 oxidation state, regional blood volume, and tissue oxyhemoglobin and O2 stores simultaneously in brain and muscle in ventilated animals. Incremental hypercapnia was produced in 10 cats by raising arterial pCO2 from 27.0 +/- 1.3 to 95.1 +/- 1.9 mmHg with inspired CO2. Hypercapnia produced progressive increases in cerebral HbO2, blood volume, and cytochrome a,a3 oxidation state (P less than 0.01). In contrast, CO2 simultaneously decreased all 3 NIR parameters in intact hindlimb muscles (P less than 0.01). Blood volume changes during hypercapnia correlated with changes in blood flow measured qualitatively by intravascular injections of indocyanine green dye. Hypocapnia produced by hyperventilation in 8 cats lowered paCO2 from 28.5 +/- 0.4 to 13.5 +/- 0.5 mmHg. Hypocapnia decreased cerebral HbO2, blood volume, and cytochrome a,a3 redox level (P less than 0.05), but NIR changes were not seen in skeletal muscle. These experiments demonstrate preferential distribution of oxygen to brain during hypercapnia and the ability of NIR spectroscopy to assess regional oxygenation in multiple tissues non-invasively.
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PMID:Near-infrared optical responses in feline brain and skeletal muscle tissues during respiratory acid-base imbalance. 211 21


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