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

Alterations in arterial oxygen and carbon dioxide influence cerebrovascular resistance and therefore cerebral blood flow (CBF), but the magnitude of these CBF responses have not been well defined in normal humans. Duplex scanning (B-mode imaging and pulsed Doppler shift analysis) was used to measure internal carotid blood flow (ICBF) as an indicator of CBF in 20 normal subjects during alterations of arterial O2 and CO2. End-tidal PCO2 (PETCO2) was measured by mass spectrometry, arterial oxygen saturation by pulse oximetry, and unilateral (right) ICBF by duplex scanning. A variety of gas mixtures were administered to achieve hypoxemia (FIO2 = 0.075-0.10) and hypercapnia (FICO2 = 0.05) or the subject was asked to hyperventilate to PETCO2 = 16-24 mm Hg. The ICBF was determined five times in each of six conditions: (1) normoxia/normocapnia; (2) normoxia/hypercapnia; (3) normoxia/hypocapnia; (4) hypoxia/normocapnia; (5) hypoxia/hypercapnia; and (6) hypoxia/hypocapnia. During normoxia and normocapnia, the mean ICBF was 330 +/- 19 (SEM) mL/min. Specific CO2 reactivity was 7.4 +/- 0.7 mL/min/mmHg, which is equivalent to 2.3% +/- 0.1% of normocapnic blood flow per mm Hg change in CO2. During normocapnia, ICBF increased by 2.9 +/- 0.9 mL/min for each percentage decrease in oxygen saturation. Using an ANOVA with repeated measures to fit the responses, the following statistically significant relationship was found: ICBF (mL/min) = 333 + 6.3.(PETCO2 - 40) + 2.7 DSO2 +/- 81 where DSO2 is arterial desaturation (100 - arterial saturation). An additional "between subject" variation had a mean of 0 and a standard deviation of 82 mL/min. There was no statistically significant evidence of an interaction between O2 and CO2 response. Our data suggest that hypoxia and carbon dioxide changes will alter CBF simultaneously and additively. Duplex scanning of the internal carotid artery, which can be performed at the bedside, is sufficiently sensitive to detect changes in ICBF and internal carotid artery oxygen delivery.
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PMID:Human cerebrovascular response to oxygen and carbon dioxide as determined by internal carotid artery duplex scanning. 158 51

Defense of ventilatory homeostasis against recurrent hypercapnia, hypoxia, and acidosis resulting from apnea in obstructive sleep apnea syndrome (OSAS) is dependent on compensatory mechanisms operative between episodes of airway obstruction. This investigation was designed to examine whether endogenous opiate activity modulates the compensatory ventilatory response to apnea in OSAS. Polysomnography and quantitative measurement of tidal volume was performed in 12 patients with moderate to severe OSAS during a morning nap study before and after intravenous administration of 10 mg of naloxone. Apnea index was not significantly altered. There was a small but significant shortening of apneas (postnaloxone apnea duration, 91.2% of prenaloxone; p = 0.002 by ANOVA). Tidal volume of the first postapnea breath and minute ventilation extrapolated from the first two postapnea breaths, but not frequency, increased significantly after naloxone (postnaloxone first breath volume, 112.7% of prenaloxone value [p = 0.03], with a similar increase for minute ventilation, 115.1% [p = 0.007]). The volume of the first postapnea breath was correlated with the duration of the previous apnea, both before (r = 0.59, p = 0.0001) and after naloxone. Despite this, analysis of covariance with apnea duration as the covariate confirmed a significant independent increase in postapnea breath volume after naloxone (p = 0.001). Naloxone also altered sleep architecture, increasing percent time awake during the study period (prenaloxone, 36.3 +/- 15.6%; postnaloxone, 56.7 +/- 22.4%; p = 0.0003) and decreasing total sleep time and percent time in Stage 1. Furthermore, naloxone increased continuity of awake periods (mean length of awake periods increased from 27.0 +/- 8.4 to 66.0 +/- 66.6 s after naloxone, p = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endogenous opiates modulate the postapnea ventilatory response in the obstructive sleep apnea syndrome. 204 14

Prompted by reports of potentially deleterious cerebral vasodilation by the synthetic opioid sufentanil, the authors compared the effects of either isoflurane/N2O and sufentanil/N2O on cerebral blood flow (CBF), arteriovenous difference in oxygen content (AVDO2), and CBF reactivity to changes in PaCO2 during carotid endarterectomy. Cerebral blood flow was measured using the iv method of 133-Xe CBF determination and AVDO2 was measured using systemic arterial-jugular venous oxygen content differences. Patients, age 68 +/- 1 yr (mean +/- SE), received either isoflurane (n = 10), 0.75% in O2 and N2O, 1:1; or sufentanil (n = 10), 1.5-2 micrograms/kg bolus and then 0.2-0.3 micrograms.kg-1.h-1 infusion in addition to O2 and N2O, 2:3. Measurements were made immediately before carotid occlusion, and then at two levels of PaCO2 (approximately 32 and 42 mmHg) after insertion of a temporary in-dwelling bypass shunt. Prior to carotid occlusion, there was no significant difference in CBF (ml.100 g-1.min-1) between patients receiving isoflurane (22 +/- 3) or sufentanil (20 +/- 2). Similarly, there was no difference in AVDO2 (vol-%) between isoflurane (4.5 +/- 0.7) and sufentanil (5.4 +/- 0.8) groups. Using a two-way ANOVA design with anesthetic as the between-group factor and elevation of PaCO2 as the within-group repeated measure, there was a significant effect of hypercarbia to increase CBF (P less than 0.0001) and decrease AVDO2 (P less than 0.001). The product of AVDO2 and CBF, which reflects cerebral metabolic oxygen consumption, remained constant (P = 0.364).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison of the cerebral hemodynamic effects of sufentanil and isoflurane in humans undergoing carotid endarterectomy. 253 61

We used large-array optical recording procedures to examine maturation of regional neural activity within the ventral medullary surface (VMS) of anaesthetized kittens during graded hypercapnic and hypoxic challenges. The VMS was exposed through a ventral surgical approach in 10, 20, 30, and 45-day-old kittens and in adult cats under sodium pentobarbital anaesthesia. Arterial pressure, costal diaphragmatic EMG, and ECG were continuously monitored. A coherent image conduit with 12 mu fibre resolution was attached to a charge-coupled-device camera and positioned over the VMS. Reflected 660 nm light was digitized continuously at 2-s intervals during a baseline period, hyperoxic hypercapnia, (3, 5, and 10% CO2 in O2), and poikylocapnic hypoxia (6%, 9%, and 12% O2 in N2), and recovery. Sixty to seventy-five images within each epoch were averaged, and subtracted from baseline. Regional differences within the image were determined by ANOVA procedures (alpha = 0.05). During hypercapnia, an overall decrease in neural activity (increase in scattered light) occurred, which was marginally age-dependent. By 30 days, regional bidirectional reflectance changes in response to CO2 emerged in a small proportion of animals, and were similar to adult responses. Hypoxia induced a dose- and age-dependent decrease in overall scattered light. Transient "on" and "off" responses were common under both ventilatory stimuli. In 20-30-day kittens, marked rebound responses in reflectance accompanied cessation of hypoxic stimuli; such patterns were absent at other ages. At 30 days, a caudal-rostral bidirectionality in response to mild hypoxia (12% O2) began to emerge in a subset of animals. We conclude that dose-dependent response to ventilatory stimuli occur in the VMS at all post-natal ages of the kitten; however, in hypoxia, the magnitude of the overall reflectance changes is diminished relative to adult patterns. Rebound responses to hypoxia are present at particular ages, and older kittens begin to show a topographical organization of neural activation.
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PMID:Optical imaging of the ventral medullary surface of developing kittens during ventilatory challenges. 871 26

The use of laparoscopy for the diagnosis or therapeutic management of abdominal disease in the horse has distinct advantages when it allows the horse to remain standing. However, distending the abdomen by insufflation of a biologically active gas in an anaesthetised horse may add to the physiological challenge of general anaesthesia and recumbency. The cardiopulmonary responses to abdominal insufflation with carbon dioxide (CO2) to 15 mmHg pressure were evaluated in 6 horses in dorsal recumbency anaesthetised with halothane in oxygen and subjected to laparoscopic colopexy. Vaporiser settings targeted a fractional expired halothane of 1.5 MAC and a clinically acceptable depth of anaesthesia. Pressure and rate controlled positive pressure ventilation was adjusted to an ETCO2 of 35 mmHg before abdominal insufflation and was not changed thereafter. Cardiopulmonary data were collected before, at 30 and 60 min during and 30 min after CO2 insufflation. ANOVA for repeated measures followed by Tukey's protected t test were used to determine differences. Partial pressure of oxygen and pH of arterial blood, tidal volume and systemic vascular resistance decreased during abdominal insufflation and laparoscopic surgery whereas mean arterial blood pressure, right atrial pressure, cardiac index, stroke index, partial pressure of CO2 in arterial blood and end tidal respiratory gases, and calculated physiological shunt increased significantly. Only systemic vascular resistance returned to the pre-insufflation level after desufflation. The hypercapnia, acidosis and apparent increase in cardiac work that accompany CO2 pneumoperitoneum for laparoscopic surgery could place the anaesthetised horse at additional risk of perioperative complications.
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PMID:Cardiopulmonary changes associated with abdominal insufflation of carbon dioxide in mechanically ventilated, dorsally recumbent, halothane anaesthetised horses. 953 71

1. Acute exposure to hypoxia stimulates ventilation and induces hypocapnia. Long-term exposure to hypoxia generates changes in respiratory control known as ventilatory acclimatization to hypoxia. The object of this study was to investigate the degree to which the hyperventilation and hypocapnia can induce the changes known as ventilatory acclimatization to hypoxia, in the absence of the primary hypoxic stimulus itself. 2. Three 6 h protocols were each performed on twelve healthy volunteers: (1) passive hypocapnic hyperventilation, with end-tidal CO2 pressure (PET,CO2) held 10 Torr below the eupnoeic value; (2) passive eucapnic hyperventilation, with PET,CO2 maintained eucapnic; (3) control. 3. Ventilatory responses to acute hypercapnia and hypoxia were assessed before and half an hour after each protocol. 4. The presence of prior hypocapnia, but not prior hyperventilation, caused a reduction in air-breathing PET,CO2 (P < 0.05, ANOVA), and a leftwards shift of the ventilatory response to hypercapnia (P < 0.05). The presence of prior hyperventilation, but not prior hypocapnia, caused an increase in the ventilatory sensitivity to CO2 (P < 0.05). No significant effects of any protocol were detected on the ventilatory sensitivity to hypoxia. 5. We conclude that following 6 h of passive hyperventilation: (i) the left shift of the VE-PET,CO2 relationship is due to alkalosis and not to hyperventilation; (ii) the increase in slope of the VE-PET,CO2 relationship is due to the hyperventilation and not the alkalosis; and (iii) ventilatory sensitivity to hypoxia is unaltered.
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PMID:Ventilatory responses to hypercapnia and hypoxia after 6 h passive hyperventilation in humans. 988 58

The gradual decay in ventilation after removal of a respiratory stimulus has been proposed to protect against cyclic breathing disorders such as obstructive sleep apnea (OSA). The male predominance of OSA, and the increased incidence of OSA in women after menopause, indicates that the respiratory-stimulating effect of progesterone may provide protection against OSA by altering the rate of poststimulus ventilatory decline (PSVD). It was therefore hypothesized that PSVD is longer in premenopausal women than in men and is longer in the luteal menstrual phase compared with the follicular phase. PSVD was measured in 12 men and in 11 women at both their luteal and follicular phases, after cessation of isocapnic hypoxia and normoxic hypercapnia. PSVD was compared between genders and between women in the luteal and follicular phases by repeated-measures ANOVA. There were no significant differences in PSVD between any of the groups after either respiratory stimulus. This suggests that the higher occurrence of OSA in men does not reflect an underlying gender difference in PSVD and implies the increased prevalence of OSA in women after menopause is not representative of an effect of progesterone on PSVD.
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PMID:Ventilatory decline after hypoxia and hypercapnia is not different between healthy young men and women. 1064 55

Six horses were randomly assigned to receive either frusemide (F) (0.5 mg/kg i.v.) or an equivalent volume of saline (S) i.v., 4 h prior to treadmill exercise. Horses were instrumented to enable measurement of heart rate (HR), systolic (SAP), mean (MAP), and diastolic (DAP) carotid arterial pressures, pulmonary artery pressure (PAP), central venous pressure (CVP), pulmonary arterial temperature (TEMP), blood gases, and cardiac output (CO). Plasma (PV) and blood volumes (BV) were measured using 2 injections of Evan's Blue dye. Baseline parameters were recorded while the horse stood quietly. Horses were then administered F or S. Four hours later, they were warmed up for 3 min at 4 m/s and then exercised to the point of fatigue at 115% VO2max. Horses were anaesthetised immediately following exercise by administration of detomidine (0.04 mg/kg bwt i.v.) followed 5 min later by tiletamine-zolazepam (1.25 mg/kg bwt i.v.). After transporting the horse to a recovery stall, anaesthesia was maintained with isoflurane in 100% O2. Data were analysed using a 2-way ANOVA with repeated measures with post hoc differences identified using the Student-Newman-Keul's procedure. Exercise was associated with increases in HR, SAP, MAP, DAP, PAP, CVP, TEMP, PCV, and BV, and decreases in PV, pH, arterial bicarbonate and base excess. Anaesthesia was associated with marked hypercapnia, a decrease in HR following detomidine administration, and persistent pulmonary hypertension despite carotid arterial pressure which returned to baseline. No effects attributable to F were identified at any time during the study.
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PMID:Effects of pre-exercise frusemide administration and post exercise anaesthesia on cardiopulmonary and acid-base parameters and blood and plasma volumes in horses exercised supramaximally to fatigue. 1065 46

Chronic hypercapnia is commonly found in patients with severe hypoxic lung disease and is associated with a greater elevation of pulmonary arterial pressure than that due to hypoxia alone. We hypothesized that hypercapnia worsens hypoxic pulmonary hypertension by augmenting pulmonary vascular remodeling and hypoxic pulmonary vasoconstriction (HPV). Rats were exposed to chronic hypoxia [inspiratory O(2) fraction (FI(O(2))) = 0.10], chronic hypercapnia (inspiratory CO(2) fraction = 0.10), hypoxia-hypercapnia (FI(O(2)) = 0.10, inspiratory CO(2) fraction = 0.10), or room air. After 1 and 3 wk of exposure, muscularization of resistance blood vessels and hypoxia-induced hematocrit elevation were significantly inhibited in hypoxia-hypercapnia compared with hypoxia alone (P < 0.001, ANOVA). Right ventricular hypertrophy was reduced in hypoxia-hypercapnia compared with hypoxia at 3 wk (P < 0.001, ANOVA). In isolated, ventilated, blood-perfused lungs, basal pulmonary arterial pressure after 1 wk of exposure to hypoxia (20.1 +/- 1.8 mmHg) was significantly (P < 0.01, ANOVA) elevated compared with control conditions (12.1 +/- 0.1 mmHg) but was not altered in hypoxia-hypercapnia (13.5 +/- 0.9 mmHg) or hypercapnia (11.8 +/- 1.3 mmHg). HPV (FI(O(2)) = 0.03) was attenuated in hypoxia, hypoxia-hypercapnia, and hypercapnia compared with control (P < 0.05, ANOVA). Addition of N(omega)-nitro-L-arginine methyl ester (10(-4) M), which augmented HPV in control, hypoxia, and hypercapnia, significantly reduced HPV in hypoxia-hypercapnia. Chronic hypoxia caused impaired endothelium-dependent relaxation in isolated pulmonary arteries, but coexistent hypercapnia partially protected against this effect. These findings suggest that coexistent hypercapnia inhibits hypoxia-induced pulmonary vascular remodeling and right ventricular hypertrophy, reduces HPV, and protects against hypoxia-induced impairment of endothelial function.
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PMID:Chronic hypercapnia inhibits hypoxic pulmonary vascular remodeling. 1066 61

In humans, 8 h of isocapnic hypoxia causes a progressive rise in ventilation associated with increases in the acute ventilatory responses to hypoxia (AHVR) and hypercapnia (AHCVR). To determine whether 8 h of hyperoxia causes the converse of these effects, three 8-h protocols were compared in 14 subjects: 1) poikilocapnic hyperoxia, with end-tidal PO(2) (PET(O(2))) = 300 Torr and end-tidal PCO(2) (PET(CO(2))) uncontrolled; 2) isocapnic hyperoxia, with PET(O(2)) = 300 Torr and PET(CO(2)) maintained at the subject's normal air-breathing level; and 3) control. Ventilation was measured hourly. AHVR and AHCVR were determined before and 0.5 h after each exposure. During isocapnic hyperoxia, after an initial increase, ventilation progressively declined (P < 0.01, ANOVA). After exposure to hyperoxia, 1) AHVR declined (P < 0.05); 2) ventilation at fixed PET(CO(2)) decreased (P < 0.05); and 3) air-breathing PET(CO(2)) increased (P < 0.05); but 4) no significant changes in AHCVR or intercept were demonstrated. In conclusion, 8 h of hyperoxia have some effects opposite to those found with 8 h of hypoxia, indicating that there may be some "acclimatization to hypoxia" at normal sea-level values of PO(2).
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PMID:Changes in respiratory control in humans induced by 8 h of hyperoxia. 1092 51


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