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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

A technique has been developed for proton magnetic resonance imaging (MRI) of perfusion, using water as a freely diffusable tracer, and its application to the measurement of cerebral blood flow (CBF) in the rat is demonstrated. The method involves labeling the inflowing water proton spins in the arterial blood by inverting them continuously at the neck region and observing the effects of inversion on the intensity of brain MRI. Solution to the Bloch equations, modified to include the effects of flow, allows regional perfusion rates to be measured from an image with spin inversion, a control image, and a T1 image. Continuous spin inversion labeling the arterial blood water was accomplished, using principles of adiabatic fast passage by applying continuous-wave radiofrequency power in the presence of a magnetic field gradient in the direction of arterial flow. In the detection slice used to measure perfusion, whole brain CBF averaged 1.39 +/- 0.19 ml.g-1.min-1 (mean +/- SEM, n = 5). The technique's sensitivity to changes in CBF was measured by using graded hypercarbia, a condition that is known to increase brain perfusion. CBF vs. pCO2 data yield a best-fit straight line described by CBF (ml.g-1.min-1) = 0.052pCO2 (mm Hg) - 0.173, in excellent agreement with values in the literature. Finally, perfusion images of a freeze-injured rat brain have been obtained, demonstrating the technique's ability to detect regional abnormalities in perfusion.
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PMID:Magnetic resonance imaging of perfusion using spin inversion of arterial water. 172 91

Cerebral hemorrhagic insults are common in neonates. However, the consequences of intracranial blood on cerebral hemodynamics are poorly understood. We examined the effects of perivascular blood on cerebrovascular dilator responses in 29 piglets. Fresh, autologous blood (n = 15) or cerebrospinal fluid (n = 14) was placed under the dura mater over the parietal cortex, and the piglets were allowed to recover from anesthesia. One to four days later, a closed cranial window was placed over the parietal cortex and pial arteriolar responses to arterial hypercapnia (PaCO2 greater than 55 mm Hg), hemorrhagic hypotension (mean arterial blood pressure less than 35 mm Hg), or topical application of 10(-6) and 10(-4) M isoproterenol were determined. Pial arterioles in the cerebrospinal fluid group dilated 27 +/- 4% (mean +/- SEM) (n = 11) in response to hypercapnia, 26 +/- 5% (n = 9) in response to hypotension, and 26 +/- 3% in response to 10(-6) M and 40 +/- 4% in response to 10(-4) M isoproterenol (n = 11). In the group in which blood was placed on the parietal cortex, pial arterioles did not dilate significantly in response to hypercapnia (8 +/- 3%, n = 11) or hypotension (2 +/- 5%, n = 13) but dilated normally in response to isoproterenol (25 +/- 5% in response to 10(-6) M and 36 +/- 7% in response to 10(-4) M, n = 13). We conclude that prolonged contact of pial arterioles with extravascular blood selectively attenuates cerebrovascular dilation in piglets.
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PMID:Selective attenuation by perivascular blood of prostanoid-dependent cerebrovascular dilation in piglets. 190 99

Arterial blood gas analysis was performed before and after 60 to 90 s of voluntary hyperventilation in 27 consecutive patients with occlusive sleep apnea syndrome (OSA) and daytime hypercapnia. The percentage of fall in PaCO2 from baseline was examined in relationship to age, body mass index, sleep-disordered breathing indices, and pulmonary function variables. In 14 subjects without airflow obstruction, only one individual could not voluntarily hyperventilate into the normal range, whereas 6 of 13 subjects with airflow obstruction could not hyperventilate to eucapnia. The average percentage of fall in PaCO2 was 16 mm Hg (SEM = 1.3 mm Hg). The percentage of fall in PaCO2 correlated significantly with FEV1/FVC ratio (r = 0.47, p = 0.01) and with FEV1 (r = 0.5, p = 0.008). Although the baseline PaCO2 did not correlate with FEV1, the posthyperventilation PaCO2 did (r = 0.54, p = 0.003). Voluntary hyperventilation studies herein suggest a predominant role for impairment of ventilatory control in the maintenance of hypercapnia in OSA since a fall of PaCO2 into the normal range can usually be obtained. The correlation between the percentage of fall in PaCO2 and spirometric measures of respiratory mechanics, as well as the inability of some subjects to normalize the PaCO2 voluntarily suggests an added role for respiratory mechanical impairment in obesity hypoventilation.
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PMID:Voluntary hyperventilation in obesity hypoventilation. 193 91

The effect of hypercarbia on ocular blood flow was studied in the newborn piglet with the isotope-labeled microsphere method. Blood flow measurements were made during spontaneous breathing and during paralyzation (pancuronium) and mechanical ventilation. Retinal blood flow increased from 0.40 +/- 0.07 (mean +/- SEM) ml/min/g at baseline levels to 0.91 +/- 0.17 ml/min/g at a PaCO2 level of 11.0 kPa during spontaneous ventilation. A similar response was observed during paralyzation and mechanical ventilation (0.89 +/- 0.15 ml/min/g at a PaCO2 of 11.1 kPa). For choroidal blood flow, however, the increase caused by hypercarbia during spontaneous ventilation (16.14 +/- 3.69 to 29.15 +/- 3.22 ml/min/g) was significantly reduced when the animals were paralyzed and mechanically ventilated (15.99 +/- 2.99 to 23.51 +/- 3.41 ml/min/g). Since choroidal blood flow accounts for 60-80% of oxygen delivery to the retina, paralyzation and mechanical ventilation may significantly reduce oxygen delivery to the retina during hypercarbia.
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PMID:Retinal, choroidal and total ocular blood flow response to hypercarbia during spontaneous breathing and mechanical ventilation. 203 72

To evaluate relative contributions of inherent versus extrinsic factors to respiratory chemosensitivity, ventilatory responses to isocapnic progressive hypoxia and normoxic progressive hypercapnia were examined at intervals of 8 to 10 yr in 32 healthy male volunteers aged 42.2 +/- 1.4 yr (SEM) in the final examination. The volunteers included 22 sons of patients with chronic obstructive pulmonary disease. The mean value for the slope factor of the end-tidal PO2-ventilation hyperbola (A) significantly decreased from 98.3 +/- 12.2 to 77.4 +/- 10.3 L/min mm Hg (p less than 0.05), but that for the end-tidal PCO2 ventilation line (S) did not change over the years. The individual values for the hypoxic ventilatory response were significantly correlated (r = 0.63, p less than 0.001) between the initial and final examinations but not so for the hypercapnic ventilatory response (r = 0.23, NS), suggesting that the latter is more subject to influence from extrinsic factors than the former in the long term. The reproducibility of both tests expressed as coefficients of variation was similar or rather small for the hypercapnic ventilatory response, which was determined by three consecutive measurements at 1 wk intervals in a different group of six subjects. From these data we conclude that hypoxic chemosensitivity is more determined by factors inherent to the individual than hypercapnic chemosensitivity and that it is more systematically influenced by temporal factors, as demonstrated by the systematic decrease over the years.
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PMID:Longitudinal analyses of respiratory chemosensitivity in normal subjects. 204 13

The effects of inhaled stable xenon gas on cerebral blood flow were studied with 23 transcranial Doppler examinations performed in 13 normal volunteers while breathing, 25, 30, or 35% xenon for 5 min. Doppler velocities from the middle cerebral artery rose significantly during inhalation in 85% of subjects and 78% of studies and decreased significantly in 15% of subjects and 17% of studies. These different velocity responses may represent different responses of pial vasculature to xenon. The mean velocity rise among those studies showing a significant increase was 38 +/- 3.6% (SEM). The velocity rise began 2 min after the start of xenon inhalation and increased rapidly, so that the velocities measured at the four times at which scans were obtained in our xenon CT protocol (0, 1.5, 3, and 5 min after the start of xenon inhalation) were significantly different. A consistent fall in the pulsatility of the Doppler waveform as the velocity increased provided evidence for xenon-induced vasodilation of the small-resistance vessels as the cause of the increase in flow velocity. Most subjects became mildly hyperventilated, so that the observed changes could not be attributed to hypercapnia. Inhalation of 25, 30, or 35% xenon for 5 min induces a delayed but significant rise in cerebral blood velocity. This suggests that cerebral blood flow itself may be rapidly changing during the process of xenon CT scanning. These changes may compromise the ability of the xenon CT technique to provide reliable quantitative measurements of cerebral blood flow.
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PMID:Effects of inhaled stable xenon on cerebral blood flow velocity. 210 2

The purpose of this study was to evaluate the effect of interruption of the descending supraspinal sympathetic outflow on heart rate control during exposures to chemical stimuli. We investigated the heart rate responses to progressive isocapnic hypoxia and hyperoxic hypercapnia using the rebreathing technique and quantified the relationship between heart rate (HR), oxygen saturation (SaO2), alveolar PCO2 (PACO2), and minute ventilation (VE) in 16 chronic tetraplegic subjects with low cervical spinal cord transection. The HR responses were determined from the linear slopes of HR on SaO2 and HR on PACO2. We found that mean resting heart rate was within normal range; 66 +/- 3 (SEM) beats min-1. HR increased as oxygenation fell or CO2 tension rose. The mean tetraplegic delta HR/delta SaO2 was 0.83 +/- 0.14 beats min-1 per 1% fall in SaO2 and that of delta HR/delta PACO2 was 0.30 +/- 0.13 beats min-1 per mmHG rise in PACO2. The HR and VE responses to either hypoxia or hypercapnia were related in the tetraplegic subjects. We conclude that the stimulatory HR responses to chemical stimuli are not suppressed by cervical spinal cord transection. Thus, the descending sympathetic activity does not underlie the HR acceleration by chemical stimuli.
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PMID:Cardiac responses to hypoxia and hypercapnia in spinal man. 211 43

The association between infections with respiratory syncytial virus and plasma concentrations of antidiuretic hormone was assessed in 48 patients who had been admitted to hospital. The mean (SEM) concentration of antidiuretic hormone was significantly raised in patients with bronchiolitis (9.3 (1.4) ng/l) compared with non-pulmonary respiratory syncytial virus infections that cause apnoea or upper respiratory tract symptoms (6.1 (1.7) ng/l). The highest concentrations of antidiuretic hormone were seen in patients receiving mechanical ventilation (18.0 (6.7) ng/l). There were no differences in mean serum sodium concentrations among the subgroups. Hypertranslucency on chest radiograph or an arterial carbon dioxide tension above 6.67 kPa were associated with a significantly higher concentration of antidiuretic hormone. Increased or normal maintenance fluid intake in children with pulmonary respiratory syncytial virus infections may cause the same symptoms of fluid overload as the syndrome of inappropriate secretion of antidiuretic hormone. Patients with pulmonary respiratory syncytial virus infection, hypertranslucency in chest radiograph, hypercapnia, or mechanical ventilation are at risk for raised concentrations of antidiuretic hormone. Restricted fluid intake and careful monitoring of fluid balance and plasma electrolyte concentrations are therefore necessary in these patients.
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PMID:Excessive secretion of antidiuretic hormone in infections with respiratory syncytial virus. 212 82

CO2 single breaths have been performed in 7 men and 7 women in conditions of normoxia (FICO2 congruent to 0.13; FIO2 congruent to 0.21; FIN2 congruent to 0.66) and of hyperoxia (FICO2 congruent to 0.13; FIO2 congruent to 0.87). Ventilatory responses of the subjects and modifications of breathing pattern in the course of the CO2 tests were also explored in the two conditions. The results (mean +/- SEM) show that, whatever the oxygenation, men and women exhibit the same ventilatory response during a CO2 test from a qualitative point of view but with a smaller intensity in women (men: 0.37 +/- 0.088 LBTPS.min-1.Torr-1; women: 0.15 +/- 0.025 LBTPS.min-1.Torr-1; p less than 0.05). Considering men and women together, CO2 tests induced an increase of minute volume VE (p less than 0.001), VT (p less than 0.01) and rate of breathing (NS) but this response is decreased in hyperoxic conditions (p less than 0.05) mainly in men (men: 0.19 +/- 0.043 LBTPS.min-1.Torr-1; women: 0.11 +/- 0.023 LBTPS.min-1.Torr-1). These results show that sensitivity to transient hypercapnia and its interaction with hyperoxia are weaker in women than in men.
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PMID:CO2 chemoreflex drive of ventilation in man: effects of hyperoxia and sex differences. 212 2


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