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

Transcranial Doppler is routinely used to assess the cerebrovascular reactivity, despite scarce information on its reproducibility. We evaluated the reproducibility of cerebrovascular reactivity measurements by this method utilizing different vasodilatory and vasoconstrictor stimuli. The cerebrovascular reactivity was measured in 45 healthy volunteers during hypercapnia induced by inhalation of a mixture of 5% CO2 and 95% O2, breath holding and rebreathing, and during hypocapnia induced by voluntary hyperventilation. Three sets of measurements were performed at times 0, 1, and 24 h to assess the within-observer short- and long-term reproducibility. The reproducibility was analyzed using the intraclass correlation coefficient. For the CO2 inhalation method, a good short-term (rI = 0.55; 95% CI = 0.39-0.68) and a good long-term (rI = 0.43; 95% CI = 0.25-0.59) reproducibility was found. For the breath-holding method a good short-term agreement was found (rI = 0.41; 95% CI = 0.22-0. 57), while the long-term reproducibility was poor (rI = 0.17; 95% CI = -0.03-0.36). Rebreathing showed a fair (rI = 0.31; 95% CI = 0.11-0. 48) short-term and a poor (rI = 0.17; 95% CI = -0.03-0.36) long-term reproducibility. For voluntary hyperventilation, the short-term reproducibility was good (rI = 0.53; 95% CI = 0.36-0.66), and the long- term reproducibility was fair (rI = 0.31; 95% CI = 0.11-0.48). In our study, CO2 inhalation and voluntary hyperventilation had the highest reproducibility and should be preferred when assessing cerebral vasoreactivity, especially in follow-up studies.
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PMID:Cerebrovascular reactivity evaluated by transcranial Doppler: reproducibility of different methods. 1020 5

In functional magnetic resonance imaging studies changes in blood oxygenation level-dependent (BOLD) signal intensities during task activation are related to multiple physiological parameters such as cerebral blood flow, volume, and oxidative metabolism, as well as to the regional microvascular anatomy. Consequently, the magnitude of activation-induced BOLD signal changes may vary regionally and between subjects. The aim of this study was to use a uniform global stimulus such as hypercapnia to quantitatively investigate the regional BOLD response in the human brain. In 10 healthy volunteers, T2*-weighted gradient echo images were acquired for a total dynamic scanning time of 9 min during alternating periods of breath holding for 30 s after expiration and self-paced normal breathing for 60 s. Hypercapnia-induced BOLD signal changes in the sensorimotor cortex, frontal cortex, basal ganglia, visual cortex, and cerebellum were significantly different (P < 0.001) and varied from 1.8 to 5.1%. The highest BOLD signal changes were found in the cerebellum and visual cortex, whereas the lowest BOLD signal increase was observed in the frontal cortex. These results demonstrate a regional dependence of the BOLD signal changes during breath hold-induced hypercapnia, indirectly supporting the notion of regional different sensitivities of BOLD responses to task activation.
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PMID:Regional variability of cerebral blood oxygenation response to hypercapnia. 1060 Apr 13

Spontaneous brain activity was measured by multichannel magnetoencephalography (MEG) during voluntary breath holds. Significant changes in the activity are limited to the alpha rhythm: 0.25 Hz frequency increase and narrowing of the peak. The area of alpha activity shifts slightly toward (fronto-) temporal. The topography of other rhythms is unaffected by breath holding. Electroencephalographic (EEG; 36 channels maximal) recordings generally made simultaneously with the MEG recordings show similar effects. However, EEG was inadequate to reveal the small topographic differences. Systemic hypercapnia caused by a long breath hold is unlikely to play an important role in producing the observed effects.
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PMID:Voluntary breath holding affects spontaneous brain activity measured by magnetoencephalography. 1064 69

The purpose of this study was to examine which physiological factors affect cerebral T2* signal intensity (SI) during breath holding (BH) (apnea after inspiration and breathing after expiration) in normal volunteers. We examined SI changes caused by anoxic gas inhalation, by respiratory movements, and by BH. High-speed echo planar images (EPI) showed changes in SI that could be divided into five phases. Reports indicate that SI changes induced by BH are due to the effects on the magnetic susceptibility of deoxygenated hemoglobin (deoxyhemoglobin (dHb)) and to hypercapnia, but these reports could not fully explain the observed five phases. In addition to deoxyhemoglobin susceptibility and hypercapnia, we found that respiratory movements play a third critical role in modifying SI by affecting blood flow into the region of interest (ROI), as judged from right carotid artery flow. Consequently, we propose that the physiological SI changes induced by BH are derived from blood oxygenation, hypercapnia, and respiratory movements.
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PMID:Chronological analysis of physiological T2* signal change in the cerebrum during breath holding. 1124 5

The length of breath-hold duration in divers is dependant on a number of interacting variables which include mechanical factors (lung volumes), chemical factors (sensitivity to hypoxia and hypercapnia), non-chemical factors (involuntary muscular contractions), psychological factors (motivation, stress, competition) and various extrinsic factors (training, muscular exercise). These stimulus provoke the unpleasant sensation of an urge to breathe at the termination point of the breath hold. Training and experience produces adaptations in divers which decreases sensitivity to CO(2) and which delays and minimises the involuntary contractions of respiratory muscles provoked by the absence of respiratory movements. These adaptations modify the breaking point of, and increase the duration of breath holding. Godfrey & Campbell's model (1968), modified by Courteix et coll. (1993) and Delapille (2000), attempts to explain the control of breathing in the context of apnea and to define the effects of each of these stimulus on the respiratory activity of divers and non-divers.
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PMID:[Ventilatory adaptations for breath holding in divers]. 1204 Mar 22

Interictal cerebrovascular reactivity and blood flow velocities were tested in 23 patients with migraine without aura and 10 age- and sex-matched healthy controls by using the breath holding index (BHI). The mean systolic, diastolic and mean velocities and pulsatility indices were not different in the controls and patients. The BHI was found to be significantly greater (P=0011) in the patients (1.64 +/- 0.33) compared with the controls (1.26 +/- 0.37), showing an exaggerated reactivity to hypercapnia in migraineurs. Reactivity to pCO2 theoretically depends on pre-existing arteriolar tone and thereby on baseline velocity. Our finding of similar blood flow velocities in controls and patients suggests that the underlying cause for this high reactivity may not be an increased vasotonus but an increased sensitivity to changes in blood CO2 levels.
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PMID:Exaggerated interictal cerebrovascular reactivity but normal blood flow velocities in migraine without aura. 1210 91

Blood oxygenation level-dependent (BOLD) signal increases induced by hypercapnia stress has been recently investigated in human brains, which may be clinically relevant because it reflects cerebral hemodynamic response to vasodilatation. The aims of this study were to investigate the detectability of BOLD signal changes due to short breath holding and the feasibility of this technique in routine clinical practice. The results showed that significant BOLD responses could be detected in the gray matter for a breath hold duration as short as 10 s. Breath hold duration correlated strongly with the full width at half maximum of the hemodynamic response (r(2) = 0.975, p < 0.02), but not with the maximum signal change or the onset time. The fraction activation volume increased as the breath hold duration lengthened, reaching a plateau approximately at 20 s. Considering breath-holding capability of patients and detectability of BOLD signal changes, breath holding with a 20-s duration is suggested to be applied for clinical applications.
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PMID:Detectability of blood oxygenation level-dependent signal changes during short breath hold duration. 1247 61

We measured ventilation, arterial O2 saturation, end-tidal CO2 (PET,CO2), blood pressure (intra-arterial catheter or photoelectric plethysmograph), and flow velocity in the middle cerebral artery (CFV) (pulsed Doppler ultrasound) in 17 healthy awake subjects while they performed 20 s breath holds under control conditions and during ganglionic blockade (intravenous trimethaphan, 4.4 +/- 1.1 mg min-1 (mean +/- S.D.)). Under control conditions, breath holding caused increases in PET,CO2 (7 +/- 1 mmHg) and in mean arterial pressure (MAP) (15 +/- 2 mmHg). A transient hyperventilation (PET,CO2 -7 +/- 1 mmHg vs. baseline) occurred post-apnoea. CFV increased during apnoeas (by 42 +/- 3 %) and decreased below baseline (by 20 +/- 2 %) during post-apnoea hyperventilation. In the post-apnoea recovery period, CFV returned to baseline in 45 +/- 4 s. The post-apnoea decrease in CFV did not occur when hyperventilation was prevented. During ganglionic blockade, which abolished the increase in MAP, apnoea-induced increases in CFV were partially attenuated (by 26 +/- 2 %). Increases in PET,CO2 and decreases in oxyhaemoglobin saturation (Sa,O2) (by 2 +/- 1 %) during breath holds were identical in the intact and blocked conditions. Ganglionic blockade had no effect on the slope of the CFV response to hypocapnia but it reduced the CFV response to hypercapnia (by 17 +/- 5 %). We attribute this effect to abolition of the hypercapnia-induced increase in MAP. Peak increases in CFV during 20 s Mueller manoeuvres (40 +/- 3 %) were the same as control breath holds, despite a 15 mmHg initial, transient decrease in MAP. Hyperoxia also had no effect on the apnoea-induced increase in CFV (40 +/- 4 %). We conclude that apnoea-induced fluctuations in CFV were caused primarily by increases and decreases in arterial partial pressure of CO2 (Pa,CO2) and that sympathetic nervous system activity was not required for either the initiation or the maintenance of the cerebrovascular response to hyper- and hypocapnia. Increased MAP or other unknown influences of autonomic activation on the cerebral circulation played a smaller but significant role in the apnoea-induced increase in CFV; however, negative intrathoracic pressure and the small amount of oxyhaemoglobin desaturation caused by 20 s apnoea did not affect CFV.
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PMID:Mechanisms of the cerebrovascular response to apnoea in humans. 1258 94

In many species of air-breathing vertebrates CO2-sensitive airway receptors play an important role in ventilatory control. In ectotherms, olfactory receptors often inhibit breathing and prolong breath holding when environmental CO2 levels are high. CO2/H+ sensitive pulmonary receptors (intra pulmonary chemoreceptors (IPC) and pulmonary stretch receptors (PSR)) regulate breathing patterns in all vertebrates in a manner that reduces dead space ventilation and enhances the efficiency of CO2 excretion under conditions of environmental hypercarbia, and/or reduces CO2 loss from hyperventilation. The greater CO2 sensitivity of IPC may allow them to also serve as a venous CO2 receptor (at least transiently when levels of metabolically produced CO2 begin to rise), prevent alkalosis during hyperpnea/polypnea, and may have contributed to the evolution of the extremely thin air/blood barrier and increased diffusion capacity associated with the rigid avian lung. The presence of all three receptor groups with different degrees of CO2 sensitivity in most reptiles, however, gives rise to what appear to be anomalous responses to environmental CO2.
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PMID:Evolutionary trends in airway CO2/H+ chemoreception. 1555 2

Breath holding maneuvers induce hypoxia, hypercapnia, and various cardiovascular responses typically including increases in total peripheral resistance, mean arterial pressure (MAP) and decreases in heart rate (HR). During dynamic exercise these responses may have a generally negative impact on performance. Moreover, they deserve particular attention in cardiovascular risk subjects. In 26 healthy sport students we studied the HR and MAP effects induced by the combination of dynamic exercise (cycle ergometry, 30 W and 250 W) with 20 s of either respiratory arrest (mouth piece pressure held constant at 20 mm Hg), free breathing, or rebreathing, i. e. periods of unimpeded breathing leading to similar levels of hypercapnia and hypoxia as the respiratory arrest. The measurements yielded no major differences between the conditions of rebreathing and free breathing. In contrast, 20 s of apnea led to a marked increase in MAP and a HR depression at both levels of exercise intensity. Additionally, there was a delayed MAP recovery after this stimulus. The present findings show that breath holding has marked effects on MAP and HR during dynamic exercise, which are essentially independent of the resulting hypoxia and of increases in intrathoracic pressure. The key factor seems to be an increase in total peripheral resistance, probably including a vasoconstriction in the exercising muscles.
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PMID:Cardiovascular responses to apnea during dynamic exercise. 1603 83


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