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

Sodium ions are intimately involved with neural activity. Thus, it is highly desirable to devise a way of mapping brain activity via sodium imaging. Sodium ions exist in the extravascular and intravascular spaces. To separate the two components, the shift reagent Tm(DOTP)(5-) was intravenously introduced into rats. Intravascular sodium changes in the rat brain were measured during increased blood flow induced by hypercapnia using volume-localized (23)Na-NMR. The intravascular sodium changes, equivalent to cerebral blood volume changes, are significant during hypercapnia conditions and correlate well with the increase in arterial pCO(2). This suggests that the intravascular sodium change is dominant in total (23)Na spectroscopy or imaging of the brain during blood flow increase induced by external perturbation.
NMR Biomed
PMID:Measurement of intravascular Na(+) during increased CBF using (23)Na NMR with a shift reagent. 1174 37

Chemoreceptors in the ventral medulla contribute to the respiratory response to hypercapnia. Do they 'sense' intracellular pH (pHi)? We measured pHi in the ventral medulla or cortex (control) using 31P-NMR obtained via a novel 3 x 5 mm2 surface coil in anesthetized rats breathing air or 7% CO2. During air breathing over 240 min, pHi decreased slightly from 7.13 +/- 0.02 to 7.05 +/- 0.02 (SEM; n = 5; 2 cortex, 3 ventral medulla). During 180 min of hypercapnia, cortical pHi (n = 4) decreased from 7.17 +/- 0.02 to 6.87 +/- 0.01 by 90 min and recovered by 150 min. Ventral medulla pHi showed no such regulation. It decreased from 7.11 +/- 0.02 to 6.88 +/- 0.02 at 90 min and recovered only after cessation of hypercapnia (n = 5), results consistent with pHi being the chemoreceptor stimulus. However, non-chemoreceptor neurons that contribute to our medullary NMR signal also do not appear to regulate pHi in vitro. Regional differences in pHi regulation between cortex and ventral medulla may be due to both chemosensitive and non-chemosensitive neurons.
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PMID:Ventral medulla pHi measured in vivo by 31P NMR is not regulated during hypercapnia in anesthetized rat. 1238 4

To decipher the biophysical mechanism behind the fMRI-BOLD response to apnea and its dependence on the baseline cerebral blood flow and oxygenation, fMRI and laser Doppler flow (LDF) studies were carried out in anesthetized rats. Baseline cerebral blood flow (CBF) and PaO2 were modulated by ventilating with different gas mixtures namely, room air (21% O2), 100% O2, carbogen (95% O2+5% CO2), 2% CO2 in air or 5% CO2 in air, respectively. A decrease in BOLD signal intensity was observed after the onset of apnea with either room air, 2% CO2 or 5% CO2 ventilation. PaO2 and cerebral tissue PO2 decreased during apnea under these conditions. However, the apnea-induced BOLD signal intensity was unaffected with carbogen ventilation and increased with 100% O2 ventilation, during which PaO2 remained constant and cerebral tissue PO2 increased. When baseline CBF was high during hypercapnia, a faster decrease occurred in the apnea-induced BOLD signal. Apnea induced the largest increase in CBF of 85 +/- 25% when ventilated with 2% CO2 while a 44 +/- 8% increase was observed with room air. During the other ventilatory conditions, minimal or no significant change in CBF was observed during apnea. These results show a significant correlation between the BOLD signal change and tissue PO2 in response to apnea under different physiological conditions. Apnea-induced increase in CBF affects the magnitude of the BOLD signal response when PaO2 remains constant or changes minimally.
NMR Biomed 2003 Aug
PMID:Baseline physiological state and the fMRI-BOLD signal response to apnea in anesthetized rats. 1464 86

Acute hypoxia (transient cycles of hypoxia-reoxygenation) is known to occur in solid tumors and is generally believed to be caused by tumor blood flow instabilities. It was recently demonstrated that T2*-weighted (T2*w) gradient echo (GRE) MRI is a powerful non-invasive method for investigating periodic changes in tumor pO2 and blood flow associated with acute hypoxia. Here, the possible correlation between tumor vessel immaturity, vessel functionality and T2*w GRE signal fluctuations was investigated. Intramuscularly implanted FSa II fibrosarcoma-bearing mice were imaged at 4.7 T. Maps of spontaneous fluctuations of MR signal intensity in tumor tissue during air breathing were obtained using a T2*w GRE sequence. This same sequence was also employed during air-5% CO2 breathing (hypercapnia) and carbogen breathing (hypercapnic hyperoxia) to obtain parametric maps representing vessel maturation and vessel function, respectively. Vascular density, vessel maturation and vessel perfusion were also assessed histologically by using CD31 labeling, alpha-smooth muscle actin immunoreactivity and Hoechst 33242 labeling, respectively. About 50% of the tumor fluctuations occurred in functional tumor regions (responsive to carbogen) and 80% occurred in tumor regions with immature vessels (lack of response to hypercapnia). The proportion of hypercapnia-responsive voxels were found to be twice as great in fluctuating than in non-fluctuating tumor areas (P: 0.22 vs 0.13). Similarly, the proportion of functional voxels was somewhat greater in fluctuating tumor areas (P: 0.54 vs 0.43). The mean values of MR signal changes during hypercapnia (VD) and during carbogen breathing (VF) (significant voxels only) were also larger in fluctuating than in non-fluctuating tumor areas (P < 0.05). This study demonstrated that adequate vessel functionality and advanced vessel maturation could explain at least in part the occurrence of spontaneous T2*w GRE signal fluctuations. Functionality and maturation are not required for signal fluctuations, however, because a large fraction of fluctuations could still occur in non-perfused and/or immature vessels.
NMR Biomed 2006 Feb
PMID:The role of vessel maturation and vessel functionality in spontaneous fluctuations of T2*-weighted GRE signal within tumors. 1641 Nov 70

Global climate change is associated with a progressive rise in ocean CO(2) concentrations (hypercapnia) and, consequently, a drop in seawater pH. However, a comprehensive picture of the physiological mechanisms affected by chronic CO(2) stress in marine biota is still lacking. Here we present an analysis of protein biosynthesis rates in isolated muscle of the marine invertebrate Sipunculus nudus, a sediment dwelling worm living at various water depths. We followed the incorporation of (13)C-labelled phenylalanine into muscular protein via high-resolution NMR spectroscopy. Protein synthesis decreased by about 60% at a medium pH of 6.70 and a consequently lowered intracellular pH (pHi). The decrease in protein synthesis rates is much stronger than the concomitant suppression of protein degradation (60% versus 10-15%) possibly posing a threat to the cellular homeostasis of structural as well as functional proteins. Considering the progressive rise in ocean CO(2) concentrations, permanent disturbances of cellular protein turnover might seriously affect growth and reproductive performance in many marine organisms with as yet unexplored impacts on species density and composition in marine ecosystems.
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PMID:Effects of environmental hypercapnia on animal physiology: a 13C NMR study of protein synthesis rates in the marine invertebrate Sipunculus nudus. 1675 22

Changes in breathing change the concentration of oxygen and carbon dioxide in arterial blood resulting in changes in cerebral blood flow (CBF). This mechanism can be described by the cerebral vascular response (CVR), which has been shown to be altered in different physiological and pathophysiological states. CBF maps of grey matter (GM) were determined with a pulsed arterial spin labelling technique at 3 T in a group of 19 subjects under baseline conditions, hypoxia, and hypercapnia. Experimental conditions allowed a change in either arterial oxygen (hypoxia) or carbon dioxide (hypercapnia) concentration compared with the baseline, leaving the other variable constant, in order to separate the effects of these two variables. From these results, maps were calculated showing the regional distribution of the CVR to hypoxia and hypercapnia in GM. Maps of CVR to hypoxia showed very high intra-subject variations, with some GM regions exhibiting a positive response and others a negative response. Per 10% decrease in arterial oxygen saturation, there was a statistically significant 7.0 +/- 2.9% (mean +/- SEM) increase in GM-CBF for the group. However, 70% of subjects showed an overall positive CVR (positive responders), and the remaining 30% an overall negative CVR (negative responders). Maps of CVR to hypercapnia showed less intra-subject variation. Per 1 mm Hg increase in partial pressure of end-tidal carbon dioxide, there was a statistically significant 5.8 +/- 0.9% increase in GM-CBF, all subjects showing an overall positive CVR. As the brain is particularly vulnerable to hypoxia, a condition associated with cardiorespiratory diseases, CVR maps may help in the clinic to identify the areas most prone to damage because of a reduced CVR.
NMR Biomed 2008 Jun
PMID:Mapping of the cerebral vascular response to hypoxia and hypercapnia using quantitative perfusion MRI at 3 T. 1785 23

Brain temperature is determined by the interplay between the cerebral metabolic rate of oxygen (CMRO2) and cerebral blood flow (CBF). In this study, single-voxel 1H nuclear MRS, with an accuracy of +/-0.2 degrees C for temperature determination, was used at 3 T to measure human brain temperature during visual stimulation (which increases both CBF and CMRO2) and hypercapnia (which increases CBF only). Visual stimulation had no detectable effect on brain temperature in the parenchyma showing blood oxygenation level dependent activation. Hypercapnia, leading to an increase in the end tidal CO2 by 8 +/- 2 mm Hg above the baseline, caused a short-lasting decrease in brain temperature of 0.30 +/- 0.33 degrees C. These results indicate that increased CBF may be a key factor, bringing about a small decrease in brain temperature during brain activation. However, the increase in CBF is not sufficient to lower brain temperature in the presence of a concomitant increase in endogenous heat production.
NMR Biomed 2008 May
PMID:Assessment of human brain temperature by 1H MRS during visual stimulation and hypercapnia. 1789 24

MRI is a powerful tool for measuring cerebral blood flow (CBF) longitudinally. However, most animal studies require anesthesia, potentially interfering with normal physiology. Isoflurane anesthesia was used here to study CBF regulation during repetitive scanning in rats. MR perfusion images were acquired using FAIR (flow-sensitive alternating inversion recovery) arterial spin labeling, and absolute CBF was calculated. CBF changes in response to a hypoxic (12% O2) and hypercapnic (5% CO2) gas stimulus were monitored. Hypercapnia led to a robust increase in CBF compared with baseline (195.5+/-21.5 vs 123.6+/-17.9 ml/100 g/min), and hypoxia caused a smaller non-significant increase in mean CBF values (145.4+/-13.4 ml/100 g/min). Strikingly, when measurements were repeated 5 days later, CBF was dramatically reduced in hypoxia (93.2+/-8.1 ml/100 g/min) compared with the first imaging session. Without application of the hypoxic and hypercapnic gases during the first MRI, baseline CBF and CBF changes in response to hypoxia at the second MRI were similar to naive rats. Blood gas analyses revealed a slight reduction in arterial oxygenation during the second period of anesthesia compared with the first. These findings indicate that, in isoflurane-anesthetized rats, even a short hypoxic episode can have long-lasting effects on cerebrovascular regulation.
NMR Biomed 2008 Aug
PMID:Longitudinal MRI studies in the isoflurane-anesthetized rat: long-term effects of a short hypoxic episode on regulation of cerebral blood flow as assessed by pulsed arterial spin labelling. 1827 45

Effective myocardial oxygen supply should not be compromised during cardiac surgery as it is essential to avoid circulatory and cardiac dysfunction. Local measurement of myocardial oxygen partial pressure (pO2) was therefore introduced into the operative monitoring of myocardial ischemia. The aim of the present study was to assess whether myocardial oxygen partial pressure correlates with the content of high energy phosphates (HEPs). Seven male rabbits were examined in parallel with measurement of myocardial pO2 by an implanted Clark electrode and 31phosphorus-NMR spectroscopy. The ventilatory management established hyperoxygenation followed by systemic hypoxia with hypercapnia for 20 min. Additionally, analysis of end-expiratory gas composition in combination with blood gas analysis was performed simultaneously, and hemodynamic parameter was recorded. Under hypoxic conditions the cardiovascular system was severely compromised, whereas the myocardial pO2 was only moderately impaired (pO2M 45.0+/-16.0 mm Hg). Immediately before cardiac arrest, low values of arterial and venous pO2 were found (17.6+/-6.0 and 12.9+/-6.1 mm Hg). In contrast to near normal myocardial pO2, HEP content in the myocardium was considerably reduced and inorganic phosphorus was increased. Artificial ventilation leading to systemic hypoxia and eventually circulatory arrest resulted in almost normal myocardial pO2 but severely compromised HEP content. This somewhat unexpected finding requires further clarification, but is in accordance with findings reported previously where regulatory mechanisms have been shown to play a role in the pathophysiology of severe hypoxic conditions such as those for cellular oxygen delivery and demand, P/O coupling and finally control of HEP production facilitating the interaction between respiratory chain and myoglobin oxygen transport.
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PMID:Direct measurement of myocardial oxygen tension and high energy phosphate content under varying ventilatory conditions in rabbits. 1980 83

Acidification of ocean surface waters by anthropogenic carbon dioxide (CO(2)) emissions is a currently developing scenario that warrants a broadening of research foci in the study of acid-base physiology. Recent studies working with environmentally relevant CO(2) levels, indicate that some echinoderms and molluscs reduce metabolic rates, soft tissue growth and calcification during hypercapnic exposure. In contrast to all prior invertebrate species studied so far, growth trials with the cuttlefish Sepia officinalis found no indication of reduced growth or calcification performance during long-term exposure to 0.6 kPa CO(2). It is hypothesized that the differing sensitivities to elevated seawater pCO(2) could be explained by taxa specific differences in acid-base regulatory capacity. In this study, we examined the acid-base regulatory ability of S. officinalis in vivo, using a specially modified cannulation technique as well as (31)P NMR spectroscopy. During acute exposure to 0.6 kPa CO(2), S. officinalis rapidly increased its blood [HCO(3)(-)] to 10.4 mM through active ion-transport processes, and partially compensated the hypercapnia induced respiratory acidosis. A minor decrease in intracellular pH (pH(i)) and stable intracellular phosphagen levels indicated efficient pH(i) regulation. We conclude that S. officinalis is not only an efficient acid-base regulator, but is also able to do so without disturbing metabolic equilibria in characteristic tissues or compromising aerobic capacities. The cuttlefish did not exhibit acute intolerance to hypercapnia that has been hypothesized for more active cephalopod species (squid). Even though blood pH (pHe) remained 0.18 pH units below control values, arterial O(2) saturation was not compromised in S. officinalis because of the comparatively lower pH sensitivity of oxygen binding to its blood pigment. This raises questions concerning the potentially broad range of sensitivity to changes in acid-base status amongst invertebrates, as well as to the underlying mechanistic origins. Further studies are needed to better characterize the connection between acid-base status and animal fitness in various marine species.
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PMID:Acid-base regulatory ability of the cephalopod (Sepia officinalis) in response to environmental hypercapnia. 1983 13


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