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

The most attractive feature of nuclear magnetic resonance spectroscopy (MRS) is the noninvasive and nondestructive measurement of chemical compounds in intact tissues. MRS already has many applications in comparative physiology, usually based on observation of 31P, since levels of phosphorus compounds indicate tissue energy status and are changed during exercise, fatigue, recovery, hypometabolism, anesthesia, hypoxia, hypercapnia, and osmotic and acid stress. Nuclei other than 31P may also be monitored, such as 1H, 13C, 15N, 19F, or 23Na, and applied in biological research. Particularly, 13C-MRS is interesting because it allows the analysis of metabolic pathways in living systems. Applications of MRS in comparative physiology and biochemistry are comprehensively discussed in this review. The main focus is on anaerobic metabolism during hypoxia, ischemia, and exercise. Species as widely different as slime molds, nematodes, frogs, turtles, and ducks have been studied by 31P-MRS. It is not surprising that striking species differences do occur, but many similarities are also observed. Unique is the occurrence of six different phosphagens with different values of Gibbs free energy in polychete worms The presence of a particular phosphagen may be related to the average oxygen tension within the tissues. Phosphagens and their kinases are also discussed in relation to hypercapnia and acid stress. Other topics discussed in this paper are enzyme kinetics, anesthetics, development and growth, parasitism, and the detection of previously unknown compounds.
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PMID:Nuclear magnetic resonance spectroscopy of living systems: applications in comparative physiology. 875 89

The present article is concerned with mechanisms which are responsible for the exaggerated brain damage observed in hyperglycemic animals subjected to transient global or forebrain ischemia. Since hyperglycemia enchances the production of lactate plus H+ during ischemia, it seems likely that aggravation of damage is due to exaggerated intra- and extracellular acidosis. This contention is supported by results showing a detrimental effect of extreme hypercapnia in normoglycemic rats subjected to transient ischemia or to hypoglycemic coma. Enhanced acidosis may exaggerate ischemic damage by one of three mechanisms: (i) accelerating free radical production via H(+)-dependent reactions, some of which are catalyzed by iron released from protein bindings by a lowering of pH, (ii) by perturbing the intracellular signal transduction pathway, leading to changes in gene expression or protein synthesis, or (iii) by activating endonucleases which cause DNA fragmentation. While activation of endonucleases must affect the nucleus, the targets of free radical attack are not known. Microvessels are considered likely targets of such attack in sustained ischemia and in trauma; however, enhanced acidosis is not known to aggravate microvascular dysfunction, or to induce inflammatory responses at the endothelial-blood interface. A more likely target is the mitochondrion. Thus, if the ischemia is of long duration (30 min) hyperglycemia triggers rapidly developing mitochondrial failure. It is speculated that this is because free radicals damage components of the respiratory chain, leading to a secondary deterioration of oxidative phosphorylation.
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PMID:Molecular mechanisms of acidosis-mediated damage. 878 Jul 90

Cystic fibrosis (CF) is a disease characterized mainly by altered exocrine gland function that eventually produces irreversible dysfunction of the pancreas and lungs. The respiratory insufficiency that develops in CF patients in the advanced stages of disease can only be corrected at this time by lung or heart-lung transplantation. We describe our experience with 6 terminal phase CF patients who underwent sequential double lung transplantation (SDLT). Anesthesia was intravenous, with exhaustive hemodynamic and respiratory monitoring. During surgery the most frequently encountered hemodynamic complications were low minute volume, arterial hypotension and irregular heart rate. The main respiratory complications were hypoxemia, hypercapnia and pulmonary edema of the implanted lung, which developed in all cases to varying degrees related to the organ's state of preservation and duration of ischemia. Other complications were the need for extracorporeal circulation in 1 case, oliguria and blood loss requiring multiple transfusions. The most critical moments were at the time of clamping the pulmonary artery, the period after revascularization of the donated lung, and at the start of patient ventilation through the first implanted lung so that the second could be implanted. Although our series is small, it is of interest given the limited Spanish experience with lung transplantation in CF patients, and the good early results obtained, which are similar to those reported for other diseases.
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PMID:[Anesthetic complications in sequential bipulmonary transplantation in patients with cystic fibrosis. Apropos of 6 cases]. 884 34

Oxygen and carbon dioxide are known to be heterogeneously distributed in tissues. Extracellular skeletal muscle tissue pH (pHt) also exhibits a spatial variability in vitro, but this has not been examined in vivo. pHt distributions in resting skeletal muscle and the effect of the dispersion of pHt on ischemia and normoxic hypercarbia was therefore studied in an animal model with a multichannel pH microelectrode. Under resting conditions and spontaneous breathing, local pHt (from all animals, n = 10) was found to vary between 6.96 and 7.68 (range), and 70% of the values were within a pH of 7.00-7.32. In each animal the maximum pHt differences (maximum range between the 6 channels of the microelectrode) found were 0.32 +/- 0.11 pH units (mean +/- SD). During tissue acidosis, induced by ischemia, no significant change in the local pHt differences in each animal was seen. During normoxic hypercarbia a 2-fold increase in pHt variability within each animal was noticed (p < 0.01), which suggests that carbon dioxide and buffering effects of the blood are significant factors for the pHt distribution. The pHt distribution range found is of similar magnitude as previously described in in vitro studies on skeletal muscle. Locally varying pHt levels may be of importance as they will affect cellular H+ extrusion, membrane potential and volume control of different cell populations differently.
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PMID:pH heterogeneity in skeletal muscle extracellular fluid. 892 50

Cerebrovascular carbon dioxide (CO2) reactivity is an important hemodynamic index in cerebrovascular disease. In the present study T2*-weighted magnetic resonance image (T2* WI) was evaluated as a non-invasive method to investigate changes in CO2 reactivity. Fourteen rats were subjected to permanent or, 30 and 90 min of temporary middle cerebral artery occlusion. A series of T2* WIs and diffusion-weighted magnetic resonance images (DWI) was performed hourly under normo- and hypercapnic conditions. Triphenyltetrazolium chloride (TTC) staining of brain sections was obtained at the end of experiment to evaluate ischemic damage. During ischemia, a 4-6% signal increase upon hypercapnia was observed on T2* WI in the non-ischemic hemisphere, while no such reactivity was seen in the putamen and cortex ipsilateral to the MCA occlusion. After reperfusion, CO2 reactivity recovered in the putamen and cortex in the 30 min ischemia group and in the cortex alone of the 90 min ischemia groups. The areas with irreversible CO2 reactivity dysfunction coincidentally revealed no recovery on DWI and lack of TTC staining. The results indicate that T2* WI can be used to monitor changes in CO2 reactivity after various ischemic insults that may indicate tissue viability.
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PMID:T2*-weighted magnetic resonance imaging of cerebrovascular reactivity in rat reversible focal cerebral ischemia. 902 80

We previously have demonstrated that hypocapnia aggravates and hypercapnia protects the immature rat from hypoxic-ischemic brain damage. To ascertain cerebral blood flow (CBF) and metabolic correlates, 7-d postnatal rats were subjected to hypoxia-ischemia during which they were rendered either hypo-(3.5 kPa), normo- (5.1 kPa), or hypercapnic (7.3 kPa) by the inhalation of either 0, 3, or 6% CO2, 8% O2, balance N2. CBF during hypoxia-ischemia was better preserved in the normo- and hypercapnic rat pups; these animals also exhibited a stimulation of cerebral glucose utilization. Brain glucose concentrations were higher and lactate lower in the normo- and hypercapnic animals, indicating that glucose was consumed oxidatively in these groups rather than by anaerobic glycolysis, as apparently occurred in the hypocapnic animals. ATP and phosphocreatine were better preserved in the normo- and hypercapnic rats compared with the hypocapnic animals. Cerebrospinal fluid glutamate, as a reflection of the brain extracellular fluid concentration, was lowest in the hypercapnic rats at 2 h of hypoxia-ischemia. The data indicate that during hypoxia-ischemia in the immature rat, CBF is better preserved during normo- and hypercapnia; the greater oxygen delivery promotes cerebral glucose utilization and oxidative metabolism for optimal maintenance of tissue high energy phosphate reserves. An inhibition of glutamate secretion into the synaptic cleft and its attenuation of N-methyl-D-aspartate receptor activation would further protect the hypercapnic animal from hypoxic-ischemic brain damage.
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PMID:Effect of carbon dioxide on cerebral metabolism during hypoxia-ischemia in the immature rat. 921 33

We have examined how various challenges to brain acid-base homeostasis, resulting in extracellular acidosis, alter N-methyl-D-aspartate (NMDA)-evoked depolarizations in vivo. Repeated stimuli were produced by perfusion of 200 microM NMDA for 2 min through a microdialysis probe implanted into the striatum of halothane anesthetized rats. Hypercapnia reduced NMDA-evoked responses in a concentration-dependent manner, with 7.5 and 15 % CO2 in the breathing mixture reducing the depolarization amplitude to 74 % and 64 % of that of the initial stimuli, respectively. Application of 50 mM NH4+ progressively reduced dialysate pH, and a further acidification was observed when NH4+ was discontinued. Perfusion of NMDA after NH4+ application evoked smaller depolarizations (56 % of the corresponding control, 5 min after NH4+ removal), and this effect persisted for over 1 h. Perfusion of acidic ACSF did not alter the amplitude of NMDA-evoked depolarization, despite changes in dialysate pH confirming that exchange/buffering of acid equivalents took place between the perfusion medium and the surrounding tissue. This negative result probably reflected the remarkable capacity of the brain to buffer H+. Together, these results demonstrate that extracellular acidosis, such as that associated with excessive neuronal activation or ischemia, inhibits NMDA-evoked responses in vivo.
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PMID:Effect of acidotic challenges on local depolarizations evoked by N-methyl-D-aspartate in the rat striatum. 924 22

We investigated the L-arginine-induced, regional cerebral blood flow (rCBF) enhancement after different durations of transient focal cerebral ischemia in the rat to determine if L-arginine increases rCBF after transient focal cerebral ischemia. Focal ischemia (5 minutes and 20 minutes) followed by 90 minutes of reperfusion was induced in a normotensive rat suture-model. Regional cerebral blood flow in both hemispheres was measured by laser-Doppler-flowmetry. Reactivity of rCBF to L-arginine (300 mg/kg) was measured 45 minutes after reperfusion, and hypercapnia 90 minutes after reperfusion. The effect of D-arginine and pretreatment with the nitric oxide (NO) synthase inhibitor N(omega)-nitro-L-arginine (L-NA) (10 mg/kg) was examined in additional groups. Hypercapnia and L-arginine increased rCBF in sham operated controls and on the nonischemic hemispheres. D-arginine did not. Twenty-minute long ischemia significantly reduced the response to L-arginine (control side: 115 +/- 5.9%; ischemic side: 107 +/- 6.1%, n = 7) and hypercapnia, 5 minutes of ischemia did not. N(omega)-nitro-L-arginine pretreatment partly restored the L-arginine-induced rCBF increase. Thus, rCBF increase caused by L-arginine in the reperfusion period was unaffected by 5 minutes of ischemia, but reduced by 20 minutes of ischemia. The restoration after pretreatment with L-NA may be caused by attenuated production of cytotoxic substances, e.g., NO and related compounds.
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PMID:L-arginine-induced regional cerebral blood flow increase is abolished after transient focal cerebral ischemia in the rat. 934 32

Preischemic hyperglycemia or superimposed hypercapnia exaggerates brain damage caused by transient forebrain ischemia. Because high regional levels of brain-derived neurotrophic factor (BDNF) protein correlate with resistance to ischemic damage, we studied the expression of BDNF mRNA using in situ hybridization in rats subjected to 10 minutes of forebrain ischemia under normoglycemic, hyperglycemic, or hypercapnic conditions. Compared with normoglycemic animals, the increase of BDNF mRNA using in situ hybridization in rats subjected to 10 minutes of forebrain ischemia under normoglycemic, or hypercapnic conditions. Compared with normoglycemic animals, the increase of BDNF mRNA in dentate granule cells was attenuated and that in CA3 pyramidal neurons completely prevented in hyperglycemic rats. No ischemia-induced increases of BDNF mRNA levels in the hippocampal formation were detected in hypercapnic animals. Hyperglycemic and hypercapnic rats showed transiently decreased expression of BDNF mRNA levels in the cingulate cortex, which was not observed in normoglycemic animals. The results suggest that suppression of the BDNF gene might contribute to the increased vulnerability of the CA3 region and cingulate cortex in hyperglycemic and hypercapnic animals.
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PMID:Hyperglycemia and hypercapnia suppress BDNF gene expression in vulnerable regions after transient forebrain ischemia in the rat. 939 29

In order to evaluate the relationship between brain oxygen supply and demand (O2 balance) in real time, it is necessary to use a multiparametric monitoring approach. Cerebral blood flow (CBF) is a representative parameter of O2 supply. The extracellular level of K+ is a reliable indicator of O2 demand since more than 60% of the energy consumed by the brain is utilized by active transport processes. Mitochondrial NADH redox state can represent the balance between O2 supply and demand. In order to monitor the brain of experimental animals or patients, we constructed the multiparametric assembly (MPA) and the following parameters were monitored simultaneously and in real time: CBF, CBV, NADH redox state, extracellular K+, DC potential, EEG, tissue temperature and ICP. Animals were exposed to hypoxia, ischemia, hypercapnia, hyperoxia and spreading depression (SD) and the relative changes in CBF and NADH were calculated and found to be significant indicators of brain energy state. Monitoring these two parameters increases the possibility of differentiating between various pathophysiological states. Each added parameter increases the power of diagnosis and determination of the functional state of the brain. Preliminary results obtained in patients monitored in the ICU or in the OR show that the responses to hypercapnia, spreading depression or ischemia are similar to those measured in experimental animals.
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PMID:Multiparametric monitoring of brain oxygen balance under experimental and clinical conditions. 958 30


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