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

In experiments with rats, subjected to single and repeated simultaneous effect of hypercapnia, hypoxia and cooling, contents of pyridine nucleotides (NAD, NADP, NAD-H2 and NADP-H2) and macroergic substances were studied and also the activity of dehydrogenases of the pentose pathway was determined in brain and myocardium. In brain NADP was not practically determined and in heart its content was increased after the first and the second treatments. Content of NADP-H2 was distinctly decreased in both tissues after the single treatment. NAD was not altered in the tissues in all the periods studied. The amount of NAD-H2 was decreased in brain after the single treatment and it was increased in myocardium after the repeated one. In the activity of dehydrogenases marked alterations were not observed. Total macroergic substances were not altered in brain after the single treatment and after the repeated one they were increased mainly due to the ATP increase. In myocardium total macroergic substances were decreased after the both treatments.
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PMID:[Pyridine nucleotide content in the brain and myocardium of rats under combined effect of hypercapnia, hypoxia and cooling]. 1 90

Cholinergic neuronal influences on the function of male rat's hypothalamo-hypophyseal-adrenocortical (HHA) system both during basal and stressful situations (hypoxia and hypercapnia) were investigated using a cholinergic agonist (eserine) and antagonists (atropine, methyl atropine, mecamylamine and 4-(1-naphthylvinyl) pyridine). The results indicate that the transmitter, acetylcholine (ACh), plays a partial role in the regulation of the HHA system. The muscarinic (m) effects of ACh were stimulatory peripherally and inhibitory centrally. The nicotinic (n) effects were stimulatory and possibly affected the HHA system by inhibiting the central m-inputs. The cholinergic regulation of the HHA system for both non-stressed and hypercapnic animals is probably mediated via a common nm-cholinergic pathway.
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PMID:Actions of cholinergic agonist and antagonists on the adrenocortical response of basal, hypoxic, and hypercapnic rats. 19 69

A new in vivo model for studying brain metabolic and haemodynamic oscillatory phenomena during ischaemia is described. In this model acute or chronic occlusion of one or two carotid arteries in the rat is performed. Due to the partial ischaemia developed, oscillations in the level of intramitochondrial pyridine nucleotides (NADH) as well as flavoproteins (Fp) were recorded from the brain by monitoring the fluorescence of these respiratory chain components. The two fluorescent signals (NADH and Fp) were measured by using the time sharing or DC fluorometer/reflectometer. The changes in the reflected light at the excitation wavelengths (366 and 450 nm) were recorded simultaneously. Bilateral carotid artery occlusion induced immediate oscillations (6-9 waves per min) in the mitochondrial redox state as well as in tissue blood volume in both hemispheres. To verify the accuracy of the NADH monitoring system, including the correction technique for haemodynamic and other artifacts, we used the intracarotid artery saline bolus injection approach. The results could be summarized as follows: (1) unilateral carotid artery occlusion resulted in delayed development of oscillations, particularly in the ipsilateral hemisphere; (2) the oscillation phenomenon was reversible if recirculation restarted within 5 min. Occlusion for more than 30 min resulted in irreversible oscillations; (3) the oscillation appearances and intensities were affected by various physiological conditions. Vasoconstriction, induced by hyperoxia, stimulated the oscillations while vasodilation, induced by hypercapnia, depressed them. Anoxia, hypoxia and spreading depression (SD) abolished the oscillations. Glucose injection was not effective.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oscillations of cortical oxidative metabolism and microcirculation in the ischaemic brain. 167 46

An attempt was made to differentiate between autoregulatory coronary vasodilation and changes in vasomotor tone produced by factors extrinsic to the heart. this was done by investigating the relation between local cardiac force and local coronary blood supply. Intracellular NADH redox levels were also measured in order to further elucidate the oxygen balance under various experimental conditions. In anaesthetized open-chest dogs, local blood supply was estimated with the aid of a thermistor probe, and the oxidation-reduction state of mitochondrial pyridine nucleotide was measured by a surface fluorometric technique. Local myocardial contractile force, as well as blood pressure and ECG were recorded simultaneously with the above parameters. The heart was paced at frequencies from 60/min to 300/min with an electronic stimulator, under both normoxic and hypopneic conditions. It was found that elevation of heart rate caused a progressive increase in local blood flow during both normal and hypopneic ventilation. The absolute flow values during hypopnea were approximately double those during normoxia. Heart rates above 120/min or 150/min resulted in a progressive increase in NADH fluorescence. This response to elevated heart rate was less prominent or absent during hypopnea. Contractile force during hypopnea was greater at elevated heart rates than during normal breathing. Data are brought which suggest that whereas vasodilation following increased heart rate is probably due to an autoregulatory mechanism, the marked vasodilatatory effect of hypopnea is related to elevated arterial CO2 levels. It is suggested that hypercapnia markedly stimulates extrinsic coronary vasodilation thereby supplying enough oxygen to maintain contractility even at very high heart rates. Moreover, intracellular O2 concentration (mitochondrial NADH level) is maintained at a normal level despite the greatly increased demand.
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PMID:Effect of coronary vasodilation produced by hypopnea upon regional myocardial oxygen balance. 617 1

Epileptogenic foci were created by topical application of penicillin to the cerebral cortex in 40 paralyzed and artificially ventilated cats receiving halothane anesthesia. The animals were divided into two equal groups to compare primary and secondary foci. The following variables were recorded at normocapnia, hypocapnia, and hypercapnia prior to and during seizure activity: cerebral blood flow (CBF), determined by clearance of xenon 133; cortical redox states, measured by the fluorescence of reduced pyridine nucleotides (PN); brain pH, measured using a lipid-soluble, pH-sensitive fluorescent indicator; and electroencephalograms (EEG). Mean arterial blood pressure, arterial pH, arterial carbon dioxide tension (PaCO2), and arterial oxygen tension (PaO2) were monitored in each animal. All animals had a normal PaCO2-CBF response prior to the creation of a seizure focus, assuring the presence of autoregulation and normal metabolic function. CBF increased equally with seizures in the primary and secondary hemispheres. The relative increase was related to the PaCO2 but approximated 68% at normocapnia. There was an alteration in the PaCO2-CBF response with seizures, but the ability of the cerebral vasculature to constrict and dilate with hypocapnia and hypercapnia was retained. There was no significant difference in the reduced PN signal with variations in PaCO2 prior to seizures, but there was an apparent 10 to 15% fall with seizures. The "equivalent" intracellular pH fell to 6.94 at normocapnia in the primary focus but remained essentially unchanged from the control value of 7.10 in the secondary focus. These differences in pH were consistent with the greater degree of seizure activity observed in the primary focus. We conclude that a nonhypoxic acidosis existed in the primary focus and that changes in CBF were not related to it because the CBF changed equally in both hemispheres.
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PMID:Correlation of intracellular redox states and pH with blood flow in primary and secondary seizure foci. 678 36

Bright-field and dark-field illumination techniques for in vivo measurements of reduced pyridine nucleotide fluorescence were compared in 15 rats during periods of normocapnia, hypocapnia, hypercapnia, and anoxia. Parameters investigated included fluorescence, cortical reflectance, cortical blood flow, and electroencephalograms. In normal brain, with preserved autoregulation, reduced pyridine nucleotide fluorescence was constant through a wide range in Pa(CO2), cortical blood flow, and cerebral blood volume in animals studied using vertical illumination (bright-field) techniques. There was a marked increase in reduced pyridine nucleotide fluorescence at death from anoxia. Artifacts were reduced by monochromators for excitation, emission, and reflected light; low-intensity vertical excitation energy and high-sensitivity recording instrumentation; and a small avascular (123 microns) field. Potential sources of error include photodecomposition, hemoglobin interference from absorption and reflectance, and light scattering. Vertical excitation techniques using a small field appeared to give more reliable and reproducible results than circumferential techniques using a larger field of observation.
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PMID:Comparison of dark-field and bright-field incident illumination for in vivo measurements of reduced pyridine nucleotides. 976 36

Chronic obstructive pulmonary disease (COPD) is a common medical disorder, which causes considerable morbidity and mortality. Given the chronic and symptomatic nature of the disease, the patient is often seen in the physician's office with complaints of dyspnea. However, more than 50% of COPD patients also have sleep complaints characterised by longer latency to falling asleep, more frequent arousals and awakenings, and/or generalised insomnia. Sleep disturbance tends to be more severe with advancing disease and substantially reduces the COPD patients' quality of life. In approaching the COPD patient who complains of insomnia it is important to take a complete sleep history. Having characterised the degree and duration of the problem, medical management of the underlying COPD must first optimise oxygen saturation while minimising the effects of many of the medications used for COPD. While aerosol therapies may be systemically absorbed and contribute to sleep disruption, anticholinergics, such as ipratropium bromide, are the least likely to do so and indeed have been shown to improve sleep quality in this population. Many of the traditional sedatives and hypnotics have been used in the COPD population including benzodiazepines, imidazopyridines, pyrazolopyrimidines and, less commonly, antidepressants and phenothiazines. Clinical trials support the role of numerous agents in treating insomnia in this population but do not always provide reassurance that these therapies can be used safely, particularly in the patient with severe COPD with hypercarbia. Benzodiazepines are among the most commonly employed agents, but case reports and series continue to describe adverse pulmonary events. Although the newer pyridine derivatives also have the potential to worsen pulmonary function, they appear less likely to do so. Data to date are limited with the tricyclic antidepressants and phenothiazines, although they appear to be very well tolerated from a respiratory point of view. Since sleep disturbances are often long-standing and associated with maladaptive behaviours towards sleep, cognitive/behavioural approaches are often useful and are more effective in the long-term than are hypnotics. When prescription of a sedative is to be made, extra caution is required for those patients at increased risk of adverse respiratory effects, such as those with advanced disease and hypercarbia in whom pharmacological therapy is often best avoided. Selection of the various options will depend upon the degree of underlying disease and the patient's specific complaints of insomnia. Finally, it is important to remember that while most hypnotics work in an acute setting, the long-term management will require an integrated approach.
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PMID:Management of insomnia in patients with chronic obstructive pulmonary disease. 1255 60

In experiments on nonlinear male mice the ability of new derivatives of nitrogen-containing heterocyclic compounds to increase the physical working capacity in conditions of hyperthermia, hypothermia and acute normobaric hypoxia and hypercapnia has been investigated. It is established, that pyridine derivative IBHF-11 has more expressed positive action in the said conditions. It provided increase of the working capacity of animals at all kinds of extreme influence, and the value of positive action was comparable, and in conditions of acute normobaric hypoxia and hypercapnia exceeded those at the reference products bemitil and bromantan.
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PMID:[Experimental evaluation of actoprotective activity of nitrogen-containing heterocyclic compounds derivatives in extreme conditions]. 2434 Oct 5

O2 sensing is essential for mammalian homeostasis. Peripheral chemoreceptors such as the carotid body (CB) contain cells with O2-sensitive K(+) channels, which are inhibited by hypoxia to trigger fast adaptive cardiorespiratory reflexes. How variations of O2 tension (PO2) are detected and the mechanisms whereby these changes are conveyed to membrane ion channels have remained elusive. We have studied acute O2 sensing in conditional knockout mice lacking mitochondrial complex I (MCI) genes. We inactivated Ndufs2, which encodes a protein that participates in ubiquinone binding. Ndufs2-null mice lose the hyperventilatory response to hypoxia, although they respond to hypercapnia. Ndufs2-deficient CB cells have normal functions and ATP content but are insensitive to changes in PO2. Our data suggest that chemoreceptor cells have a specialized succinate-dependent metabolism that induces an MCI state during hypoxia, characterized by the production of reactive oxygen species and accumulation of reduced pyridine nucleotides, which signal neighboring K(+) channels.
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PMID:Oxygen Sensing by Arterial Chemoreceptors Depends on Mitochondrial Complex I Signaling. 2653 83