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

Studies were performed to determine the pH relationships among the extracellular, intracellular, and arterial blood compartments in the brain in vivo. Resolution of the extracellular monophosphate resonance peak from the intracellular peak in 31P nuclear magnetic resonance (NMR) spectra of sheep brain with the calvarium intact enabled pH measurement in these respective compartments. Sheep were then subjected to both hyper- and hypoventilation, which resulted in a wide range of arterial PCO2 and pH values. Linear regression analysis of pH in these compartments yielded slopes of 0.56 +/- 0.05 for extracellular pH (pHe) vs. arterial pH, 0.43 +/- 0.078 for intracellular pH (pHi) vs. pHe, and 0.23 +/- 0.056 for pHi vs. arterial pH. These data indicate that CO2 buffering capacity is different and decreases from the intracellular to extracellular to arterial blood compartments. Separation of the extracellular space from the vascular space may be a function of the blood-brain barrier, which contributes to the buffering capability of the extracellular compartment. A marked decrease in the pH gradient between the extracellular and intracellular space occurs during hypercarbia and may influence mechanisms of central respiratory control.
J Appl Physiol (1985) 1991 Dec
PMID:Intra- and extracellular pH of the brain in vivo studied by 31P-NMR during hyper- and hypocapnia. 177 8

To determine whether the intensity of dyspnea at a given level of respiratory motor output differs between bronchoconstriction and the presence of an external resistance, we compared the sensation of difficulty in breathing during isocapnic voluntary hyperventilation in six normal subjects. An external resistance of 1.9 cmH2O.1-1.s was applied during both inspiration and expiration. To induce bronchoconstriction, histamine aerosol (5 mg/ml) was inhaled until airway resistance (Raw) increased to a level approximately equal to the subject's control Raw plus the added external resistance. To clarify the role of vagal afferents on the genesis of dyspnea during both forms of obstruction to airflow, the effect of airway anesthesia by lidocaine aerosol inhalation was also examined after histamine and during external resistive loading. The sensation of difficulty in breathing was rated at 30-s intervals on a visual analog scale during isocapnic voluntary hyperpnea, in which the subjects were asked to copy an oscilloscope volume trace obtained previously during progressive hypercapnia. Histamine inhalation significantly increased the intensity of the dyspneic sensation over the equivalent external resistive load at the same levels of ventilation and occlusion pressure during voluntary hyperpnea. Inhaled lidocaine decreased the sensation of dyspnea during bronchoconstriction with no change in Raw, but it did not significantly change the sensation during external resistive loading. These results suggest that afferent vagal activity plays a role in the genesis of dyspnea during bronchoconstriction.
J Appl Physiol (1985) 1991 Dec
PMID:Effects of bronchoconstriction and external resistive loading on the sensation of dyspnea. 177 11

Phrenic and cervical sympathetic nerve responses to hypercapnia were examined before and after anesthesia in twelve midcollicularly decerebrated, vagotomized, glomectomized, paralyzed and ventilated cats. We measured responses of integrated phrenic and cervical sympathetic nerve activities to increases in end-tidal PCO2 (PETCO2) from apneic threshold to approximately 30 torr above threshold. All cats were studied first in the unanesthetized state. Six cats were then restudied after a quarter of a usual dose of chloralose/urethane (10 mg/kg and 62.5 mg/kg, respectively) and then after half the usual dose of chloralose/urethane (20 mg/kg and 125 mg/kg). The other six animals were restudied after quarter of a standard dose of pentobarbital (9 mg/kg), after half the standard dose (18 mg/kg) and then after the full (35 mg/kg) dose. Both anesthetic agents led to significant increases in apneic thresholds for both phrenic and sympathetic nerve activities. These agents also caused dose-dependent decreases in peak, tonic and respiratory-related sympathetic nerve activities. Peak (tidal) phrenic nerve activities, in comparison, were much less affected by the anesthetic agents. CO2 response curves showed that both of these anesthetic agents depressed, at any given level of PETCO2, respiratory-related sympathetic nerve responses more than the responses found in the phrenic nerve. We conclude that the relations between peak, tonic (i.e. between phasic bursts) and respiratory-related sympathetic nerve activities and phrenic nerve activity can be altered by anesthesia.
J Auton Nerv Syst 1991 Dec
PMID:Anesthesia affects respiratory and sympathetic nerve activities differentially. 178 59

The pathogenesis of vertebrobasilar ischemia (VBI) is still uncertain. Embolism and systemic hypotension have been discussed as possible causes. We evaluated the basilar arteries of 35 VBI-patients by transcranial Doppler-sonography at rest and under hypercapnic conditions and compared these findings with the basilar flow velocities in 10 healthy volunteers matched by age. We found no difference between the controls and the VBI-patients for the basilar flow velocities at rest. Under hypercapnia (end-tidal CO2-concentration 8.5%), the basilar blood flow velocities in the healthy controls increased by an average of 53.0% but only by 32.3% in the VBI-patients (p less than 0.005). The reduction of CO2 dependent vasomotor reactivity was observed in all VBI-patients, except in patients with infarction in the posterior cerebral artery area, possibly indicating a different pathogenic mechanism of stroke. The results in all other patients revealed no obvious correlation to the clinical course or angiographic or dopplersonographic findings. As CO2 dependent vasomotor reactivity and brain perfusion pressure dependent cerebral autoregulation have similar mechanisms, we conclude that systemic hypotension might play an important part in VBI.
Acta Neurol Scand 1991 Dec
PMID:Doppler CO2-test in patients with vertebrobasilar ischemia. 179 55

We performed inhalation anesthetic therapy in an attempt to produce improvement in cause of life-threatening asthma, which were standard pharmacological therapy. We analysed the results obtained in 6 cases given inhalation anesthetic therapy (4 cases were treated with halothane and 2 cases with enflurane). The following observations were made: 1) The criteria for starting inhalation anesthetic therapy were persistent hypoxycemia or hypercapnia, persistently high inspiratory intra-airway pressure, clinical exhaustion and bronchial toilet with bronchofiberscope. 2) We treated the patients with halothane concentrations of between 1.0 and 2.0% and enflurane concentrations of between 1.0 to 4.2%. 3) No major complications were observed in inhalation anesthetic therapy.
Arerugi 1991 Dec
PMID:[Halothane or enflurane treatment in life-threatening asthma]. 179 65

To learn if chemoreceptor control of breathing is abnormal in babies whose mothers took narcotics, cocaine, or both drugs during pregnancy, we performed hypoxia and hypercapnia challenges on 28 babies (greater than or equal to 36 weeks gestation). Six babies were exposed to narcotics, six to cocaine, nine to both drugs, and seven babies were controls. Studies were done at 3 and 8 weeks and 3 and 5 months of age. Gestational ages were similar, but birth weight was lower in the cocaine group. Respiratory rate was higher in both groups of cocaine-exposed babies at 3 weeks. End-tidal partial pressure of CO2 (PCO2) was decreased and partial pressure of O2 (PO2) increased at 3 and 8 weeks in babies exposed to narcotics plus cocaine. At 3 weeks, babies exposed to narcotics plus cocaine had a shift to the left in CO2 response with a normal slope; at 8 weeks, both intercept and slope were decreased. Responses to hypoxia were similar among the four groups. Babies exposed to narcotics plus cocaine before birth have abnormalities in control of breathing in the first months after birth.
Early Hum Dev 1991 Dec
PMID:Control of breathing in babies of narcotic- and cocaine-abusing mothers. 180 70

A 18-year-old boy was admitted to hospital in an unconsciousness state as a result of taking a large dose of several psychotropic drugs simultaneously in an attempt to commit suicide. Blood studies revealed hypoxia (55.7 mmHg) and hypercapnia (59.7 mmHg). Hypoxia (74.3 mmHg) and hypercapnia (46.7 mmHg) were still present on the fourth day after admission, and the patient was becoming lethargic. Reduced vascular markings in the right upper lung field on chest roentgenogram in spite of hypercapnia suggested that the persistent hypoxia was the result of a pulmonary embolism. This diagnosis was supported by a perfusion defect on 99mTc-MAA scintigram and arterial obstruction in right pulmonary angiogram. Hypercapnia is an unusual finding in pulmonary embolism, and in this case was considered due to depression of respiration by psychotropic drugs.
Nihon Kyobu Shikkan Gakkai Zasshi 1991 Dec
PMID:[A case of pulmonary embolism following acute respiratory failure with hypercapnia]. 180 86

To investigate the factors that modulate exercise performance at extreme altitude, the role of the following variables was analyzed in 16 climbers: 1) ventilatory response to chemical stimuli (hypoxia and hypercapnia); and, 2) maximum exercise performance while breathing room air and during acute hypoxia (F1O2, 0.11). Seven climbers (elite climbers, AE) had previously ascended to 8,000 m or more above sea level, and 9 (A) had never achieved such extreme altitude. Then healthy sedentary subjects (C) of similar age (31.1 +/- 6.0 SD years) were used as control group. Elite climbers showed higher ventilatory responses to both transient hypoxia (-0.49 +/- 0.13 L x min-1 x %-1) (p less than 0.05) and progressive hypoxia (-0.47 +/- 0.13 L x min-1 x %-1) than C (-0.33 +/- 0.14 and -0.30 +/- 0.15 L x min-1 x %-1, respectively). By contrast, no differences were observed between the two groups of climbers. The ventilatory response to hypercapnia was higher in AE (3.04 +/- 1.03 L x min-1 mmHg-1) compared to A (1.85 +/- 0.73 L x min-1 mmHg-1) (p less than 0.05) but similar to that observed in C. Breathing 11% O2, maximum workload and oxyhemoglobin desaturation during maximum exercise were similar in both groups of climbers. Additionally, the ventilatory response to hypoxia did not correlate with maximum workload (F1O2, 0.11), maximal ventilation during exercise (F1O2, 0.11), nor with the altitude score. The present study supports previous reports that inform about the role of the ventilatory response to hypoxia in the exercise performance at high altitude.(ABSTRACT TRUNCATED AT 250 WORDS)
Rev Esp Fisiol 1991 Dec
PMID:[Respiratory response to chemical stimuli and exercise capacity under conditions of acute hypoxia in elite mountain climbers]. 181 41

Exposure to hypercapnia (8.2 +/- 0.7% CO2) for 3 weeks failed to change the morphometric characteristics (mean cell area, nuclear, mitochondria and vesicle volume density) of the recurrent laryngeal nerve paraganglia of the rat. Moreover, this treatment had no effect on the dopamine and noradrenaline content of the superior and recurrent laryngeal nerves. The results are in contrast to what is found after exposure to hypoxia which increases the dopamine content and the cell area of the paraganglia and indicate that the mechanisms of the paraganglia in long-term hypoxia and hypercapnia differ.
Neurosci Lett 1991 Dec 16
PMID:Laryngeal nerve paraganglia of the rat are morphologically and biochemically unchanged by long-term hypercapnia. 181 49

Dynamic cerebral blood flow (CBF) studies using acetazolamide or hypercapnia as a vasodilatory challenge have attempted to evaluate intracranial hemodynamics. We report two patients with asymptomatic internal carotid artery occlusion in whom the vasodilatory stimulus was a single oral dose of antihypertensive medication (prazosin hydrochloride or enalapril maleate). In both patients, changes in regional CBF occurred that were larger than those seen in nine normal controls. One patient experienced an improvement in regional CBF with a reduction in probe pair asymmetry. In the other patient, who had bilateral carotid artery disease, a decrease in regional CBF in all 16 probes (mean decrease 12 percent) and an accentuation of the predose asymmetry were observed. Both patients remained asymptomatic throughout the study. Assessing these effects on cerebral circulation may help identify patients at risk for iatrogenic focal cerebral ischemia and provide information regarding the functional status of the cerebral vasculature.
DICP 1991 Dec
PMID:Assessing the effects of antihypertensive medication on cerebral blood flow: demonstration in internal carotid artery occlusion. 181 20


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