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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess the possibility that climbing to extremely high altitude may result in hypoxic injury to the brain, we performed neuropsychological and physiologic testing on 35 mountaineers before and 1 to 30 days after ascent to altitudes between 5488 and 8848 m, and on 6 subjects before and after simulation in an altitude chamber of a 40-day ascent to 8848 m. Neuropsychological testing revealed a decline in visual long-term memory after ascent as compared with before; of 14 visual items of information on the Wechsler Memory Scale, fewer were recalled after ascent by both the simulated-ascent group (a mean [+/- SD] of 10.14 +/- 1.68 items before, as compared with 7.00 +/- 3.35 items after; P less than 0.05) and the mountaineers (12.33 +/- 1.96 as compared with 11.36 +/- 1.88; P less than 0.05). Verbal long-term memory was also affected, but only in the simulated-ascent group; of a total of 10 words, an average of 8.14 +/- 1.86 were recalled before simulated ascent, but only 6.83 +/- 1.47 afterward (P less than 0.05). On the aphasia screening test, on which normal persons make an average of less than one error in verbal expression, the mountaineers made twice as many aphasic errors after ascent (1.03 +/- 1.10) as before (0.52 +/- 0.80; P less than 0.05). A higher ventilatory response to hypoxia correlated with a reduction in verbal learning (r = -0.88, P less than 0.05) and with poor long-term verbal memory (r = -0.99, P less than 0.01) after ascent. An increase in the number of aphasic errors on the aphasia screening test also correlated with a higher ventilatory response to hypoxia in both the simulated-ascent group (r = 0.94, P less than 0.01) and a subgroup of 11 mountaineers (r = 0.59, P less than 0.05). We conclude that persons with a more vigorous ventilatory response to hypoxia have more residual neurobehavioral impairment after returning to lower elevations. This finding may be explained by poorer oxygenation of the brain despite greater ventilation, perhaps because of a decrease in cerebral blood flow caused by hypocapnia that more than offsets the increase in arterial oxygen saturation.
N Engl J Med 1989 Dec 21
PMID:The cost to the central nervous system of climbing to extremely high altitude. 251 83

We evaluated the topographic distributions of regional cerebral blood flow in 51 normal subjects (mean age 41 years) by the xenon-133 inhalation technique. Forty-five of these subjects were divided by age into young normals less than 30 years old (mean age 24 years), middle-aged normals 30-50 years old (mean age 40 years), and elderly normals greater than 50 years old (mean age 62 years); there were 15 subjects in each group. The distributions of vascular CO2 reactivity to hypocapnia were also evaluated in 20 of the normal subjects (mean age 34 years), including 11 younger normals less than 30 years old (mean age 24 years) and nine older (middle-aged or elderly) normals greater than or equal to 30 years old (mean age 45 years). The hyperfrontal distribution of regional cerebral blood flow observed in the young and middle-aged normals was not observed in the elderly normals. The hyperfrontal distribution of vascular CO2 reactivity observed in the younger normals was absent in the older normals. In addition, the correlation between regional cerebral blood flow and vascular CO2 reactivity observed in the younger normals was disturbed in the older normals. The data show a hyperfrontal distribution of regional cerebral blood flow in normal subjects that diminishes during the fifth and sixth decades, along with a distribution of vascular CO2 reactivity in younger normal subjects that is not homogeneous throughout the frontoparietal regions.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1989 Dec
PMID:Changes in hyperfrontality of cerebral blood flow and carbon dioxide reactivity with age. 251 91

Regional cerebral blood flow was simultaneously determined using the stable xenon computed tomographic and the radioactive microsphere techniques over a wide range of blood flow rates (less than 10-greater than 300 ml/100 g/min) in 12 baboons under conditions of normocapnia, hypocapnia, and hypercapnia. A total of 31 pairs of determinations were made. After anesthetic and surgical preparation of the baboons, cerebral blood flow was repeatedly determined using the stable xenon technique during saturation with 50% xenon in oxygen. Concurrently, cerebral blood flow was determined before and during xenon administration using 15-microns microspheres. In Group 1 (n = 7), xenon and microsphere determinations were made repeatedly during normocapnia. In Group 2 (n = 5), cerebral blood flow was determined using both techniques in each baboon during hypocapnia (PaCO2 = 20 mm Hg), normocapnia (PaCO2 = 40 mm Hg), and hypercapnia (PaCO2 = 60 mm Hg). Xenon and microsphere values in Group 1 were significantly correlated (r = 0.69, p less than 0.01). In Group 2, values from both techniques also correlated closely across all levels of PaCO2 (r = 0.92, p less than 0.001). No significant differences existed between the slopes or y intercepts of the regression lines for either group and the line of identity. Our data indicate that the stable xenon technique yields cerebral blood flow values that correlate well with values determined using radioactive microspheres across a wide range of cerebral blood flow rates.
Stroke 1989 Dec
PMID:Stable xenon versus radiolabeled microsphere cerebral blood flow measurements in baboons. 251 92

The effect of cyclooxygenase inhibition by indomethacin on regional cerebral blood flow (CBF) during hypocapnia induced by hyperventilation and during hypercapnia induced by CO2 inhalation was examined. CBF was measured in 27 anesthetized, ventilated piglets (2-8 d) using microspheres in control and indomethacin treated animals (5 mg/kg) after hyperventilation or inhalation of 6% CO2. In the control group (n = 6), CBF decreased significantly (p less than 0.05) to all regions of the brain after hyperventilation with a 32% decrease in the cerebral cortex. In the indomethacin-treated group (n = 6), blood flow significantly decreased by 35 to 49% in all regions of the brain, except the cerebral white matter, during normocapnia with no further decrease in flow during subsequent hypocapnia. Although CBF increased significantly after indomethacin treatment during hypercapnia the response was markedly attenuated with blood flow to the cerebral gray matter, hippocampus and pons rising only 42, 25, and 42% in contrast to 108, 75, and 225% in the control group. Since indomethacin decreased resting CBF, unilateral sympathetic nerve stimulation at 15 Hz was used to test the specificity of indomethacin on hypocapnic vasoconstriction (n = 5). Unilateral sympathetic nerve stimulation caused a further statistically significant decrease in CBF on the stimulated side after hyperventilation with indomethacin (12%), which was comparable to that which occurred during normocapnia (16%). The data demonstrate that indomethacin attenuates the cerebrovascular sensitivity to both increases and decreases in CO2/H+ and implicate a possible role for vasoactive prostanoids in mediating the response of CBF to fluctuations in CO2 in newborn piglets.
Pediatr Res 1989 Dec
PMID:Effect of indomethacin on the regulation of cerebral blood flow during respiratory alkalosis in newborn piglets. 251 48

The normal relationship between arterial and venous acid-base composition is altered in hemodynamic compromise. Because the mechanism of this phenomenon remains conjectural, we have studied the acid-base profile and the end-tidal PCO2 of dogs with normal or depressed hemodynamic status in association with either normal ventilation or respiratory arrest. Reductions in cardiac output widened the arteriovenous difference in PCO2 and pH, largely due to arterial hypocapnia but also to venous hypercapnia, and decreased end-tidal PCO2. The arteriovenous gradients for PCO2 and pH of -5.1 +/- 0.4 mmHg and 0.02 +/- 0.01, respectively, during normal hemodynamics widened progressively with graded circulatory compromise reaching values of -30 +/- 5 mmHg for PCO2 (P less than 0.01) and 0.35 +/- 0.05 for pH (P less than 0.01) during cardiac arrest. Development of this disparity, however, required the presence of substantial pulmonary ventilation, since respiratory arrest obliterated the arteriovenous gradients. We propose that arterial hypocapnia, which occurs in association with reduced CO2 excretion, is secondary to an increased ventilation-to-perfusion ratio that reflects a disproportionate decrement in cardiac output. Venous hypercapnia, on the other hand, results from a greater than normal addition of CO2 per unit of blood traversing the capillaries of the hypoperfused peripheral tissues and a diminished CO2 excretion because of pulmonary hypoperfusion. Titration of bicarbonate stores by ongoing production of organic acids might also contribute to venous hypercapnia.
Am J Physiol 1989 Dec
PMID:Arteriovenous acid-base disparity in circulatory failure: studies on mechanism. 251 27

The aim of this study was to determine whether hypocapnia causes bronchoconstriction by releasing tachykinins (TKs) from C-afferent nerves in airways. Hypocapnia-induced bronchoconstriction (HIBC) was induced in anesthetized vagotomized guina pigs by ventilating lungs with a heated humidified hypocapnic gas mixture for 15 min after sudden circulatory arrest. The intensity of bronchoconstriction was assessed by calculating changes in dynamic compliance and by measuring the relaxation lung volume at the completion of experiments. Visualization of the airways by tantalum bronchography showed constriction of segmental bronchi with relative sparing of more proximal airways. Hypocapnia-induced bronchoconstriction was prevented by prior administration of salbutamol aerosol. Three experimental interventions were used to investigate the role of TKs in HIBC: 1) repeated capsaicin injections to deplete airway sensory nerves of TKs, 2) treatment with phosphoramidon, an inhibitor of enkephalinase, the main enzyme responsible for TK inactivation, and 3) topical airway anesthesia. Capsaicin pretreatment markedly attenuated the hypocapnia-induced changes in dynamic compliance (P less than 0.0005) and relaxation lung volume (P less than 0.0002), whereas phosphoramidon augmented these changes (P less than 0.02, P less than 0.03, respectively). Topical anesthesia of airways with lignocaine postponed the onset of bronchoconstriction, whereas the longer-acting, more lipid-soluble local anesthetic, bupivacaine, almost completely prevented HIBC. We conclude that, in the guinea pig lung, HIBC is mediated by TKs that are released after the activation of bronchial axonal reflexes.
J Appl Physiol (1985) 1989 Dec
PMID:Tachykinins mediate hypocapnia-induced bronchoconstriction in guinea pigs. 251 77

Cerebral computed tomography (CT) was performed before and after right-sided electroconvulsive therapy (ECT) in 40 patients aged 26-87 years with major affective disorders. Nine patients with a concomitant definite or possible non-acute organic brain disorder were included. Several patients had long seizure durations, maximum 6.5 min, caused by hyperventilation-induced hypocapnia. Twenty-nine patients received at least 16 treatments (maximum 46). No CT changes occurred following ECT. A questionable dilatation of the left temporal horn in a 69-year-old hypertensive man who recovered completely without side effects after 3 ECT sessions was probably unrelated to the ECT. Provided sufficient oxygenation, even relatively long ECT series and seizures lasting several minutes do not cause any brain damage visible on CT.
Acta Psychiatr Scand 1989 Dec
PMID:Electroconvulsive therapy and cerebral computed tomography. A prospective study. 261 80

The first 5 days of treatment of 98 patients with acute disorders of the cerebral blood circulation revealed hypophosphatemia and related reduction of the level of 2, 3 DPG, ATP in the erythrocytes. The causes of hypophosphatemia in these patients were absence of entrance of phosphorus to the body, its loss with the urine and gastrointestinal contents and hypocapnia. The possible ways of correction of these disorders are discussed.
Vrach Delo 1989 Dec
PMID:[Characteristics of phosphorus metabolism in patients with acute disorders of cerebral circulation]. 262 71

Previously we reported that activities of certain chemoreflex sensitive cervical preganglionic sympathetic nerves (PSN) were augmented by carotid chemoreceptor stimulation independently of phrenic nerve (PN) activity in the cat. To test the hypothesis that the PSN carotid chemoreflex could have been mediated by the expiratory neuron activity, we studied the relationship between PSN, internal intercostal expiratory nerve (IICEN) and PN activities in vagotomized, anesthetized, paralysed and artificially ventilated cats. We made the following observations. (1) Hypoxia often inhibited IICEN activity while the PN and PSN activities were stimulated. (2) during normoxia, cyanide strongly stimulated PN and PSN discharges but only moderately IICEN discharges. (3) Hyperventilation hypocapnia suppressed or eliminated PSN and PN rhythms and activities, but made some IICEN fibers fire continuously. (4) During hypocapnic apnea, cyanide stimulated PSN activity before PN and IICEN activities, although some PSN fibers were stimulated simultaneously with PN fibers. Accordingly we conclude that IICEN activity does not significantly influence chemoreflex stimulation of PSN activity and that a direct chemoreflex stimulation of IICEN is minimal in the cat. Thus, the chemoreflex PSN response is in part independent of respiratory chemoreflex pathways.
J Auton Nerv Syst 1989 Dec 30
PMID:Sympathetic peripheral chemoreflex is independent of expiratory output neurons in the cat. 263 35

The sensation of disrupted sleep following ascent to high altitude is associated with frequent awakenings, which may reflect sleep disruption due to respiratory dysrhythmia consisting typically of monotonously repetitive periodic breathing. This seems to arise from the combined effects of hypocapnia, which leads to suppression of respiratory effort in NREM sleep, and hypoxia, which stimulates termination of apnea and hyperpnea with consequent hypocapnia, leading to perpetuation of periodicity. Sleep disruption and periodic breathing decrease with time at altitude but may also be considerably reduced by pretreatment with acetazolamide, which may act by correction of alkalosis or through some other mechanism. In long-term residents of high altitude less distinctive, undulating respiratory dysrhythmias are described with unstable and decreased arterial oxygenation.
Clin Chest Med 1985 Dec
PMID:Sleep at high altitude. 293 58


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