Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pyrenebutyric acid (PBA), the intracellular fluorescent indicator, was used to measure the partial pressure of oxygen (PO2) in the exposed cerebral cortex of anesthetized cats at hyperbaric pressures up to 4 ATA. The validity of the PBA method for determining cortical PO2 was confirmed by demonstrating a precise linear relationship between Pao2 and the reciprocal of the fluorescence of PBA in the brain as the cat was ventilated with sequentially greater oxygen pressures while holding the Paco2 nearly constant. Increments in the Paco2 while the Pao2 was maintained at a high (about 2,000 Torr) level resulted in stepwise greater oxygen tensions in the brain until an oxygenation end point was reached with a Paco2 averaging near 122 Torr. Greater amounts of CO2 did not bring the mean PO2 of the brain, 1,017 Torr, closer to 2,000 Torr. During normocapnia the cortical PO2 was greater than the PO2 of cerebral venous blood collected from the superior sagittal sinus; however, in hypercapnia (PaCO greater than 45 Torr), the PO2 of the sinus blood exceeded the value determined in the cortex. This latter observation is taken as evidence for convective shunting of cerebral arterial blood to venous circulation when hypercapnia is present.
 ...
PMID:Oxygen tensions measured in cat cerebral cortex under hyperbaric conditions. 45 30

The ventilatory response of four subjects was measured at rest and various intensities of exercise. Experiments were conducted in a dry pressure chamber (1) at 1 ATA and 4 ATA with the subjects breathing from a low-resistance mouthpiece, and (2) at ATA with the subjects breathing from open-circuit breathing apparatus (Royal Naval Swimmers' Air Breathing Apparatus). At 4 ATA there was significant hypoventilation and hypercapnia, together with an increased tidal volume and lower respiratory frequency. The use of the breathing apparatus tended to amplify these changes in ventilatory response. In addition, the extent of hypercapnia at 4 ATA was related to the exercise intensity. When subjects breathed from a low-resistance mouthpiece, oxygen uptake was significantly greater at 4 ATA than at the surface for the same ergometric work load, but when they breathed from the breathing apparatus, the increase in oxygen uptake was not significant in comparison to surface values. At 4 ATA bradycardia was evident at all levels of exercise but was not affected significantly by the presence of the breathing apparatus.
 ...
PMID:Effects of increased O2-N2 pressure and breathing apparatus on respiratory function. 96 25

Because the pulmonary endothelium is sensitive to O2-induced damage, we studied in vivo angiotensin-converting enzyme (ACE) activity in the lungs of 14 catheterized unanesthetized dogs exposed either to air or continuous 100% O2 at 1 ATA. For 5 days, or until the dog died, we measured physiological variables and lung ACE activity. The metabolic data were analyzed with a model that accounted for the effect of changes in cardiac output. Nine dogs breathing O2 lived 88 +/- 21.8 (SD) h and except for blood O2 tensions were indistinguishible from controls until development of a terminal response lasting only a few hours. Hemodynamic instability preceded a precipitous terminal change in blood gas tensions which resulted in impairment of arterial oxygenation, hypercapnia, and acidosis. Plasma renin activity increased. The metabolic capacity of the pulmonary endothelium of O2-exposed animals decreased with time so that after 96 h it was 50% of the control. That of five control animals did not change with time. Thus changes in lung ACE activity preceded alterations in hemodynamics or gas exchange, and the contributions of each are discussed.
 ...
PMID:Pulmonary oxygen toxicity in awake dogs: metabolic and physiological effects. 609 73

To define the effects of hypoxia adaptation on tolerance to a useful range of O2 pressures, groups of 20 or more rats were exposed to O2 at 1.0, 1.5, 2.0, 3.0, and 4.0 ATA before and after adaptation to an inspired PO2 (PIO2) of 71 Torr for 5 days. Effects of acute hypercapnia on O2 tolerance in hypoxia-adapted rats were also determined by exposing rats to the same O2 pressures with an inspired PCO2 (PICO2) of 60 Torr. In nonadapted rats exposed to O2 at 1.0, 1.5, 2.0, 3.0, and 4.0 ATA, 50% mortality (LD50) occurred at 76.4, 26.8, 17.4, 9.0, and 6.4 h, respectively. LD50 values in O2-CO2 at the same pressures were 77.1, 24.5, 15.6, 3.4, and 1.7 h. Hypoxia-adapted rats had only 20% mortality in O2 at 1.0 ATA, and survivors were killed at 336 h. In O2-CO2 at 1.0 ATA, mortality was 85% with an LD50 at 282 h. LD50 values in hypoxia-adapted rats at O2 pressures of 1.5, 2.0, 3.0, and 4.0 ATA were 63.1, 22.5, 7.9, and 3.8 h, respectively. Corresponding values in O2-CO2 were 29.5, 18.7, 4.9, and 1.9 h. Exposure to O2 at 4.0 ATA caused nearly immediate onset of violent convulsions in hypoxia-adapted rats compared with a 50% incidence of convulsions at 3.2 h in nonadapted rats. These data indicate that hypoxia-adaptation increases pulmonary O2 tolerance but reduces central nervous system (CNS) O2 tolerance. However, the enhanced pulmonary O2 tolerance in hypoxia-adapted rats is greatly diminished when acute hypercapnia is superimposed on O2 exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Interacting effects of hypoxia adaptation and acute hypercapnia on oxygen tolerance in rats. 632 81

Five male volunteers served as subjects for exercise studies during three dives to pressures of 47 and 66 ATA while breathing gases containing 0.5 ATA PO2 and varying amounts of N2 and He. The inspired gas density ranged from 1.1 g/l (BTPS) at the surface to 17.1 g/l at the highest pressure. Dyspnea at rest and during exercise was evident in all divers and was predominantly inspiratory in nature. Despite the dyspnea, divers were able to perform work requiring an O2 consumption larger than 2 l/min STPD at each depth. Compared with surface measurements, moderate work at depth was associated with alveolar hypoventilation, arterial hypercapnia, very large physiological dead space, and higher levels of arterial lactate and signs of simultaneous respiratory and metabolic acidosis. The increase of ventilation that accompanies the onset of acidemia at the surface was not present at depth. Acidemia at depth was more severe, and its onset occurred at lesser work rates than at 1 ATA. No large differences could be ascertained when a variety of responses obtained with inspired gas having a density of 7.9 g/l at 47 ATA were compared with those obtained with an inspired gas density of 17.1 g/l at 66 ATA. It appears that the major impact of the environment on the physiological responses to work was almost fully manifested at a pressure of 47 ATA with a He-O2 gas mixture. It is cautioned that maximum work tolerance may be an insufficient assessment of the physiological condition of a diver exposed to these high pressures.
 ...
PMID:Physiological responses to exercise at 47 and 66 ATA. 643 26

The study was undertaken to determine the changes in plasma catecholamine levels in response to the combined stresses of cool water immersion and hyperbaric exposure. Plasma catecholamines were measured in seven thermally unprotected trained male U.S. Navy divers immersed in water at 25 degrees C and 35 degrees C at 1 ATA and 4 ATA. All measurements were made prior to any decompression procedures. Plasma norepinephrine (NE) levels were higher during cool immersions at both 1 ATA and 4 ATA. Hyperbaric exposure during warm immersion was associated with a small but significant increase in plasma NE levels. Hyperbaric exposure during cool immersion was associated with an increase in plasma NE levels, but this increase was not statistically significant. Hyperbaric exposure in both the cool and warm immersions was associated with a moderate degree of hypoventilation and carbon dioxide retention. Plasma NE levels reflect the overall stress imposed on an individual. This study indicates that plasma NE levels may be too variable to be useful as indicators of specific stress.
 ...
PMID:Catecholamine levels in divers subjected to stresses of immersion and hyperbaric exposure. 661 1

Groups of 16-52 normal or CO2-adapted rats were exposed top 100% O2 or to O2 with 60 Torr PICO2 (O2-CO2) at pressures of 1.0, 1.5, 2.0, 3.0, and 4.0 ATA. Exposure durations for 50% mortality (LD50) in normal rats at 4.0, 3.0, 2.0, 1.5, and 1.0 ATA O2 were 6.3, 9.3, 17.2, 27.4, and 76.1 h, respectively. Corresponding LD50 values for normal rats exposed to O2-CO2 were 2.0, 2.9, 16.3, 24.8, and 74.8 h. Survival times of CO2-adapted rats exposed to O2 were nearly identical to those of normal rats. LD50 values for CO2-adapted rat exposed to O2-CO2 were 4.1, 7.5, 17.9, 23.6, and 65.4 h, respectively. These data confirm acceleration of O2 intoxication by acute hypercapnia at 4.0 and 3.0 ATA, but they show less prominent effects at 2.0, 1.5, and 1.0 ATA. Hypercapnia adaptation clearly has a protective effect in rats exposed to O2-CO2 at 4.0 and 3.0 ATA. At 2.0, 1.5, and 1.0 ATA, where acute hypercapnia has less effect, the effects of CO2 adaptation are also less prominent. The observed changes in oxygen tolerance can be explained by cerebral vasodilation with increased brain oxygenation in acute hypercapnia and by significant amelioration of this response during chronic hypercapnia.
 ...
PMID:Effects of acute and chronic hypercapnia on oxygen tolerance in rats. 678 62

In a study of respiratory function under hyperbaric conditions one diver (TM) was found to have an extremely low ventilatory response to exercise with a postinspiratory pause typical of certain "carbon dioxide retaining divers." The respiratory function of diver TM is compared with that of four other divers having a normal ventilatory response. In exercise at 4 ATA hypoventilation and hypercapnia were potentiated to a greater extent in TM than in the other divers. Diver TM maintained a ventilation 25%-50% lower than that of the other divers and whereas their end-tidal Pco2 remained within reasonable limits (Pco2 less than or equal to 55 mmHg), that of TM rose to levels considered hazardous (Pco2 less than or equal to 76 mmHg). Results suggest that when a diver exhibits a postinspiratory pause in the breathing cycle, mixing of alveolar and dead space gas takes place. As a result, physiological dead space calculated according to the Bohr formula is unusually small. As alveolar Pco2 will rise during postinspiratory pause, mean arterial Pco2 may be lower than end-tidal Pco2. Such a respiratory pattern has a greater ventilatory efficiency than normal and may afford the diver some protection, albeit incomplete, from hypercapnia.
 ...
PMID:Effects of CO2 insensitivity and respiratory pattern on respiration in divers. 679 30

Transcutaneous PO2 and PCO2 measurements and estimates of skin respiration were monitored at different levels of inspired PO2 in 20 healthy adults during the first 4 days of the tuberculin reaction, a convenient model of acute inflammation. Hyperoxia at 1 and 2 ATA significantly increased transcutaneous PO2 levels in undisturbed and in inflamed skin but did not fully correct the relative hypoxia at the site of inflammation. Hypercapnia was reduced with O2 breathing at 2 ATA. The apparent rate of O2 consumption at the reaction site was raised during hyperoxia, most prominently at 2 ATA. The most intense reactions showed a central relative slowing of laser-Doppler blood flow indicative of microcirculatory impairment. The extent of the relative hypoxia and hypercapnia was greatest in these strongest reactions. The density of lymphocytes and monocytes in biopsies of 48-h reactions was loosely related to the corresponding transcutaneous PO2 measurements. The present study provides evidence that diffusion barriers, in addition to increased local respiration, can contribute to the apparent hypoxia and hypercapnia of this inflammatory model.
 ...
PMID:Effect of hyperoxia at 1 and 2 ATA on hypoxia and hypercapnia in human skin during experimental inflammation. 800 26