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Hogan, M. C., D. E. Bebout, P. D. Wagner y J. B. West. "Maximal O2 uptake of in situ dog muscle during acute hypoxemia with constant perfusion". Journal of Applied Physiology 69, n.º 2 (1 de agosto de 1990): 570–76. http://dx.doi.org/10.1152/jappl.1990.69.2.570.
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We investigated the relationships among maximal O2 uptake (VO2max), effluent venous PO2 (PvO2), and calculated mean capillary PO2 (PCO2) in isolated dog gastrocnemius in situ as arterial PO2 (PaO2) was progressively reduced with muscle blood flow held constant. The hypothesis that VO2max is determined in part by peripheral tissue O2 diffusion predicts proportional declines in VO2max and PCO2 if the diffusing capacity of the muscle remains constant. The inspired O2 fraction was altered in each of six dogs to produce four different levels of PaO2 [22 +/- 2, 29 +/- 1, 38 +/- 1, and 79 +/- 4 (SE) Torr]. Muscle blood flow, with the circulation isolated, was held constant at 122 +/- 15 ml.100 g-1.min-1 while the muscle worked maximally (isometric twitches at 5-7 Hz) at each of the four different values of PaO2. Arterial and venous samples were taken to measure lactate, pH, PO2, PCO2, and muscle VO2. PCO2 was calculated using Fick's law of diffusion and a Bohr integration procedure. VO2max fell progressively (P less than 0.01) with decreasing PaO2. The decline in VO2max was proportional (R = 0.99) to the fall in both muscle PvO2 and calculated PCO2 while the calculated muscle diffusing capacity was not different among the four conditions. Fatigue developed more rapidly with lower PaO2, although lactate output from the muscle was not different among conditions. These results are consistent with the hypothesis that resistance to O2 diffusion in the peripheral tissue may be a principal determinant of VO2max.
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Franchini, K. G., I. A. Cestari y E. M. Krieger. "Restoration of arterial blood oxygen tension increases arterial pressure in sinoaortic-denervated rats". American Journal of Physiology-Heart and Circulatory Physiology 266, n.º 3 (1 de marzo de 1994): H1055—H1061. http://dx.doi.org/10.1152/ajpheart.1994.266.3.h1055.
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The objective of the present study was to analyze whether the hypoxemia produced by chemoreceptor elimination influences the arterial pressure level after sinoaortic denervation (SAD) in rats. Hypoxemia and hypercapnia were observed in acute (1 day) and chronic (20 days) SAD rats [arterial PO2 (PaO2) = 65 +2- 1.6 and 71 +2- 2.2 mmHg and arterial PCO2 (PaCO2) = 46 +/- 1.3 and 37 +/- 1.8 mmHg, respectively] compared with control rats (PaO2 = 85 +/- 1.6 mmHg, PaCO2 = 31 +/- 1.07 mmHg). Increasing inspired PO2 (PIO2) from 138 mmHg (room air) to 155 mmHg restored the PaO2 of SAD rats to control levels (acute = 81 +/- 2.21 mmHg, chronic = 85 +/- 2.35 mmHg). PaO2. restoration produced pronounced elevation of mean arterial pressure (MAP) of acute (from 121 +/- 4 to 147 +/- 3.5 mmHg) and chronic (from 121 +/- 3 to 134 +/- 3.5 mmHg) SAD rats. Progressive stepwise increase of PIO2 (from 138 to 175, 210, and 235 mmHg) produced no additional elevation of MAP of acute (113 +/- 4, 137 +/- 5, 143 +/- 5, and 147 +/- 5 mmHg) and chronic (111 +/- 3.6, 131 +/- 7.4, 130 +/- 8.7, and 130 +/- 7 mmHg) SAD rats. Otherwise, the arterial pressure of control rats remained unchanged to progressive stepwise increase of PIO2 (118 +/- 5, 117 +/- 4, 118 +/- 4, 116 +/- 4 mmHg). These data suggest that the elimination of chemoreceptors in SAD rats produces hypoxemia responsible for hypotensive influences that counteract the pressor effects produced by baroreceptor elimination.
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Roca, J., M. C. Hogan, D. Story, D. E. Bebout, P. Haab, R. Gonzalez, O. Ueno y P. D. Wagner. "Evidence for tissue diffusion limitation of VO2max in normal humans". Journal of Applied Physiology 67, n.º 1 (1 de julio de 1989): 291–99. http://dx.doi.org/10.1152/jappl.1989.67.1.291.
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We recently found [at approximately 90% maximal O2 consumption (VO2max)] that as inspiratory PO2 (PIO2) was reduced, VO2 and mixed venous PO2 (PVO2) fell together along a straight line through the origin, suggesting tissue diffusion limitation of VO2max. To extend these observations to VO2max and directly examine effluent venous blood from muscle, six normal men cycled at VO2max while breathing air, 15% O2 and 12% O2 in random order on a single day. From femoral venous, mixed venous, and radial arterial samples, we measured PO2, PCO2, pH, and lactate and computed mean muscle capillary PO2 by Bohr integration between arterial (PaO2) and femoral venous PO2 (PfvO2). VO2 and CO2 production (VCO2) were measured by expired gas analysis, VO2max averaged 61.5 +/- 6.2 (air), 48.6 +/- 4.8 (15% O2), and 38.1 +/- 4.1 (12% O2) ml.kg-1.min-1. Corresponding values were 16.8 +/- 5.6, 14.4 +/- 5.0, and 12.0 +/- 5.0 Torr for PfVO2; 23.6 +/- 3.2, 19.1 +/- 4.2, and 16.2 +/- 3.5 Torr for PVO2; and 38.5 +/- 5.4, 30.3 +/- 4.1, and 24.5 +/- 3.6 Torr for muscle capillary PO2 (PmCO2). Each of the PO2 variables was linearly related to VO2max (r = 0.99 each), with an intercept not different from the origin. Similar results were obtained when the subjects were pushed to a work load 30 W higher to ensure that VO2max had been achieved. By extending our prior observations 1) to maximum VO2 and 2) by direct sampling of femoral venous blood, we conclude that tissue diffusion limitation of VO2max may be present in normal humans. In addition, since PVO2, PfVO2, and PmCO2 all linearly relate to VO2max, we suggest that whichever of these is most readily obtained is acceptable for further evaluation of the hypothesis.
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Norton, J. M. "A visual aid for teaching ventilation-perfusion relationships." Advances in Physiology Education 24, n.º 1 (diciembre de 2000): 38–42. http://dx.doi.org/10.1152/advances.2000.24.1.38.
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To help students understand the concept of the ventilation-perfusion ratio (VA/Q) and the effects that VA/Q mismatching has on pulmonary gas exchange, a "sliding rectangles" visual aid was developed to teach VA/Q relationships. Adjacent rectangles representing "ventilation" and "perfusion" are slid past one another so that portions of the ventilation and perfusion rectangles are not touching, illustrating the concepts of dead-space ventilation (VD) and shunt flow (QS). The portion of the ventilation bar representing VD is further subdivided into anatomical and alveolar VD and used to show the effects of alveolar dead space on the PO2 (PAO2) and PCO2 of alveolar air (PACO2); movement away from the "ideal" point). Similarly, the portion of the perfusion bar representing QS is used to define anatomical and physiological shunts and the effect of shunts on the PO2 (PaO2) and PCO2 of arterial blood (PaCO2). The genesis of the PAO2-PaO2 (A-a) PO2 difference as well as the effects of VA/Q mismatching and diffusion abnormalities can all be discussed with this visual aid. This approach has greatly assisted some students in mastering this traditionally difficult area of respiratory physiology.
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Demchenko, Ivan T., Yuriy I. Luchakov, Alexander N. Moskvin, Diana R. Gutsaeva, Barry W. Allen, Edward D. Thalmann y Claude A. Piantadosi. "Cerebral Blood Flow and Brain Oxygenation in Rats Breathing Oxygen under Pressure". Journal of Cerebral Blood Flow & Metabolism 25, n.º 10 (23 de marzo de 2005): 1288–300. http://dx.doi.org/10.1038/sj.jcbfm.9600110.
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Hyperbaric oxygen (HBO2) increases oxygen tension (PO2) in blood but reduces blood flow by means of O2-induced vasoconstriction. Here we report the first quantitative evaluation of these opposing effects on tissue PO2 in brain, using anesthetized rats exposed to HBO2 at 2 to 6 atmospheres absolute (ATA). We assessed the contribution of regional cerebral blood flow (rCBF) to brain PO2 as inspired PO2 (PiO2) exceeds 1 ATA. We measured rCBF and local PO2 simultaneously in striatum using collocated platinum electrodes. Cerebral blood flow was computed from H2 clearance curves in vivo and PO2 from electrodes calibrated in vitro, before and after insertion. Arterial PCO2 was controlled, and body temperature, blood pressure, and EEG were monitored. Scatter plots of rCBF versus pO2 were nonlinear ( R2 = 0.75) for rats breathing room air but nearly linear ( R2 = 0.88–0.91) for O2 at 2 to 6 ATA. The contribution of rCBF to brain PO2 was estimated at constant inspired PO2, by increasing rCBF with acetazolamide (AZA) or decreasing it with N-nitro-l-arginine methyl ester (l-NAME). At basal rCBF (78 mL/100 g min), local PO2 increased 7- to 33-fold at 2 to 6 ATA, compared with room air. A doubling of rCBF increased striatal PO2 not quite two-fold in rats breathing room air but 13- to 64-fold in those breathing HBO2 at 2 to 6 ATA. These findings support our hypothesis that HBO2 increases PO2 in brain in direct proportion to rCBF.
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Lahiri, S., W. L. Rumsey, D. F. Wilson y R. Iturriaga. "Contribution of in vivo microvascular PO2 in the cat carotid body chemotransduction". Journal of Applied Physiology 75, n.º 3 (1 de septiembre de 1993): 1035–43. http://dx.doi.org/10.1152/jappl.1993.75.3.1035.
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To understand the interplay between microcirculatory control and carotid body (CB) function, we simultaneously measured carotid body microvascular PO2 (CBM PO2) and chemosensory activity in the cat in vivo under several experimental conditions. Cats were anesthetized with pentobarbital sodium, paralyzed, and artificially ventilated. CBs were exposed, and steady-state CBM PO2 was measured by the O2-dependent quenching of the phosphorescence of Pd-meso-tetra-(4-carboxyphenyl)porphine, which was administered intravenously. A few fibers of the carotid sinus nerve were used to record chemosensory discharges. At arterial PO2 (PaO2) of 103.4 +/- 4.1 Torr, CBM PO2 was 52.5 +/- 3.6 Torr (n = 9). Graded lowering of PaO2 from 160 to 50 Torr resulted in nearly proportional decreases in CBM PO2, but at lower PaO2 the decrease in CBM PO2 became more substantial. As PaO2 decreased, chemosensory discharge increased in parallel with CBM PO2. Hypercapnia and hypocapnia did not significantly change the relationship between PaO2 and CBM PO2, although the chemosensory discharge responded significantly. CBM PO2 and chemosensory discharge were not affected by hemorrhagic hypotension until arterial blood pressure fell below approximately 50 Torr and then CBM PO2 decreased and chemosensory discharge increased. The lack of a significant effect of hemorrhagic hypotension indicated that O2 delivery to CB was almost independent of the systemic blood pressure. Taken together, the observations suggest that CB microcirculation and PO2 are subject to control by intrinsic mechanisms and that CBM PO2 is compatible with oxidative metabolism playing a role in O2 chemoreception during hypoxia.
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Bickler, P. E., L. Litt, D. L. Banville y J. W. Severinghaus. "Effects of acetazolamide on cerebral acid-base balance". Journal of Applied Physiology 65, n.º 1 (1 de julio de 1988): 422–27. http://dx.doi.org/10.1152/jappl.1988.65.1.422.
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Acetazolamide (AZ) inhibition of brain and blood carbonic anhydrase increases cerebral blood flow by acidifying cerebral extracellular fluid (ECF). This ECF acidosis was studied to determine whether it results from high PCO2, carbonic acidosis (accumulation of H2CO3), or lactic acidosis. Twenty rabbits were anesthetized with pentobarbital sodium, paralyzed, and mechanically ventilated with 100% O2. The cerebral cortex was exposed and fitted with thermostatted flat-surfaced pH and PCO2 electrodes. Control values (n = 14) for cortex ECF were pH 7.10 +/- 0.11 (SD), PCO2 42.2 +/- 4.1 Torr, PO2 107 +/- 17 Torr, HCO3- 13.8 +/- 3.0 mM. Control values (n = 14) for arterial blood were arterial pH (pHa) 7.46 +/- 0.03 (SD), arterial PCO2 (PaCO2) 32.0 +/- 4.1 Torr, arterial PO2 (PaO2) 425 +/- 6 Torr, HCO3- 21.0 +/- 2.0 mM. After intravenous infusion of AZ (25 mg/kg), end-tidal PCO2 and brain ECF pH immediately fell and cortex PCO2 rose. Ventilation was increased in nine rabbits to bring ECF PCO2 back to control. The changes in ECF PCO2 then were as follows: pHa + 0.04 +/- 0.09, PaCO2 -8.0 +/- 5.9 Torr, HCO3(-)-2.7 +/- 2.3 mM, PaO2 +49 +/- 62 Torr, and changes in cortex ECF were as follows: pH -0.08 +/- 0.04, PCO2 -0.2 +/- 1.6 Torr, HCO3(-)-1.7 +/- 1.3 mM, PO2 +9 +/- 4 Torr. Thus excess acidity remained in ECF after ECF PCO2 was returned to control values. The response of intracellular pH, high-energy phosphate compounds, and lactic acid to AZ administration was followed in vivo in five other rabbits with 31P and 1H nuclear magnetic resonance spectroscopy.(ABSTRACT TRUNCATED AT 250 WORDS)
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Wimberley, P. D., K. Grønlund Pedersen, J. Olsson y O. Siggaard-Andersen. "Transcutaneous carbon dioxide and oxygen tension measured at different temperatures in healthy adults." Clinical Chemistry 31, n.º 10 (1 de octubre de 1985): 1611–15. http://dx.doi.org/10.1093/clinchem/31.10.1611.
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Abstract Transcutaneous carbon dioxide tension (tc-pco2) at 37, 39, 41, 43, and 45 degrees C, and transcutaneous oxygen tension (tc-po2) at 41, 43, and 45 degrees C were measured simultaneously in 10 healthy adults during hyperventilation and inhalation of O2/CO2 gas. Nine electrodes were applied to each subject: Five CO2 electrodes, one O2 electrode, and three combined O2/CO2 electrodes. The CO2 electrodes had negligible temperature coefficients in the calibration gases, but the O2 electrodes showed an increase in po2 of 4.5% per degree C. With skin application, tc-pco2 increased approximately 4% per degrees C between 37 and 45 degrees C, which is close to the anaerobic temperature coefficient of pco2 in blood. The tc-po2 increases on the skin with increasing temperature appeared to be more dependent on changes in blood flow in skin, but in the temperature range 43 to 45 degrees C, tc-po2 showed the expected decrease in the temperature coefficient with increasing po2. The correlation between transcutaneous and capillary pco2 was close at all transcutaneous electrode temperatures, even 37 degrees C, provided the skin was preheated (via the electrode) to 45 degrees C. For tc-po2, an electrode temperature of at least 43 degrees C was necessary to produce a reasonable correlation between tc-po2 and capillary po2. The combined O2/CO2 electrodes measured slightly higher pco2 values than the single CO2 electrodes, but there were no differences in po2 readings, stabilization time, imprecision, or electrode drift between the two electrode types. The imprecision (CV, %) of tc-pco2 and tc-po2 measurements was approximately twice that of the corresponding capillary blood-gas measurements.
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FORGUE, JEAN, BERNARD BURTIN y JEAN-CHARLES MASSABUAU. "MAINTENANCE OF OXYGEN CONSUMPTION IN RESTING SILURUS GLANIS AT DIFFERENT LEVELS OF AMBIENT OXYGENATION". Journal of Experimental Biology 143, n.º 1 (1 de mayo de 1989): 305–19. http://dx.doi.org/10.1242/jeb.143.1.305.
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The mechanisms of adaptation that allow the teleost Silurus glanis to maintain its resting oxygen consumption constant when the O2 partial pressure (PO2) m the inspired water (PIO2) varied between 40 and 3kPa were studied at 13 °C. Steadystate values of oxygen consumption, ventilatory and circulatory flow rates, PO2 in the inspired and expired water, PO2 and O2 concentration in the arterial and venous blood, haematocrit and acid--base status in the arterial blood were determined after 1-day exposures at selected PIO2 values. Whole-blood O2-binding characteristics were also determined. The key adaptation after 1 day of acclimation was maintenance of oxygen consumption by ventilatory adjustment with no change in blood flow rate or pH (no Bohr effect). At each PIO2 value (i) the ventilatory adjustment was minimal as the O2 extraction coefficient from water always remained around 80–90 % and (ii) PaO2 stayed constant at about 2kPa. Data are compared with previous results in crayfish and other teleosts. It is concluded that the principle of a constant O2 status in themilieu intérieur -- independent of large changes in PIO2 for a given state of activity -- should be valid in many crustaceans and teleosts.
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Gutierrez, G., N. Lund, A. L. Acero y C. Marini. "Relationship of venous PO2 to muscle PO2 during hypoxemia". Journal of Applied Physiology 67, n.º 3 (1 de septiembre de 1989): 1093–99. http://dx.doi.org/10.1152/jappl.1989.67.3.1093.
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Anesthetized mechanically ventilated rabbits were subjected to progressive hypoxemia (n = 7) to determine the relationship of venous PO2 (PvO2) to skeletal muscle PO2 (PtiO2). Measures of arterial PO2 (PaO2), right atrial PO2 [(PvO2)RA], and hindlimb PO2 [(PvO2)limb], were obtained from the carotid artery, right atrium, and inferior vena cava, just above the level of the iliac bifurcation. Biceps femoris muscle PtiO2 was measured with a surface O2 microelectrode having eight measuring points. PaO2 was decreased from 90.3 +/- 5.4 to 26.8 +/- 0.8 Torr in five consecutive steps, followed by reoxygenation to 105.6 +/- 10.5 (SE) Torr. Measurements were obtained after each decrement in PaO2. A total of 128 measures of PtiO2 were obtained per experimental stage. The mean and distribution of the muscle PtiO2 histogram were determined. Measurements were compared with analysis of variance and the Newman-Keuls post hoc method. (PvO2)limb had similar values as the average muscle PtiO2 (PtiO2) for PaO2 values greater than 52.1 +/- 4.3 Torr, where (PvO2)limb became greater than PtiO2 (P less than 0.05). The lowest measures of (PvO2)limb and PtiO2 were 15.9 +/- 0.7 and 4.0 +/- 0.1 Torr, respectively (P less than 0.01). The PtiO2 histograms showed no evidence of increased microvascular heterogeneity with hypoxemia. We conclude that in hypoxemia PvO2 is greater than muscle PtiO2. This difference may be related to the establishment of significant physicochemical O2 gradients from erythrocyte to tissue cell.
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Fonzi, C. E., J. L. Clausen y J. Mahoney. "Aberrant PO2 values in proficiency testing". Clinical Chemistry 39, n.º 3 (1 de marzo de 1993): 467–71. http://dx.doi.org/10.1093/clinchem/39.3.467.
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Abstract We prospectively determined the frequency of aberrant vials of fluorocarbon/buffer used for proficiency testing of measurements of pH, PCO2, and PO2, using 20 duplicate vials from 12 lots of fluorocarbon/buffer and two arterial blood gas analyzers in eight reference laboratories. We defined aberrant vials as vials for which both duplicate measurements differed from the mean value of repeated measurements for the specific instrument (for each lot of testing materials) by > 0.04 for pH, > 10% of the mean or 3.0 mm Hg, whichever was greater, for PCO2; or > 10% of the mean or 6 mm Hg, whichever was greater, for PO2. Four of 1620 vials (0.25%) were aberrant, all based on PO2 measurements (< 70 mm Hg); all would have failed in both American/California Thoracic Societies and College of American Pathologists proficiency programs. The average intra-instrument SDs of repeated measures (range of mean values: pH, 7.181-7.631; PCO2, 12.7-65.9; PO2, 32.5-150.1) were 0.0055 for pH, 0.67 mm Hg for PCO2, and 1.65 mm Hg for PO2. Deliberate contamination of the fluorocarbon emulsion with room air, as might occur during sampling from the vial, indicated that only minor increases in PO2 (e.g., 1.0 mm Hg at PO2 of 56 mm Hg) occur when samples are aspirated. Larger increases in PO2 (mean 7.1 mm Hg at a PO2 of 66 mm Hg) occurred when the syringe samples were contaminated with room air. We conclude that isolated aberrant measurements of PO2 in blood gas proficiency testing attributable to vial contents can occur, but the frequency is very low.
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Bisoi, Soumendu, Arun Kumar Mandal, Asheesh Singh y Susanta Banerjee. "Gas separation properties of Troeger’s base-bridged polyamides". e-Polymers 17, n.º 4 (27 de junio de 2017): 283–93. http://dx.doi.org/10.1515/epoly-2016-0291.
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AbstractA series of new polyamides (PAs) has been prepared from a Troeger base-bridged diamine (TB), 2,8- diamino-4,10-dimethyl-6H,12H-5,11-methanodibenzo[1,5]-diazocine and different commercially available diacid monomers via the conventional polycondensation method. Dense membranes were prepared from the PAs by solution casting and solvent evaporation techniques. The synthesized PAs showed high glass transition temperature (283–290°C), 10% weight loss up to temperature 431°C in air, and tensile strength up to 91 MPa. The PA membranes showed higher permeability than some commercially used glassy polymers (PCO2 up to 109 and PO2 up to 21 Barrer) and permselectivity (PCO2/PCH4 up to 53.7 and PO2/PN2 up to 7.52) in comparison to many other PAs published in the literature.
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Wilson, D. F., A. Pastuszko, J. E. DiGiacomo, M. Pawlowski, R. Schneiderman y M. Delivoria-Papadopoulos. "Effect of hyperventilation on oxygenation of the brain cortex of newborn piglets". Journal of Applied Physiology 70, n.º 6 (1 de junio de 1991): 2691–96. http://dx.doi.org/10.1152/jappl.1991.70.6.2691.
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A new phosphorescence imaging method (Rumsey et al. Science Wash. DC 241: 1649-1651, 1988) has been used to continuously monitor the PO2 in the blood of the cerebral cortex of newborn pigs. A window was prepared in the skull and the brain superfused with artificial cerebrospinal fluid. The phosphorescent probe for PO2, Pd-meso-tetra(4-carboxyphenyl)porphine, was injected directly into the systemic blood. The phosphorescence of the probe was imaged, and the lifetimes were measured using flash illumination and a gated video camera. The PO2 in the blood of the veins and capillary beds of the cortex was calculated from the lifetimes. Systemic blood pressure was continuously monitored while the systemic arterial PCO2, PO2, and blood pH were measured periodically. The PO2 in the blood was quantitated for 60- to 200 microns2 regions within the image (from a total field of approximately 3 mm diam). The PO2 in the microvasculature was not uniform across the viewing field but increased or decreased in each region independently of the other regions. Thus at any point in time the PO2 in a region could be substantially above or below the average value. During hyperventilation, which lowered arterial PCO2 and increased pH of the blood, the average PO2 decreased in proportion to the decrease in arterial PCO2. For example, hyperventilation, which decreased arterial PCO2 from its normal value of 40 Torr to 10 Torr, caused a rapid (within 5 min) decrease in PO2 in the blood of capillaries and veins to approximately one-third of normal.
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Mover-Lev, Haya, Moshe Harell, Dalia Levy, Amos Ar, Michal Luntz y Jacob Sadé. "Dependence of Middle Ear Gas Composition on Pulmonary Ventilation". Annals of Otology, Rhinology & Laryngology 106, n.º 4 (abril de 1997): 314–19. http://dx.doi.org/10.1177/000348949710600410.
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The middle ear (ME) steady state gas composition resembles that of mixed venous blood. We changed arterial and venous blood gases by artificially ventilating anesthetized guinea pigs and measured simultaneous ME gas changes during spontaneous breathing, hyperventilation, and hypoventilation. During hyperventilation, PaCO2 and PvCO2 (a = arterial, v = venous) decreased from 46.0 and 53.0 mm Hg to 17.9 and 37.5 mm Hg, respectively, while PaO2 and PvO2 (85.6 and 38.2 mm Hg) did not change. This was accompanied by an ME PCO2 decrease from 70.4 to 58.8 mm Hg and a PO2 decrease from 36.8 to 25.4 mm Hg. During hypoventilation, PaCO2 and PvCO2 increased to 56.8 and 66.4 mm Hg, while PvO2 decreased to 21.8 mm Hg. The ME PCO2 increased simultaneously to 88.8 mm Hg and the ME PO2 decreased to 25.4 mm Hg. The ME PO2 decrease during hyperventilation may be explained by a 33% decrease in ME mucosa perfusion, calculated from the ME ventilation-perfusion ratio. This study shows that ME gas composition follows fluctuations of blood gas levels and thus may affect total ME pressure.
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Kerger, H., I. P. Torres Filho, M. Rivas, R. M. Winslow y M. Intaglietta. "Systemic and subcutaneous microvascular oxygen tension in conscious Syrian golden hamsters". American Journal of Physiology-Heart and Circulatory Physiology 268, n.º 2 (1 de febrero de 1995): H802—H810. http://dx.doi.org/10.1152/ajpheart.1995.268.2.h802.
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Arteriolar and venular oxygen tension distribution was studied in the subcutaneous connective tissue of the chamber window preparation in conscious Syrian golden hamsters as a function of the systemic PO2, PCO2, pH, arterial pressure and hematocrit, microvascular red blood cell (RBC) velocity, vessel diameter, and blood flow in the same microvessels. PO2 was measured with the phosphorescence decay technique using Pd-meso-tetra(4-carboxyphenyl)porphyrin (30 mg/kg body wt iv). Systemic arterial and venous PO2s were 71.6 +/- 13.1 and 28.4 +/- 5.1 mmHg, while oxygen tension was 45.1 +/- 13.3 mmHg in arterioles and 30.1 +/- 10.7 mmHg in venules. The relatively low arteriolar PO2 and the small arteriolar-venular PO2 gradient indicate that some blood oxygen exits directly to the tissue or is shunted before reaching the capillaries. RBC velocity was the strongest correlate of microvascular PO2 (arterial correlation coefficient = 0.503 and venous correlation coefficient = 0.560, P < 0.001). Microvascular PO2 was also correlated with blood flow, vessel diameter, blood pH, and PCO2 but not with systemic PO2. Arterial oxygen tension was only significantly related to PCO2, pH, and hematocrit. These findings suggest that oxygen delivery to the tissue improves with increasing blood flow velocity and that microvascular PO2 is a locally regulated parameter in the absence of major systemic perturbations.
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Hogan, M. C., J. Roca, P. D. Wagner y J. B. West. "Limitation of maximal O2 uptake and performance by acute hypoxia in dog muscle in situ". Journal of Applied Physiology 65, n.º 2 (1 de agosto de 1988): 815–21. http://dx.doi.org/10.1152/jappl.1988.65.2.815.
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The factors that determine maximal O2 uptake (VO2max) and muscle performance during severe, acute hypoxemia were studied in isolated, in situ dog gastrocnemius muscle. Our hypothesis that VO2max is limited by O2 diffusion in muscle predicts that decreases in VO2max, caused by hypoxemia, will be accompanied by proportional decreases in muscle effluent venous PO2 (PvO2). By altering the fraction of inspired O2, four levels of arterial PO2 (PaO2) [21 +/- 2, 28 +/- 1, 44 +/- 1, and 80 +/- 2 (SE) Torr] were induced in each of eight dogs. Muscle arterial and venous circulation was isolated and arterial pressure held constant by pump perfusion. Each muscle worked maximally (3 min at 5-6 Hz, isometric twitches) at each PaO2. Arterial and venous samples were taken to measure lactate, [H+], PO2, PCO2, and muscle VO2. Muscle biopsies were taken to measure [H+] (homogenate method) and lactate. VO2max decreased with PaO2 and was linearly (R = 0.99) related to both PVO2 and O2 delivery. As PaO2 fell, fatigue increased while muscle lactate and [H+] increased. Lactate release from the muscle did not change with PaO2. This suggests a barrier to lactate efflux from muscle and a possible cause of the greater fatigue seen in hypoxemia. The gas exchange data are consistent with the hypothesis that VO2max is limited by peripheral tissue diffusion of O2.
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Kayama, Takamasa, Takashi Yoshimoto, Shunichi Fujimoto y Yoshiharu Sakurai. "Intratumoral oxygen pressure in malignant brain tumor". Journal of Neurosurgery 74, n.º 1 (enero de 1991): 55–59. http://dx.doi.org/10.3171/jns.1991.74.1.0055.
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✓ Oxygen pressure (pO2) in brain tumors, pO2 in brain cortex surrounding the tumors, and PaO2 were measured simultaneously during total resection in 16 patients with previously untreated brain tumors in order to detect hypoxic regions within the tumors. When the inhaled O2:N2O ratio was 1:3 under enflurane anesthesia, mean PaO2 was 109.2 ± 5.8 mm Hg, a rather high value when compared with that obtained when air is inhaled under atmospheric pressure. The simultaneously measured intratumoral pO2 and pO2 in brain cortex surrounding the tumor were 15.3 ± 2.3 and 59.8 ± 6.5 mm Hg, respectively. Each intratumoral pO2 value was significantly lower than that of pO2 in brain cortex surrounding the tumor (mean < 30 mm Hg, Wilcoxon signed rank test, p < 0.005) and influenced the oxygen effects on radiation. These results appear to confirm that there are hypoxic regions within human brain tumors. A comparison between intratumoral pO2 and either the angiographic or contrast-enhanced computerized tomography scans of the tumor vasculature disclosed no correlation.
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Steinacker, J. M. y W. Spittelmeister. "Dependence of transcutaneous O2 partial pressure on cutaneous blood flow". Journal of Applied Physiology 64, n.º 1 (1 de enero de 1988): 21–25. http://dx.doi.org/10.1152/jappl.1988.64.1.21.
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Transcutaneous PO2 was measured using a transcutaneous PO2 electrode heated to 45 degrees C on the forearm of 19 healthy volunteers. Cutaneous blood flow (CBF) was estimated indirectly from the heating power of the electrode (HP) and with an 8-MHz bidirectional ultrasonic probe by Doppler shift in a fingertip at 45 degrees C (DF). Blood flow was regulated by an upper arm cuff. Mean transcutaneous PO2 during air respiration was 86.0 +/- 6.2 Torr, and the correlation to arterial PO2 (Pao2) was 0.96 at normal blood flow. The arterial inflow was intermittently reduced in 10-15% stages of effective perfusion pressure (Peff). There was a hyperbolic decrease in PO2 when CBF was restricted in stages. A linear dependence between Peff, HP, and DF was found, which means that there is no autoregulation in the capillary bed at 45 degrees C. Transcutaneous PO2 can be also taken as an indication of CBF. The transcutaneous index, transcutaneous PO2/Pao2, is helpful for estimating local O2 availability.
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Hoffman, William E., Fady T. Charbel, Guy Edelman, Mukesh Misra y James I. Ausman. "Comparison of the Effect of Etomidate and Desflurane on Brain Tissue Gases and pH during Prolonged Middle Cerebral Artery Occlusion". Anesthesiology 88, n.º 5 (1 de mayo de 1998): 1188–94. http://dx.doi.org/10.1097/00000542-199805000-00008.
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Background The authors compared the effects of etomidate and desflurane on brain tissue oxygen pressure (PO2), carbon dioxide pressure (PCO2), and pH in patients who had middle cerebral artery occlusion for > 15 min. Methods After a craniotomy, a probe that measures PO2, PCO2, and pH was inserted into cortical tissue at risk for ischemia during middle cerebral artery occlusion. A burst suppression pattern of the electroencephalogram was induced with etomidate (n = 6) or 9% end-tidal desflurane (n = 6) started before middle cerebral artery occlusion. Mean blood pressure was supported with phenylephrine to 90-95 mmHg. Results During baseline conditions, tissue PO2, PCO2, and pH were similar between the two groups (PO2 = 15 mmHg, PCO2 = 60 mmHg, pH = 7.1). During administration of etomidate before middle cerebral artery occlusion, tissue PO2 decreased in five of six patients without a change in PCO2 or pH. During administration of 9% desflurane, tissue PO2 and pH increased before middle cerebral artery clipping. Middle cerebral artery occlusion for an average of 33 min with etomidate and 37 min with desflurane produced a decrease in pH with etomidate (7.09 to 6.63, P < 0.05) but not with desflurane (7.12 to 7.15). Conclusion These results suggest that tissue hypoxia and acidosis are often observed during etomidate treatment and middle cerebral artery occlusion. Treatment with desflurane significantly increases tissue PO2 alone and attenuates acidotic changes to prolonged middle cerebral artery occlusion.
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Gulinson, S. y J. Harrison. "Control of resting ventilation rate in grasshoppers". Journal of Experimental Biology 199, n.º 2 (1 de febrero de 1996): 379–89. http://dx.doi.org/10.1242/jeb.199.2.379.
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We examined the effect of extracellular acid-base status and tracheal gas levels on the ventilation rate of resting Romalea guttata and Schistocerca americana grasshoppers. We manipulated haemolymph pH and [HCO3-] within normal physiological ranges using injections of HCl, NaOH, NaHCO3 and NaCl into the haemocoel. In contrast to terrestrial vertebrates, there was no evidence that extracellular acidification increases ventilation rate in grasshoppers. Elevation of haemolymph bicarbonate levels (by NaHCO3 injection) increased ventilation rate, while depression of haemolymph bicarbonate levels (HCl injection) had no effect. Injection of NaHCO3 also increased tracheal PCO2, suggesting that the effect of the NaHCO3 injection might be mediated by a sensitivity of the ventilatory system to tracheal gases. We tested for effects of tracheal gases on ventilation rate by independently manipulating tracheal PCO2 and PO2 using tracheal perfusions. Ventilation rate was positively correlated with tracheal PCO2 and negatively correlated with tracheal PO2. Increasing tracheal PO2 above normal resting levels or decreasing tracheal PCO2 below normal levels decreased ventilation rate. We conclude that quiescent grasshoppers regulate tracheal PCO2 and PO2 by varying ventilation rate and that both PCO2 and PO2 in the trachea stimulate ventilation in normal, resting grasshoppers.
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Hogan, M. C., D. E. Bebout y P. D. Wagner. "Effect of hemoglobin concentration on maximal O2 uptake in canine gastrocnemius muscle in situ". Journal of Applied Physiology 70, n.º 3 (1 de marzo de 1991): 1105–12. http://dx.doi.org/10.1152/jappl.1991.70.3.1105.
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O2 delivery to maximally working muscle was decreased by altering hemoglobin (Hb) concentration and arterial PO2 (PaO2) to investigate whether the reductions in maximal O2 uptake (VO2max) that occur with lowered [Hb] are in part related to changes in the effective muscle O2 diffusing capacity (DmO2). Two sets of experiments were conducted. In the initial set (n = 8), three levels of Hb [5.8 +/- 0.3, 9.4 +/- 0.1, and 14.4 +/- 0.6 (SE) g/100 ml] in the blood were used in random order to pump perfuse, at equal muscle blood flows and PaO2, maximally working isolated dog gastrocnemius muscle. VO2max declined with decreasing [Hb], but the relationship between VO2max and both the effluent venous PO2 (PvO2) and the calculated mean capillary PO2 (PcO2) was not linear through the origin and, therefore, not compatible with a single value of DmO2 (as calculated by Bohr integration using a model based on Fick's law of diffusion). To clarify these results, a second set of experiments (n = 6) was conducted in which two levels of Hb (14.0 +/- 0.6 and 6.9 +/- 0.6 g/100 ml) were each combined with two levels of oxygenation (PaO2 79 +/- 8 and 29 +/- 2 Torr) and applied in random sequence to again pump perfuse maximally working dog gastrocnemius muscle at constant blood flow. In these experiments, the relationship between VO2max and both PvO2 and calculated PcO2 for each [Hb] was consistent with a constant estimate of DmO2 as PaO2 was reduced, but the calculated DmO2 for the lower [Hb] was 33% less than that at the higher [Hb] (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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West, John B., Matthew A. Liu, Phoebe C. Stark y G. Kim Prisk. "Measuring the efficiency of pulmonary gas exchange using expired gas instead of arterial blood: comparing the “ideal” Po2 of Riley with end-tidal Po2". American Journal of Physiology-Lung Cellular and Molecular Physiology 319, n.º 2 (1 de agosto de 2020): L289—L293. http://dx.doi.org/10.1152/ajplung.00150.2020.
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When using a new noninvasive method for measuring the efficiency of pulmonary gas exchange, a key measurement is the oxygen deficit, defined as the difference between the end-tidal alveolar Po2 and the calculated arterial Po2. The end-tidal Po2 is measured using a rapid gas analyzer, and the arterial Po2 is derived from pulse oximetry after allowing for the effect of the Pco2 on the oxygen affinity of hemoglobin. In the present report we show that the values of end-tidal Po2 and Pco2 are highly reproducible, providing a solid foundation for the measurement of the oxygen deficit. We compare the oxygen deficit with the classical ideal alveolar-arterial Po2 difference (A-aDO2) as originally proposed by Riley, and now extensively used in clinical practice. This assumes Riley’s criteria for ideal alveolar gas, namely no ventilation-perfusion inequality, the same Pco2 as arterial blood, and the same respiratory exchange ratio as the whole lung. It transpires that, in normal subjects, the end-tidal Po2 is essentially the same as the ideal value. This conclusion is consistent with the very small oxygen deficit that we have reported in young normal subjects, the significantly higher values seen in older normal subjects, and the much larger values in patients with lung disease. We conclude that this noninvasive measurement of the efficiency of pulmonary exchange is identical in many respects to that based on the ideal alveolar Po2, but that it is easier to obtain.
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Broten, T. P. y E. O. Feigl. "Role of myocardial oxygen and carbon dioxide in coronary autoregulation". American Journal of Physiology-Heart and Circulatory Physiology 262, n.º 4 (1 de abril de 1992): H1231—H1237. http://dx.doi.org/10.1152/ajpheart.1992.262.4.h1231.
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Myocardial oxygen (PO2) and carbon dioxide tensions (PCO2) are likely mediators of the local control of coronary blood flow. A previous study demonstrated that myocardial PO2 and PCO2, estimated by coronary venous values, interact synergistically to determine coronary flow. This synergistic relation was used in a prospective study to test the hypothesis that myocardial PO2 and PCO2 mediate changes in coronary vascular conductance during autoregulation. The left main coronary artery was pump perfused at controlled pressures in closed-chest anesthetized dogs. Autoregulation curves were obtained by increasing coronary perfusion pressure from 80 to 160 mmHg in 20-mm increments. Steady-state measurements of coronary venous PO2 and PCO2 and coronary conductance were obtained at each perfusion pressure. The coronary venous PO2 and PCO2 were used in the previously determined synergistic relation to predict the coronary vascular conductance during autoregulation. The predicted changes in coronary vascular conductance were compared with the actual changes in coronary vascular conductance for the pressure range of 80-160 mmHg. The data indicate that the synergistic interaction of oxygen and carbon dioxide accounts for approximately 23% of the change in coronary vascular conductance during autoregulation. These results suggest that other factors are also involved in autoregulation.
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Krolikowski, K. y J. Harrison. "Haemolymph acid-base status, tracheal gas levels and the control of post-exercise ventilation rate in grasshoppers". Journal of Experimental Biology 199, n.º 2 (1 de febrero de 1996): 391–99. http://dx.doi.org/10.1242/jeb.199.2.391.
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In grasshoppers, ventilation rate increases after jumping, in association with decreases in haemolymph pH and tracheal PO2 and increases in haemolymph and tracheal PCO2. Are these changes in haemolymph acid-base status or tracheal gas composition causally responsible for the increases in post-locomotion ventilation rate? To answer this question, we manipulated haemolymph acid-base status with injections into the haemocoel and independently manipulated tracheal PO2 and PCO2 with tracheal perfusions. Using a new technique, we continuously monitored ventilation rate and ventilatory pressures on virtually unrestrained insects. Changes in haemolymph acid-base status or tracheal PCO2 did not affect post-exercise ventilation rate, clearly demonstrating that the ventilatory stimulus associated with locomotion is not dependent on negative feedback from these variables. Post-exercise ventilation rate varied with tracheal PO2, with the lowest ventilation rates observed at the lowest tracheal PO2 values, a result opposite to that expected if negative feedback from internal PO2 levels were to drive the increase in ventilation rate. Particularly after activity, there was considerable heterogeneity in unperfused animals between tracheal and haemolymph PCO2, and between tracheal PCO2 in the thorax and leg, consistent with unidirectional airflow and a considerable role for diffusion gradients in the gas exchange of grasshoppers.
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Linsenmeier, R. A. y R. D. Braun. "Oxygen distribution and consumption in the cat retina during normoxia and hypoxemia." Journal of General Physiology 99, n.º 2 (1 de febrero de 1992): 177–97. http://dx.doi.org/10.1085/jgp.99.2.177.
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Oxygen tension (PO2) was measured with microelectrodes within the retina of anesthetized cats during normoxia and hypoxemia (i.e., systemic hypoxia), and photoreceptor oxygen consumption was determined by fitting PO2 measurements to a model of steady-state oxygen diffusion and consumption. Choroidal PO2 fell linearly during hypoxemia, about 0.64 mmHg/mmHg decrease in arterial PO2 (PaO2). The choroidal circulation provided approximately 91% of the photoreceptors' oxygen supply under dark-adapted conditions during both normoxia and hypoxemia. In light adaptation the choroid supplied all of the oxygen during normoxia, but at PaO2's less than 60 mmHg the retinal circulation supplied approximately 10% of the oxygen. In the dark-adapted retina the decrease in choroidal PO2 caused a large decrease in photoreceptor oxygen consumption, from approximately 5.1 ml O2/100 g.min during normoxia to 2.6 ml O2/100 g.min at a PaO2 of 50 mmHg. When the retina was adapted to a rod saturating background, normoxic oxygen consumption was approximately 33% of the dark-adapted value, and hypoxemia caused almost no change in oxygen consumption. This difference in metabolic effects of hypoxemia in light and dark explains why the standing potential of the eye and retinal extracellular potassium concentration were previously found to be more affected by hypoxemia in darkness. Frequency histograms of intraretinal PO2 were used to characterize the oxygenation of the vascularized inner half of the retina, where the oxygen distribution is heterogeneous and simple diffusion models cannot be used. Inner retinal PO2 during normoxia was relatively low: 18 +/- 12 mmHg (mean and SD; n = 8,328 values from 36 profiles) in dark adaptation, and significantly lower, 13 +/- 6 mmHg (n = 4,349 values from 19 profiles) in light adaptation. Even in the dark-adapted retina, 30% of the values were less than 10 mmHg. The mean PO2 in the inner (i.e., proximal) half of the retina was well regulated during hypoxemia. In dark adaptation it was significantly reduced only at PaO2's less than 45 mmHg, and it was reduced less at these PaO2's in light adaptation.
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Seylaz, J., H. Hara, E. Pinard, S. Mraovitch, E. T. MacKenzie y L. Edvinsson. "Effect of Stimulation of the Sphenopalatine Ganglion on Cortical Blood Flow in the Rat". Journal of Cerebral Blood Flow & Metabolism 8, n.º 6 (diciembre de 1988): 875–78. http://dx.doi.org/10.1038/jcbfm.1988.145.
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The effects of electrical stimulation of the sphenopalatine ganglion on cortical blood flow and gas partial pressures (Po2 and PCo2) were studied in the anesthetized rat. Tissue Po2, PCo2, and local CBF were measured simultaneously in both parietal cortices by means of mass spectrometry. Stimulation of the sphenopalatine ganglion increased CBF and tissue Po2 by —50 and 20%, respectively, in the ipsilateral parietal cortex. Smaller but significant increases in CBF and tissue Po2 were simultaneously seen in the contralateral parietal cortex. These variations were also accompanied by small decreases in PCo2 in both parietal cortices and a 5% increase in mean arterial pressure, whereas cortical electrical activity did not change. We conclude that the cholinergic (and vasoactive intestinal polypeptidergic) innervation of the cerebral blood vessels, arising from the sphenopalatine ganglion has significant vasomotor potential and that this system may be of functional importance.
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Zang, Yu, Toshiki Aoki, Masahiro Teraguchi, Takashi Kaneko, Hongge Jia, Liqun Ma y Fengjuan Miao. "New Synthetic Methods of Novel Nanoporous Polycondensates and Excellent Oxygen Permselectivity of Their Composite Membranes". Nanomaterials 9, n.º 6 (5 de junio de 2019): 859. http://dx.doi.org/10.3390/nano9060859.
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Two kinds of novel nanoporous polycondensates (sc(Rf)) have been synthesized by two new preparation methods consisting of polycondensation and highly selective photocyclicaromataization of 1/3 helical cis-cis polyphenylacetylenes with polymerizable groups. By the original methods, new well-defined sheet polymers having nanopores or nanospaces have been synthesized for the first time. Their composite membranes, containing small amounts (1.0 wt%) of sc(Rf), had ultrahigh oxygen permeability (Po2 > 1000 barrer), and their plots were beyond the Robeson’s upper bound line in the graph of oxygen permselectivity (α = Po2/PN2) versus Po2. Both α and Po2 values were enhanced by adding only small amounts (1.0 wt%) of sc(Rf). One of the sc(Rf)s synthesized on the base membrane surface showed the best performance, i.e., Po2 = 5300 barrer and α = 2.5. The membrane surface was effectively covered by sc(Rf), judging from the contact angle values. It is thought that nanopores and nanospaces created in and between sc(Rf) molecules played an important role for the enhancement of both α and Po2/PN2.
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Primashanti, Dewa Ayu Dini, Putu Siadi Purniti y I. Gusti Ayu Trisna Windiani. "Forced expiratory volume in 1-second and blood gas analysis in children during asthma attacks". Paediatrica Indonesiana 58, n.º 5 (4 de octubre de 2018): 221–6. http://dx.doi.org/10.14238/pi58.5.2018.221-6.
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Background Asthma is the most common chronic disease in the world, with a high incidence in children. Blood gas analysis and pulmonary function test using spirometry are recommended to evaluate the degree of asthma in children. Spirometry test is non-invasive and easier to implement compared to blood gas analysis.
Objective To evaluate for a possible correlation between forced expiratory volume in 1 second (FEV1) measured by spirometry test and blood gas analysis (pO2 and pCO2 levels) in children during an asthma attack.
Methods This cross-sectional study was done in children with asthma attacks who were admitted to Sanglah Hospital, Denpasar, Bali, between November 2016 and April 2017. Subjects underwent spirometry tests and blood gas analyses. Potential correlations between FEV1 and pO2 and pCO2 levels were analyzed by Spearman’s correlation test.
Results A total of 50 subjects, consisting of children aged 6 to 12 years, were diagnosed with asthma attacks during the study period. Subjects’ mean FEV1 level was 43.6%, mean pCO2 was 38.36 mmHg, and mean pO2 was 121.92 mmHg. There were no significant correlations between FEV1 and pCO2 level (r=0.206; P=0.152) or FEV1 and pO2 (r=0.157; P=0.277) found in this study.
Conclusion FEV1 does not correlate with pCO2 and pO2 level in children during asthma attacks.
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Abitbol, M. Maurice, Alan G. Monheit y Martin L. Stone. "Arterial Po2, Pco2, and pH versus transcutaneous Po2 and Pco2 and tissue pH in the fetal dog". American Journal of Obstetrics and Gynecology 155, n.º 2 (agosto de 1986): 437–43. http://dx.doi.org/10.1016/0002-9378(86)90848-3.
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Sérvio, Thaianne Cavalcante, Rodrigo Severo de Camargo Pereira y Daniele Cristina Cataneo. "Study on functional cardiorespiratory changes after laparoscopic Nissen fundoplication". Acta Cirurgica Brasileira 27, n.º 7 (julio de 2012): 499–504. http://dx.doi.org/10.1590/s0102-86502012000700012.
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PURPOSE: To analyze the behavior of cardiopulmonary function in postoperative of laparoscopic Nissen fundoplication. METHODS: Thirty-two patients, 13 males (41%) and 19 females (59%), were evaluated. Their age ranged from 25 to 67 years, with a mean of 44.4 ± 10.9. Pulmonary volumes, respiratory pressures and exercise tests were performed in the preoperative period (PRE) and in the first (PO1), second (PO2), fifth (PO5) and thirtieth (PO30) postoperative periods. RESULTS: Thirty-two patients were evaluated, of whom 59% were females. Mean age was 44.4 ± 10.9 years. Lung volumes had significant decrease at PO1 and PO2 and were similar to PRE values at PO5. Respiratory pressures were altered only at PO1. The distance covered in the 6-minute walk test had significant reduction until PO2, and climbing time in the stair-climbing test significantly increased at PO2. CONCLUSION: Patients submitted to LNF surgery have decreased cardiorespiratory function in the early postoperative period; however, they soon return to preoperative conditions.
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Torbati, D., A. Mokashi y S. Lahiri. "Effects of acute hyperbaric oxygenation on respiratory control in cats". Journal of Applied Physiology 67, n.º 6 (1 de diciembre de 1989): 2351–56. http://dx.doi.org/10.1152/jappl.1989.67.6.2351.
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We studied ventilatory responsiveness to hypoxia and hypercapnia in anesthetized cats before and after exposure to 5 atmospheres absolute O2 for 90-135 min. The acute hyperbaric oxygenation (HBO) was terminated at the onset of slow labored breathing. Tracheal airflow, inspiratory (TI) and expiratory (TE) times, inspiratory tidal volume (VT), end-tidal PO2 and PCO2, and arterial blood pressure were recorded simultaneously before and after HBO. Steady-state ventilation (VI at three arterial PO2 (PaO2) levels of approximately 99, 67, and 47 Torr at a maintained arterial PCO2 (PaCO2, 28 Torr) was measured for the hypoxic response. Ventilation at three steady-state PaCO2 levels of approximately 27, 36, and 46 Torr during hyperoxia (PaO2 450 Torr) gave a hypercapnic response. Both chemical stimuli significantly stimulated VT, breathing frequency, and VI before and after HBO. VT, TI, and TE at a given stimulus were significantly greater after HBO without a significant change in VT/TI. The breathing pattern, however, was abnormal after HBO, often showing inspiratory apneusis. Bilateral vagotomy diminished apneusis and further prolonged TI and TE and increased VT. Thus a part of the respiratory effects of HBO is due to pulmonary mechanoreflex changes.
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Gronlund, J. "Evaluation of factors affecting relationship between transcutaneous PO2 and probe temperature". Journal of Applied Physiology 59, n.º 4 (1 de octubre de 1985): 1117–27. http://dx.doi.org/10.1152/jappl.1985.59.4.1117.
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Several studies on transcutaneous O2 probes have shown that the transcutaneous PO2 increases to approximately 80% of the arterial PO2 when the probe is heated to 44 degrees C. It is not known whether this result reflects near-complete thermic arterialization or rather other factors such as the temperature-linked right shift of the hemoglobin O2-binding curve. In many clinical applications of transcutaneous probes the use of 44 degrees C is a major disadvantage because of the risk of skin burns. The development of new probes operating at lower temperatures is hampered by the lack of data on the temperature dependence of the factors influencing the relationship between the transcutaneous PO2 and the probe temperature. The present study attempts to estimate the temperature dependence of 1) the degree of arterialization of the blood in the skin capillaries, 2) the PO2 difference across the epidermis caused by the diffusion gradient and the epidermal O2 consumption, and 3) the arteriovenous saturation difference over the skin capillaries. The estimation is based on simultaneously measured transcutaneous PO2, PCO2, and argon partial pressure (PAr) values at seven different probe temperatures. The transcutaneous PCO2 is assumed equal to the mean capillary PCO2, which is used to calculate the mean capillary PO2 by the aid of a skin model. The O2 diffusion gradient is estimated from the transcutaneous PAr, and the PO2 difference caused by the epidermal O2 consumption is set equal to the difference between the mean capillary and transcutaneous PO2 less the partial pressure difference caused by the diffusion gradient. The degree of arterialization was found to be 53% at 38 degrees C and 65% at 44 degrees C. The partial pressure difference caused by the epidermal O2 consumption decreased from 33 Torr at 38 degrees C to 6 Torr at 44 degrees C. The PO2 difference across the epidermis caused by the diffusion gradient was 7 Torr at 38 degrees C and 5 Torr at 44 degrees C. The arteriovenous saturation difference fell from 31% at 38 degrees C to 12% at 44 degrees C.
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Burnett, R. W. y M. Itano. "An interlaboratory study of blood-gas analysis: dependence of pO2 and pCO2 results on atmospheric pressure." Clinical Chemistry 35, n.º 8 (1 de agosto de 1989): 1779–81. http://dx.doi.org/10.1093/clinchem/35.8.1779.
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Abstract Blood-gas data from a large interlaboratory survey were analyzed to determine whether pO2 and pCO2 results are affected by the atmospheric pressure at the measuring location. A small but statistically significant dependence was found, averaging about 2.3% per 100 mmHg (1.7% per 10 kPa) for pO2 and 1.0% per 100 mmHg (0.75% per 10 kPa) for pCO2.
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Gronlund, J., E. R. Swenson, J. Ohlsson y M. P. Hlastala. "Contribution of continuing gas exchange to phase III exhaled PCO2 and PO2 profiles". Journal of Applied Physiology 62, n.º 6 (1 de junio de 1987): 2467–76. http://dx.doi.org/10.1152/jappl.1987.62.6.2467.
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Changes in PCO2 and PO2 during expiration have been ascribed to simultaneous gas exchange, but other factors such as ventilation-perfusion inhomogeneity in combination with sequential emptying may also contribute. An experimental and model approach was used to study the relationship between gas exchange and changes in expired PCO2 and PO2 in anesthetized dogs during prolonged high tidal volume expirations. Changes in PCO2 and PO2 were quantified by taking the area bounded by the sloping exhalation curve and a line drawn horizontally from a point where the Fowler dead space plus 250 ml had been expired. This procedure is similar to using the slope of the exhalation curve but it circumvents problems caused by nonlinearity of the PCO2 and PO2 curves. The gas exchange components of the CO2 and O2 areas were calculated using a single-alveolus lung model whose input parameters were measured in connection with each prolonged expiration. The relationship between changes in experimental CO2 areas caused by sudden reductions in mixed venous PCO2 (produced by right atrial infusions of NaOH) and those calculated by the model was also studied. In seven dogs, calculated CO2 and O2 areas were 13% higher and 25% lower than the respective experimental areas, but interindividual variations were large. Changes in experimental CO2 areas caused by step changes in mixed venous PCO2 were almost identical to changes in the calculated areas. We conclude that the changes in PCO2 and PO2 during expiration cannot be explained solely by gas exchange. However, the single-alveolus lung model accurately predicts changes in the CO2 exhalation curve caused by alterations in the alveolar CO2 flow.
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Paulev, P. E. y O. Siggaard-Andersen. "Clinical application of the pO2-pCO2 diagram". Acta Anaesthesiologica Scandinavica 48, n.º 9 (octubre de 2004): 1105–14. http://dx.doi.org/10.1111/j.1399-6576.2004.00487.x.
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Gardner, William. "Measurement of end-tidal PCO2 and PO2". Biofeedback and Self-Regulation 19, n.º 2 (junio de 1994): 103–13. http://dx.doi.org/10.1007/bf01776484.
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Schwemmer, T. G., H. Baumann, C. S. Murray, A. I. Molina y J. A. Nye. "Acidification and hypoxia interactively affect metabolism in embryos, but not larvae, of the coastal forage fish Menidia menidia". Journal of Experimental Biology 223, n.º 22 (12 de octubre de 2020): jeb228015. http://dx.doi.org/10.1242/jeb.228015.
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ABSTRACTOcean acidification is occurring in conjunction with warming and deoxygenation as a result of anthropogenic greenhouse gas emissions. Multistressor experiments are critically needed to better understand the sensitivity of marine organisms to these concurrent changes. Growth and survival responses to acidification have been documented for many marine species, but studies that explore underlying physiological mechanisms of carbon dioxide (CO2) sensitivity are less common. We investigated oxygen consumption rates as proxies for metabolic responses in embryos and newly hatched larvae of an estuarine forage fish (Atlantic silverside, Menidia menidia) to factorial combinations of CO2×temperature or CO2×oxygen. Metabolic rates of embryos and larvae significantly increased with temperature, but partial pressure of CO2 (PCO2) alone did not affect metabolic rates in any experiment. However, there was a significant interaction between PCO2 and partial pressure of oxygen (PO2) in embryos, because metabolic rates were unaffected by PO2 level at ambient PCO2, but decreased with declining PO2 under elevated PCO2. For larvae, however, PCO2 and PO2 had no significant effect on metabolic rates. Our findings suggest high individual variability in metabolic responses to high PCO2, perhaps owing to parental effects and time of spawning. We conclude that early life metabolism is largely resilient to elevated PCO2 in this species, but that acidification likely influences energetic responses and thus vulnerability to hypoxia.
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Arquint, P., M. Koudelka-Hep, B. H. van der Schoot, P. van der Wal y N. F. de Rooij. "Micromachined analyzers on a silicon chip". Clinical Chemistry 40, n.º 9 (1 de septiembre de 1994): 1805–9. http://dx.doi.org/10.1093/clinchem/40.9.1805.
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Abstract For an example of a silicon-based micromachined analyzer, we describe a combined PO2, PCO2, and pH sensor designed for extracorporeal blood gas monitoring. The clinically well-accepted amperometric (PO2) and potentiometric (PCO2, pH) sensing principles are used, realized in a planar and miniaturized form on a single silicon chip (6 x 22 mm). The transducer part of the chip is fabricated by standard silicon technology. Polyacrylamide and polysiloxane polymeric layers, which are used as internal electrolyte and gas-permeable membrane, respectively, are deposited and patterned by photopolymerization. The entire sensor is fabricated on the wafer level by using integrated-circuit-compatible processes, thus allowing mass production. By integrating a flow-through channel directly on the chip, the sample size and the reagent consumption are substantially reduced. The device was characterized in aqueous solutions and in blood intended for transfusion. The sensor has a typical sensitivity of 0.36 nA/mmHg (PO2), -39 mV/decade (PCO2), and 51 mV/pH (pH); low drift; and a functional lifetime of > 2 months. The analytical precision in the physiologically expected range is better than 2 mmHg for the PO2 and PCO2 sensor, and 0.02 pH unit for the pH sensor.
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Hoffman, William E., Fady T. Charbel, Guy Edelman y Chris Abood. "Brain Tissue Response to CO2 in Patients with Arteriovenous Malformation". Journal of Cerebral Blood Flow & Metabolism 16, n.º 6 (noviembre de 1996): 1383–86. http://dx.doi.org/10.1097/00004647-199611000-00038.
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We tested whether cerebral arteriovenous malformations (AVM) alter brain tissue oxygen pressure, Po2, carbon dioxide pressure Pco2, and pH before, during, and after hypercapnia. A craniotomy was performed and a sensor inserted into normal brain tissue (control) (n = 7) or into tissue adjacent to an AVM (n = 9). Under baseline conditions, tissue Po2 was 80% lower in AVM compared to control patients, but Pco2 and pH were normal. During a 10 mm Hg increase in Paco2, tissue Po2 increased only in AVM patients, Pco2 increased in both groups, and pH decreased only in controls. When hypercapnia was reversed, tissue Pco2 decreased below baseline and pH increased in AVM patients. Results suggest that tissue CO2 washout and elevated pH result from increases in blood flow during hypercapnia. This response may be related to symptoms of hyperperfusion during AVM resection.
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Carter, B. G., J. Tibballs, M. Hochmann, A. Osborne, A. Chiriano y G. Murray. "A Comparison of Syringes to Collect Blood for Analysis of Gases, Electrolytes and Glucose". Anaesthesia and Intensive Care 22, n.º 6 (diciembre de 1994): 698–702. http://dx.doi.org/10.1177/0310057x9402200610.
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We studied the interchangeability of two blood gas syringes (Johns, Hardie Health Care Products Pty Ltd and Marksman, Martell Medical Products Inc) for the collection of blood for the analysis of PCO2, PO2, pH, sodium, potassium and glucose in 71 intensive care unit patients. The interchangeability of these two syringes with a specially designed syringe (Radiometer, Radiometer A/S) for the collection of blood for the analysis of ionized calcium was also studied. Analysis of pH, sodium, potassium and glucose showed no clinically significant differences between samples collected with Johns and Marksman syringes. However, differences in PCO2 and PO2 in samples collected with these syringes may be clinically significant if the PO2 is less than 100 mmHg. There were no clinically significant differences in ionized calcium levels in blood samples collected with Johns, Marksman and Radiometer syringes. We conclude that Johns and Marksman syringes are interchangeable for the collection of blood for the analysis of PCO2, PO2, pH, sodium, potassium and glucose and they are also interchangeable with Radiometer syringes for the collection of blood for ionized calcium analysis.
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Chandrasekharan, Praveen, Munmun Rawat y Satyan Lakshminrusimha. "How Do We Monitor Oxygenation during the Management of PPHN? Alveolar, Arterial, Mixed Venous Oxygen Tension or Peripheral Saturation?" Children 7, n.º 10 (13 de octubre de 2020): 180. http://dx.doi.org/10.3390/children7100180.
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Oxygen is a pulmonary vasodilator and plays an important role in mediating circulatory transition from fetal to postnatal period. Oxygen tension (PO2) in the alveolus (PAO2) and pulmonary artery (PaO2) are the main factors that influence hypoxic pulmonary vasoconstriction (HPV). Inability to achieve adequate pulmonary vasodilation at birth leads to persistent pulmonary hypertension of the newborn (PPHN). Supplemental oxygen therapy is the mainstay of PPHN management. However, optimal monitoring and targeting of oxygenation to achieve low pulmonary vascular resistance (PVR) and optimizing oxygen delivery to vital organs remains unknown. Noninvasive pulse oximetry measures peripheral saturations (SpO2) and a target range of 91–95% are recommended during acute PPHN management. However, for a given SpO2, there is wide variability in arterial PaO2, especially with variations in hemoglobin type (HbF or HbA due to transfusions), pH and body temperature. This review evaluates the role of alveolar, preductal, postductal, mixed venous PO2, and SpO2 in the management of PPHN. Translational and clinical studies suggest maintaining a PaO2 of 50–80 mmHg decreases PVR and augments pulmonary vasodilator management. Nevertheless, there are no randomized clinical trials evaluating outcomes in PPHN targeting SpO2 or PO2. Also, most critically ill patients have umbilical arterial catheters and postductal PaO2 may not be an accurate assessment of oxygen delivery to vital organs or factors influencing HPV. The mixed venous oxygen tension from umbilical venous catheter blood gas may assess pulmonary arterial PO2 and potentially predict HPV. It is crucial to conduct randomized controlled studies with different PO2/SpO2 target ranges for the management of PPHN and compare outcomes.
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MacDonald, V. W. y R. M. Winslow. "Oxygen delivery and myocardial function in rabbit hearts perfused with cell-free hemoglobin". Journal of Applied Physiology 72, n.º 2 (1 de febrero de 1992): 476–83. http://dx.doi.org/10.1152/jappl.1992.72.2.476.
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Isolated rabbit hearts were perfused with Krebs-Henseleit buffer that contained 1.5 g/dl hemoglobin Ao [HbAo; PO2 at which half-saturation of hemoglobin occurs = 12 Torr], human hemoglobin cross-linked between alpha-chains with bis(3,5-dibromosalicyl)fumarate (alpha alpha-Hb; PO2 at which half-saturation of hemoglobin occurs = 30 Torr), or fatty acid-free bovine serum albumin (BSA). Myocardial performance and oxygen uptake were determined at different aortic PO2's [arterial PO2 (PaO2)] by use of an isovolumic Langendorff preparation. Function and oxygen uptake were comparable among the three different groups of hearts at an average mean PaO2 of 557 Torr. As PaO2 decreased, myocardial function was preserved better in hearts perfused with hemoglobin than in hearts perfused with Krebs-Henseleit buffer alone or with BSA. Hearts perfused with either HbAo or alpha alpha-Hb exhibited similar 10% decreases in left ventricular developed pressure and rate of change in left ventricular developed pressure at PaO2 of 141 Torr compared with a 58% decrease with BSA. However, corresponding venous PO2's were lower with HbAo (20 Torr) than with alpha alpha-Hb (35 Torr), and oxygen uptake decreased by 36% with HbAo but remained constant with alpha alpha-Hb. These data suggest that although myocardial function can be sustained over a fairly broad range of hemoglobin oxygen affinities, tissue oxygen gradients and myocardial oxygen uptake are maintained better by cell-free hemoglobin with an oxygen affinity in the normal physiological range.
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Rodrigues, Cristiane Delgado Alves, Caroline Andréia Pizano, Melina Tarossi, Ligia dos Santos Roceto y Desanka Dragosavac. "Análise da correlação do índice de Helkimo com a função respiratória no pré e pós-operatório de pacientes submetidos à cirurgia cardíaca: estudo piloto". Fisioterapia e Pesquisa 18, n.º 1 (marzo de 2011): 67–71. http://dx.doi.org/10.1590/s1809-29502011000100012.
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Avaliar a articulação temporomandibular (ATM) e a função respiratória no pré e pós-operatório de pacientes submetidos à cirurgia cardíaca eletiva, com intubação orotraqueal (IOT) e verificar se há correlação entre o Índice de disfunção clínica craniomandibular (IDCCM) com a função respiratória. Foram avaliados pacientes no pré, primeiro e segundo dias de pós-operatório (PO1, PO2) de cirurgia cardíaca com até 24 horas IOT. Na avaliação da ATM foi utilizado o IDCCM e para a avaliação respiratória foram utilizados a cirtometria axilar, xifoideana e umbilical, ventilometria, incluindo capacidade vital (CV), volume minuto (VM) e frequência respiratória (FR). Completaram o estudo 13 pacientes. Não foi encontrada diferença estatística entre o IDCCM nos diferentes períodos de avaliação. Houve diminuição significativa dos valores de cirtometria nas três medidas e da CV com p<0, 001. A FR apresentou aumento significativo, com p=0,01. Foi encontrada correlação negativa entre o IDCCM no PO1 e a cirtometria axilar no PO1; correlação negativa entre o IDCCM no PO2 e a cirtometria xifoideana no PO2, e correlação positiva entre o IDCCM no PO2 e FR no PO2. Pode-se concluir que o IDCCM não se alterou significativamente após intubação orotraqueal ao longo dos tempos estudados. A função respiratória apresentou diminuição dos volumes e capacidades pulmonares. A cirtometria axilar e xifoideana, assim como a FR apresentaram correlação com o IDCCM em diferentes tempos.
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Daristotle, L., M. J. Engwall, W. Z. Niu y G. E. Bisgard. "Ventilatory effects and interactions with change in PaO2 in awake goats". Journal of Applied Physiology 71, n.º 4 (1 de octubre de 1991): 1254–60. http://dx.doi.org/10.1152/jappl.1991.71.4.1254.
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We utilized selective carotid body (CB) perfusion while changing inspired O2 fraction in arterial isocapnia to characterize the non-CB chemoreceptor ventilatory response to changes in arterial PO2 (PaO2) in awake goats and to define the effect of varying levels of CB PO2 on this response. Systemic hyperoxia (PaO2 greater than 400 Torr) significantly increased inspired ventilation (VI) and tidal volume (VT) in goats during CB normoxia, and systemic hypoxia (PaO2 = 29 Torr) significantly increased VI and respiratory frequency in these goats. CB hypoxia (CB PO2 = 34 Torr) in systemic normoxia significantly increased VI, VT, and VT/TI; the ventilatory effects of CB hypoxia were not significantly altered by varying systemic PaO2. We conclude that ventilation is stimulated by systemic hypoxia and hyperoxia in CB normoxia and that this ventilatory response to changes in systemic O2 affects the CB O2 response in an additive manner.
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GLASS, M. L., N. A. ANDERSEN, M. KRUHøFFER, E. M. WILLIAMS y N. HEISLER. "Combined Effects of Environmental PO2 and Temperature on Ventilation and Blood Gases in the Carp Cyprinus Carpio L". Journal of Experimental Biology 148, n.º 1 (1 de enero de 1990): 1–17. http://dx.doi.org/10.1242/jeb.148.1.1.
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The effects of changes in environmental temperature and oxygen tension on gill ventilation, arterial PO2, PCO2 pH and [HCO3−] were evaluated in carp (Cyprinus carpio L.). Gill ventilation was measured continuously in specimens acclimated to 10 or 20°C, combining the method of electromagnetic flow determination with the application of a rubber mask technique. After establishing control values in airequilibrated water the environmental water PO2 (PwO2) was reduced from about 150 mmHg (20 kPa) during control conditions to 110 or 75 mm Hg (14.7 or 10 kPa), respectively. Measurements of blood gases and acid-base parameters were performed repeatedly before, and 1 and 4 h after, initiation of hypoxia. Regardless of temperature, these moderately hypoxic conditions caused considerable and lasting increases in gill ventilation of about 70% (PWO2=110 mm Hg/l4.7kPa) or 180% (PwO2=75 mm Hg/10kPa), relative to the respective normoxic control values of about 50 ml kg−1min−1 at 10°C and 230 ml kg −1min−1 at 20°C. These increases in ventilation reduced PCO2 substantially, resulting in a rise in pHa by about 0.1 units at PwO2 of 110 mmHg (14.7 kPa) and by about 0.2 units at PwCO2 of 75 mmHg (lOkPa). Arterial PO2 was low under normoxic conditions at both temperatures (≈15 mmHg, ≈2kPa). During hypoxia, PaO2 was marginally reduced, whereas the arterial O2 content and saturation remained at normoxic levels, mainly because of the increase in the blood O2-affinity induced by respiratory alkalosis. Thislack of any clear relationship between arterial O2 content and ventilatory response to moderate hypoxia contrasts with previously reported data for trout, and supports the hypothesis that a change in PO2 is an adequate stimulus for the adjustment of ventilation in carp.
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Bacher, Andreas, Jae Young Kwon y Mark H. Zornow. "Effects of Temperature on Cerebral Tissue Oxygen Tension, Carbon Dioxide Tension, and pH during Transient Global Ischemia in Rabbits". Anesthesiology 88, n.º 2 (1 de febrero de 1998): 403–9. http://dx.doi.org/10.1097/00000542-199802000-00019.
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Background A decrease in brain temperature (Tbrain) causes a decrease in the cerebral metabolic rate for oxygen (CMRO2) and provides potent neuroprotection against ischemic damage. In the present study, the effects of mild to moderate hypothermia on cerebral tissue oxygen tension (PO2 brain), carbon dioxide tension (PCO2 brain), and pH (pHbrain) were monitored during short episodes of global cerebral ischemia. Methods After approval by the Animal Care and Use Committee, 10 New Zealand white rabbits were anesthetized (1% halothane in air) and mechanical ventilation was adjusted to maintain the arterial carbon dioxide tension at 35 mmHg (alpha-stat). A sensor to measure PO2 brain, PCO2 brain, pHbrain, and Tbrain was inserted into the brain through a burr hole in the skull. Tbrain was adjusted to 38 degrees C, 34.4 degrees C, and 29.4 degrees C in a random sequence in each animal. PO2 brain, PCO2brain, and pHbrain (all variables are reported at the actual Tbrain) were recorded every 10 s during a 5-min baseline, 3 min of cerebral ischemia induced by inflation of a neck tourniquet, and 10 min of reperfusion at each level of Tbrain. Analysis of variance and Dunnett's test were used for statistical analysis. Data are presented as means +/- SD. Results During ischemia, PO2 brain decreased from 56 +/- 3 to 33 +/- 2 mmHg at 38 degrees C, from 58 +/- 3 to 32 +/- 3 mmHg at 34.4 degrees C, and from 51 +/- 2 to 32 +/- 2 mmHg at 29.4 degrees C (p = NS). PCO2 brain increased by 6.7 +/- 2 mmHg at 38 degrees C, by 5.1 +/- 1.4 mmHg at 34.4 degrees C, and by 2.3 +/- 0.8 mmHg at 29.4 degrees C. pHbrain inversely followed the trend of PCO2 brain. Conclusions The attenuated increase in PCO2 brain during hypothermic ischemia results from the reduced CMRO2. The similar decrease in PO2 brain at all temperature levels indicates that despite the reduction in CMRO2, PO2 brain is no better preserved during brief episodes of hypothermic ischemia than during normothermic ischemia.
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Kett-White, Rupert, Peter J. Hutchinson, Pippa G. Al-Rawi, Marek Czosnyka, Arun K. Gupta, John D. Pickard y Peter J. Kirkpatrick. "Cerebral oxygen and microdialysis monitoring during aneurysm surgery: effects of blood pressure, cerebrospinal fluid drainage, and temporary clipping on infarction". Journal of Neurosurgery 96, n.º 6 (junio de 2002): 1013–19. http://dx.doi.org/10.3171/jns.2002.96.6.1013.
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Object. The aim of this study was to investigate potential episodes of cerebral ischemia during surgery for large and complicated aneurysms, by examining the effects of arterial temporary clipping and the impact of confounding variables such as blood pressure and cerebrospinal fluid (CSF) drainage. Methods. Brain tissue PO2, PCO2, and pH, as well as temperature and extracellular glucose, lactate, pyruvate, and glutamate were monitored in 46 patients by using multiparameter sensors and microdialysis. Baseline data showed that brain tissue PO2 decreased significantly, below a mean arterial pressure (MAP) threshold of 70 mm Hg. Further evidence of its relationship with cerebral perfusion pressure was shown by an increase in mean brain tissue PO2 after drainage of CSF from the basal cisterns (Wilcoxon test, p < 0.01). Temporary clipping was required in 31 patients, with a mean total duration of 14 minutes (range 3–52 minutes), causing brain tissue PO2 to decrease and brain tissue PCO2 to increase (Wilcoxon test, p < 0.01). In patients in whom no subsequent infarction developed in the monitored region, brain tissue PO2 fell to 11 mm Hg (95% confidence interval 8–14 mm Hg). A brain tissue PO2 level below 8 mm Hg for 30 minutes was associated with infarction in any region (p < 0.05 according to the Fisher exact test); other parameters were not predictive of infarction. Intermittent occlusions of less than 30 minutes in total had little effect on extracellular chemistry. Large glutamate increases were only seen in two patients, in both of whom brain tissue PO2 during occlusion was continuously lower than 8 mm Hg for longer than 38 minutes. Conclusions. The brain tissue PO2 decreases with hypotension, and, when it is below 8 mm Hg for longer than 30 minutes during temporary clipping, it is associated with increasing extracellular glutamate levels and cerebral infarction.
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Torre-Bueno, J. R., P. D. Wagner, H. A. Saltzman, G. E. Gale y R. E. Moon. "Diffusion limitation in normal humans during exercise at sea level and simulated altitude". Journal of Applied Physiology 58, n.º 3 (1 de marzo de 1985): 989–95. http://dx.doi.org/10.1152/jappl.1985.58.3.989.
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The relative roles of ventilation-perfusion (VA/Q) inequality, alveolar-capillary diffusion resistance, postpulmonary shunt, and gas phase diffusion limitation in determining arterial PO2 (PaO2) were assessed in nine normal unacclimatized men at rest and during bicycle exercise at sea level and three simulated altitudes (5,000, 10,000, and 15,000 ft; barometric pressures = 632, 523, and 429 Torr). We measured mixed expired and arterial inert and respiratory gases, minute ventilation, and cardiac output. Using the multiple inert gas elimination technique, PaO2 and the arterial O2 concentration expected from VA/Q inequality alone were compared with actual values, lower measured PaO2 indicating alveolar-capillary diffusion disequilibrium for O2. At sea level, alveolar-arterial PO2 differences were approximately 10 Torr at rest, increasing to approximately 20 Torr at a metabolic consumption of O2 (VO2) of 3 l/min. There was no evidence for diffusion disequilibrium, similar results being obtained at 5,000 ft. At 10 and 15,000 ft, resting alveolar-arterial PO2 difference was less than at sea level with no diffusion disequilibrium. During exercise, alveolar-arterial PO2 difference increased considerably more than expected from VA/Q mismatch alone. For example, at VO2 of 2.5 l/min at 10,000 ft, total alveolar-arterial PO2 difference was 30 Torr and that due to VA/Q mismatch alone was 15 Torr. At 15,000 ft and VO2 of 1.5 l/min, these values were 25 and 10 Torr, respectively. Expected and actual PaO2 agreed during 100% O2 breathing at 15,000 ft, excluding postpulmonary shunt as a cause of the larger alveolar-arterial O2 difference than accountable by inert gas exchange.
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Murtisiwi, Lusia. "EVALUATION OF TREATMENT BRONCHODILATORS AND CORTICOSTEROIDS IN COPD INPATIENT IN HOSPITALS DR. MOEWARDI SURAKARTA JANUARY 2016-JUNE 2017". Jurnal Farmasi (Journal of Pharmacy) 1, n.º 1 (20 de octubre de 2018): 73–80. http://dx.doi.org/10.37013/jf.v1i1.67.
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Chronic Obstructive Pulmonary Disease (COPD) is one of the cause of mortality and morbidity in worldwide. This study aims to determine the pattern of treatment of bronchodilators with or without corticosteroids and their effects on changes carbon dioxide pressure in blood (PCO2) and oxygen pressure in blood (PO2) in COPD patients of inpatient in RSUD Dr. Moewardi Surakarta January 2016-June 2017. This research is a retrospective descriptive research design, data collecting by tracking medical records patients with 195 samples. The results showed that treatment of COPD patient using single bronchodilator of 30,8%, bronchodilator combination of 57,1%, bronchodilator combination with corticosteroid of 1% and corticosteroid equal to 91,3%.Effect of bronchodilator treatment without corticosteroids on changes in the largest largest PCO2 change of 14.8%, the smallest change in PCO25.9%, the largest PO2 change was 19%, the smallest PO2 change was 5.6%, whereas in patients who received bronchodilator treatment with corticosteroids there was the largest PCO2 change of 87.4%, the smallest PCO2 cha
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Kadam, Paulina, Ni Putu Rahayu Artini y I. Wayan Tanjung Aryasa. "GAMBARAN NILAI SATURASI OKSIGEN (SO2) DENGAN TEKANAN OKSIGEN (PO2) PADA PASIEN PENYAKIT JANTUNG KORONER (PJK) DI RUMAH SAKIT UMUM DAERAH JAYAPURA". JOURNAL OF MUHAMMADIYAH MEDICAL LABORATORY TECHNOLOGIST 3, n.º 2 (12 de diciembre de 2020): 57. http://dx.doi.org/10.30651/jmlt.v3i2.5861.
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Coronary heart disease (CHD) patients are equipped with blood tests to reinforce the diagnosis of the patient's disease. One of the parameters that is usually checked is blood gas analysis (AGD). One of the parameters of blood gas analysis (BGA) is oxygen saturation (SO2), oxygen pressure (PO2), and carbon dioxide pressure (PCO2). The purpose of this study was to determine the relationship between SO2, and PO2,at the Jayapura Regional General Hospital. This type of research is retrospective analytic. The sample of this study were coronary heart patients who underwent BGA xamination at the Jayapura General Hospital who met the inclusion criteria, so that 30 samples were obtained. The type of data is secondary data. With the mean value of SO2 is 96,1% and PO2 is 133,2 mmHg. The results of the relationship between SO2 and PO2 in coronary heart disease patients at Jayapura Regional Hospital are directly proportional, namely the decrease in SO2, PO2 will also decrease in CHD patients, with four people experiencing moderate hypoxemia, five people with normal PO2, and 21 people with PO2 is high because you have got a ventilator device.