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1
Bordi, Christophe, Chantal Iobbi-Nivol, Vincent Méjean, and Jean-Claude Patte. "Effects of ISSo2 Insertions in Structural and Regulatory Genes of the Trimethylamine Oxide Reductase of Shewanella oneidensis." Journal of Bacteriology 185, no. 6 (March 15, 2003): 2042–45. http://dx.doi.org/10.1128/jb.185.6.2042-2045.2003.
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ABSTRACT We have isolated three Shewanella oneidensis mutants specifically impaired in trimethylamine oxide (TMAO) respiration. The mutations arose from insertions of an ISSo2 element into torA, torR, and torS, encoding, respectively, the TMAO reductase TorA, the response regulator TorR, and the sensor TorS. Although TorA is not the sole enzyme reducing TMAO in S. oneidensis, growth analysis showed that it is the main respiratory TMAO reductase. Use of a plasmid-borne torE′-lacZ fusion confirmed that the TorS-TorR phosphorelay mediates TMAO induction of the torECAD operon.
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Bordi, Christophe, Mireille Ansaldi, Stéphanie Gon, Cécile Jourlin-Castelli, Chantal Iobbi-Nivol, and Vincent Méjean. "Genes Regulated by TorR, the Trimethylamine Oxide Response Regulator of Shewanella oneidensis." Journal of Bacteriology 186, no. 14 (July 15, 2004): 4502–9. http://dx.doi.org/10.1128/jb.186.14.4502-4509.2004.
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ABSTRACT The torECAD operon encoding the trimethylamine oxide (TMAO) respiratory system of Shewanella oneidensis is positively controlled by the TorS/TorR two-component system when TMAO is available. Activation of the tor operon occurs upon binding of the phosphorylated response regulator TorR to a single operator site containing the direct repeat nucleotide sequence TTCATAN4TTCATA. Here we show that the replacement of any nucleotide of one TTCATA hexamer prevented TorR binding in vitro, meaning that TorR specifically interacts with this DNA target. Identical direct repeat sequences were found in the promoter regions of torR and of the new gene torF (SO4694), and they allowed TorR binding to both promoters. Real-time PCR experiments revealed that torR is negatively autoregulated, whereas torF is strongly induced by TorR in response to TMAO. Transcription start site location and footprinting analysis indicate that the operator site at torR overlaps the promoter −10 box, whereas the operator site at torF is centered at −74 bp from the start site, in agreement with the opposite role of TorR in the regulation of the two genes. Since torF and torECAD are positively coregulated by TorR, we propose that the TorF protein plays a role related to TMAO respiration.
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Ebell, Mark H., Akke Vellinga, Siobhan Masterson, and Phillip Yun. "Meta-analysis of the accuracy of termination of resuscitation rules for out-of-hospital cardiac arrest." Emergency Medicine Journal 36, no. 8 (May 29, 2019): 479–84. http://dx.doi.org/10.1136/emermed-2018-207833.
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BackgroundOur objective was to perform a systematic review of studies reporting the accuracy of termination of resuscitation rules (TORRs) for out-of-hospital cardiac arrest (OHCA).MethodsWe performed a comprehensive search of the literature for studies evaluating the accuracy of TORRs, with two investigators abstracting relevant data from each study regarding study design, study quality and the accuracy of the TORRs. Bivariate meta-analysis was performed using the mada procedure in R.ResultsWe identified 14 studies reporting the performance of 9 separate TORRs. The sensitivity (proportion of eventual survivors for whom the TORR recommends resuscitation and transport) was generally high: 95% for the European Resuscitation Council (ERC) TORR, 97% for the basic life support (BLS) TORR and 99% for the advanced life support (ALS) TORR. The BLS and ERC TORR were more specific, which would lead to fewer futile transports, and all three of these TORRs had a miss rate of ≤0.13% (defined as a case where a patient is recommended for termination but survives). The pooled proportion of patients for whom each rule recommends TOR was much higher for the ERC and BLS TORRs (93.5% and 74.8%, respectively) than for the ALS TORR (29.0%).ConclusionsThe BLS and ERC TORRs identify a large proportion of patients who are candidates for termination of resuscitation following OHCA while having a very low rate of misclassifying eventual survivors (<0.1%). Further prospective validation of the ERC TORR and direct comparison with BLS TORR are needed.
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Ansaldi, Mireille, Gwénola Simon, Michèle Lepelletier, and Vincent Méjean. "The TorR High-Affinity Binding Site Plays a Key Role in Both torR Autoregulation and torCADOperon Expression in Escherichia coli." Journal of Bacteriology 182, no. 4 (February 15, 2000): 961–66. http://dx.doi.org/10.1128/jb.182.4.961-966.2000.
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ABSTRACT In the presence of trimethylamine N-oxide (TMAO), the TorS-TorR two-component regulatory system induces thetorCAD operon, which encodes the TMAO respiratory system ofEscherichia coli. The sensor protein TorS detects TMAO and transphosphorylates the response regulator TorR which, in turn, activates transcription of torCAD. The torRgene and the torCAD operon are divergently transcribed, and the short torR-torC intergenic region contains four direct repeats (the tor boxes) which proved to be TorR binding sites. The tor box 1-box 2 region covers thetorR transcription start site and constitutes a TorR high-affinity binding site, whereas box 3 and box 4 correspond to low-affinity binding sites. By using torR-lacZ operon fusions in different genetic backgrounds, we showed that thetorR gene is negatively autoregulated. Surprisingly, TorR autoregulation is TMAO independent and still occurs in atorS mutant. In addition, this negative regulation involves only the TorR high-affinity binding site. Together, these data suggest that phosphorylated as well as unphosphorylated TorR binds the box 1-box 2 region in vivo, thus preventing RNA polymerase from binding to the torR promoter whatever the growth conditions. By changing the spacing between box 2 and box 3, we demonstrated that the DNA motifs of the high- and low-affinity binding sites must be close to each other and located on the same side of the DNA helix to allow induction of the torCAD operon. Thus, prior TorR binding to the box 1-box 2 region seems to allow cooperative binding of phosphorylated TorR to box 3 and box 4.
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Ansaldi, Mireille, Cécile Jourlin-Castelli, Michèle Lepelletier, Laurence Théraulaz, and Vincent Méjean. "Rapid Dephosphorylation of the TorR Response Regulator by the TorS Unorthodox Sensor in Escherichia coli." Journal of Bacteriology 183, no. 8 (April 15, 2001): 2691–95. http://dx.doi.org/10.1128/jb.183.8.2691-2695.2001.
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ABSTRACT Induction of the torCAD operon, encoding the trimethylamine N-oxide (TMAO) respiratory system, is tightly controlled by the TorS-TorR phosphorelay system in response to TMAO availability. TorS is an unorthodox sensor that contains three phosphorylation sites and transphosphorylates TorR via a four-step phosphorelay, His443→Asp723→His850→Asp(TorR). In this study, we provide genetic evidence that TorS can dephosphorylate phospho-TorR when TMAO is removed. Dephosphorylation probably occurs by a reverse phosphorelay, Asp(TorR)→His850→Asp723, since His850 and Asp723 are both essential in this process. By using reverse transcriptase PCR, we also show that TMAO removal results in shutoff of toroperon transcription in less than 2 min. Based on our results and on analogy to other phosphorelay signal transduction systems, we propose that reverse phosphotransfer could be a rapid and efficient mechanism to inactivate response regulators.
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Shi, X., C. G. Crandall, and P. B. Raven. "Hemodynamic responses to graded lower body positive pressure." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 1 (July 1, 1993): H69—H73. http://dx.doi.org/10.1152/ajpheart.1993.265.1.h69.
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Fourteen healthy young men were exposed to progressive increases in lower body positive pressure (LBPP) from 0 to 40 Torr in the supine position. Central venous pressure (CVP) increased 1.09 mmHg (P < 0.05) at 5 Torr LBPP. Between 20 and 40 Torr LBPP CVP increased 0.85 mmHg, resulting in a total increase of 2.06 mmHg (P < 0.05). During 0–20 Torr LBPP mean arterial pressure (MAP) increased from 86 to 89 mmHg with a slope of 0.15 mmHg/Torr LBPP. Stroke volume and cardiac output were significantly increased at 20 Torr LBPP. Beyond 20 Torr LBPP, MAP increased to 95 mmHg at 40 Torr (P < 0.05) with a slope of 0.32 mmHg/Torr LBPP. Forearm blood flow increased above rest at 40 Torr LBPP (P< 0.05). However, neither peripheral nor forearm vascular resistance decreased significantly from rest. Despite the significant increases in MAP, heart rate was unchanged above 20 Torr LBPP. These data suggest that LBPP produces increases in CVP at 0–20 Torr by translocation of blood volume from the legs to the thorax. At LBPP > 20 Torr, further increases in CVP and MAP were produced by other mechanisms possibly related to an activation of intramuscular pressure-sensitive receptors.
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Lucero, M., J. R. Barrow, P. Osuna, and I. Reyes. "A cryptic microbial community persists within micropropagated Bouteloua eriopoda (Torr.) Torr. cultures." Plant Science 174, no. 6 (June 2008): 570–75. http://dx.doi.org/10.1016/j.plantsci.2008.02.012.
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Osuna, Pedro, and Jerry R. Barrow. "Regeneration of black grama (Bouteloua eriopoda torr. torr) plants via somatic embryogenesis." In Vitro Cellular & Developmental Biology - Plant 40, no. 3 (May 2004): 299–302. http://dx.doi.org/10.1079/ivp2003533.
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Eno, N. Clare. "The morphometrics of cephalopod gills." Journal of the Marine Biological Association of the United Kingdom 74, no. 3 (August 1994): 687–706. http://dx.doi.org/10.1017/s0025315400047743.
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The capacity for oxygen uptake of a respiratory organ can be estimated using morpho-metric techniques, the two essential measurements being respiratory surface-area and thickness of the tissue barrier across which oxygen diffuses. In cephalopods, the gills are the main site of respiratory exchange and this study was designed to estimate oxygen uptake capacity of the gills of four different genera of cephalopods. A preliminary study was required to determine the form and structure of the gills. Light microscopy showed the surface of the gills to be highly folded, particularly in Octopus. A level of microscopy was chosen at which the outline of the smallest folds of the epithelium and the blood vessels of the gills could be easily resolved. Stereological techniques were then employed to obtain values for the respiratory surface-area related to body weight (cm2 g-1), tissue barrier thickness (μm) and oxygen-diffusing capacity (ml O2 min1 Torr·1 kg1). Values for these three variables obtained for the different species were as follows: Octopus vulgaris 2·9 cm2 g-1, 10 μm, 0·05 ml O2 min-1 Torr-1 kg1; Alloteuthis subulata 10·6 cm2 g1,6 μm, 0·27 ml O2 min-1 Torr-1 kg-1; Nautilus sp. 4·9 cm2 g-1,15 μm, 0·05 ml O2 min-1 Torr1 kg-1; Sepia hatchlings 13·3 cm2 g-1, 4 μm, 0·52 ml O2 min-1 Torr-1 kg-1.
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Mertens, S., T. Noll, R. Spahr, A. Krutzfeldt, and H. M. Piper. "Energetic response of coronary endothelial cells to hypoxia." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 3 (March 1, 1990): H689—H694. http://dx.doi.org/10.1152/ajpheart.1990.258.3.h689.
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The response of endothelial energy metabolism to oxygen supply was studied in cultured coronary endothelial cells from the rat at defined PO2 levels between 0.1 and 100 Torr. In the presence of glucose (5 mM), endothelial respiration (4 nmol O2.min-1.mg protein-1) was independent of the exterior PO2 greater than 3 Torr; oxygen consumption was half maximal at 0.8 Torr. At 100 Torr, lactate production was 26 nmol.min-1.mg protein-1; the decrease of the PO2 to 0.1 Torr resulted in a 2.2-fold increase in lactate production. The contents of ATP, ADP, and AMP were 21, 4, and 2 nmol/mg protein, respectively; they remained constant for 2.5-h incubations at PO2 levels between 0.1 and 100 Torr. In the presence of palmitate (100 microM) plus glutamine (0.5 mM), oxygen consumption was 8 nmol.min-1.mg protein-1 at PO2 levels greater than 3 Torr, and the half-maximal rate was again observed at 0.8 Torr. Lactate production was negligible. At PO2 levels greater than 3 Torr, the cells remained well energized. Below 3 Torr, however, the adenine nucleotide contents rapidly declined. These results demonstrate that the oxygen demand of coronary endothelial cells is low compared with the beating myocardium. In the presence of glucose, aerobic glycolysis is pronounced and the Pasteur effect small. In severe hypoxia (PO2 less than 0.1 Torr) the energetic state remained stable. In the absence of glucose, the energetic state of coronary endothelial cells is sensitive to the exterior PO2 less than 3 Torr, declining concomitantly with the decrease in respiration.
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Young, P. M., J. R. Sutton, H. J. Green, J. T. Reeves, P. B. Rock, C. S. Houston, and A. Cymerman. "Operation Everest II: metabolic and hormonal responses to incremental exercise to exhaustion." Journal of Applied Physiology 73, no. 6 (December 1, 1992): 2574–79. http://dx.doi.org/10.1152/jappl.1992.73.6.2574.
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The reasons for the reduced exercise capacities observed at high altitudes are not completely known. Substrate availability or accumulations of lactate and ammonium could have significant roles. As part of Operation Everest II, peak oxygen uptakes were determined in five normal male volunteers with use of progressively increasing cycling work loads at ambient barometric pressures of 760, 380, and 282 Torr. Decrements from sea level (SL) to 380 and 282 Torr occurred in peak power output (19 and 47%), time to exhaustion (19 and 48%), and oxygen uptake (41 and 61%), respectively. Arterial saturations after exhaustive exercise were decreased to 63% at 380 Torr and 39% at 282 Torr. At 380 and 282 Torr, postexercise plasma concentrations of glucose and free fatty acids were not increased, whereas plasma glycerol concentrations were decreased relative to SL (145 +/- 24 microM at 380 Torr and 77 +/- 10 microM at 282 Torr vs. 213 +/- 24 microM at SL). Preexercise plasma insulin concentrations were elevated at both 380 and 282 Torr (87 +/- 16 pM at 380 Torr and 85 +/- 18 pM at 282 Torr vs. 41 +/- 30 pM at SL). In general, postexercise concentrations of plasma catecholamines were decreased at altitude compared with SL. Preexercise lactate and ammonium concentrations were not different at any simulated altitude. From these data neither substrate availability nor metabolic product accumulation limited exercise capacity at extreme simulated altitude.
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Morelli, Chris, M. Safwan Badr, and Jason H. Mateika. "Ventilatory responses to carbon dioxide at low and high levels of oxygen are elevated after episodic hypoxia in men compared with women." Journal of Applied Physiology 97, no. 5 (November 2004): 1673–80. http://dx.doi.org/10.1152/japplphysiol.00541.2004.
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We hypothesized that the acute ventilatory response to carbon dioxide in the presence of low and high levels of oxygen would increase to a greater extent in men compared with women after exposure to episodic hypoxia. Eleven healthy men and women of similar race, age, and body mass index completed a series of rebreathing trials before and after exposure to eight 4-min episodes of hypoxia. During the rebreathing trials, subjects initially hyperventilated to reduce the end-tidal partial pressure of carbon dioxide (PetCO2) below 25 Torr. Subjects then rebreathed from a bag containing a normocapnic (42 Torr), low (50 Torr), or high oxygen gas mixture (150 Torr). During the trials, PetCO2 increased while the selected level of oxygen was maintained. The point at which minute ventilation began to rise in a linear fashion as PetCO2 increased was considered to be the carbon dioxide set point. The ventilatory response below and above this point was determined. The results showed that the ventilatory response to carbon dioxide above the set point was increased in men compared with women before exposure to episodic hypoxia, independent of the oxygen level that was maintained during the rebreathing trials (50 Torr: men, 5.19 ± 0.82 vs. women, 4.70 ± 0.77 l·min−1·Torr−1; 150 Torr: men, 4.33 ± 1.15 vs. women, 3.21 ± 0.58 l·min−1·Torr−1). Moreover, relative to baseline measures, the ventilatory response to carbon dioxide in the presence of low and high oxygen levels increased to a greater extent in men compared with women after exposure to episodic hypoxia (50 Torr: men, 9.52 ± 1.40 vs. women, 5.97 ± 0.71 l·min−1·Torr−1; 150 Torr: men, 5.73 ± 0.81 vs. women, 3.83 ± 0.56 l·min−1·Torr−1). Thus we conclude that enhancement of the acute ventilatory response to carbon dioxide after episodic hypoxia is sex dependent.
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Chandel, N., G. R. Budinger, R. A. Kemp, and P. T. Schumacker. "Inhibition of cytochrome-c oxidase activity during prolonged hypoxia." American Journal of Physiology-Lung Cellular and Molecular Physiology 268, no. 6 (June 1, 1995): L918—L925. http://dx.doi.org/10.1152/ajplung.1995.268.6.l918.
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During acute (< 30 min) hypoxia, cellular respiration is independent of the O2 concentration as long as PO2 remains above a critical value (5–10 Torr). Similarly, state 3 respiration by isolated mitochondria is independent of PO2 above a critical tension of 2–4 Torr. However, rat hepatocytes demonstrate a reversible suppression of respiration and an increase in NAD(P)H concentration during prolonged (2–24 h), but not acute hypoxia [P. T. Schumacker, N. Chandel, and A. G. N. Augusti. Am. J. Physiol. 265 (Lung Cell. Mol. Physiol. 9): L395–L402, 1993]. This study tested whether respiration is similarly inhibited in isolated mitochondria exposed to low PO2 for prolonged periods and whether cytochrome-c oxidase participates in this response. Coupled rat liver mitochondria were incubated under low oxygen conditions (PO2 < 2 Torr) for 2 h. State 3 respiration after reoxygenation to PO2 = 20 Torr was then compared with the value obtained subsequently at 100 Torr. Using succinate and ADP as substrates, we determined that state 3 respiration at 20 Torr was 61.0 +/- 8.4% of the subsequent value at 100 Torr (P < 0.05). By contrast, control mitochondria reoxygenated to 100 Torr first and 20 Torr subsequently showed no significant difference at the two O2 tensions (P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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Papelier, Y., P. Escourrou, J. P. Gauthier, and L. B. Rowell. "Carotid baroreflex control of blood pressure and heart rate in men during dynamic exercise." Journal of Applied Physiology 77, no. 2 (August 1, 1994): 502–6. http://dx.doi.org/10.1152/jappl.1994.77.2.502.
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The degree of control of blood pressure (BP) and heart rate (HR) by arterial baroreflex during exercise is still controversial. We studied baroreflex control of BP and HR in seven normal young men by a noninvasive procedure employing a neck suction chamber that delivers pulsatile positive and negative pressures to the carotid sinus (CS). Pressures applied to the CS ranged from -80 to +60 Torr in steps of 20 Torr. Pressure stimuli were triggered by electrocardiogram R wave, and each pressure step was maintained for 20 s in a continuous sequence. One baroreflex-response curve was obtained during the last 3 min of each 6-min period of exercise. The four levels of upright (cycle) exercise were 60, 120, 180, and 240 W, the highest requiring approximately 75% of maximal O2 uptake. The sensitivity of the HR baroreflex response assessed by linear regression of HR vs. CS pressure (CSP) did not significantly decrease from rest (-0.09 +/- 0.053 beat/Torr) to 240 W (-0.06 +/- 0.025 beat/Torr). The BP above or below which CSP was increased or decreased by neck collar pressure was significantly increased from rest (76 +/- 6.5 Torr) to 240 W (111.2 +/- 4.0 Torr). The sensitivity of baroreflex response was assessed by linear regression of BP vs. CSP and was not significantly different from rest (-0.29 +/- 0.054 Torr/Torr) up to exercise at 240 W (-0.29 +/- 0.048 Torr/Torr). We conclude that mild to severe exercise does not reduce the gain of the CS reflex below resting values.(ABSTRACT TRUNCATED AT 250 WORDS)
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Gon, Stéphanie, Jean-Claude Patte, Jean-Philippe Dos Santos, and Vincent Méjean. "Reconstitution of the Trimethylamine Oxide Reductase Regulatory Elements of Shewanella oneidensis in Escherichia coli." Journal of Bacteriology 184, no. 5 (March 1, 2002): 1262–69. http://dx.doi.org/10.1128/jb.184.5.1262-1269.2002.
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ABSTRACT Several bacteria can grow by using small organic compounds such as trimethylamine oxide (TMAO) as electron acceptors. In Shewanella species, the TMAO reductase respiratory system is encoded by the torECAD operon. We showed that production of the TMAO reductase of S. oneidensis was induced by TMAO and repressed by oxygen, and we noticed that a three-gene cluster (torSTR) encoding a complex two-component regulatory system was present downstream of the torECAD operon. We introduced the torSTR gene cluster into Escherichia coli and showed that this regulatory gene cluster is involved in TMAO induction of the torE promoter but plays no role in the oxygen control. The TorR response regulator was purified, and gel shift and footprinting experiments revealed that TorR binds to a single region located about 70 bases upstream of the transcription start site of the tor structural operon. By deletion analysis, we confirmed that the TorR operator site is required for induction of the tor structural promoter. As the TMAO regulatory system of S. oneidensis is homologous to that of E. coli, we investigated a possible complementation between the TMAO regulatory components of the two bacteria. Interestingly, TorSec, the TMAO sensor of E. coli, was able to transphosphorylate TorRso, the TMAO response regulator of S. oneidensis.
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Shah, Sidharth, Julie Allen, John G. Wood, and Norberto C. Gonzalez. "Dissociation between skeletal muscle microvascular Po2and hypoxia-induced microvascular inflammation." Journal of Applied Physiology 94, no. 6 (June 1, 2003): 2323–29. http://dx.doi.org/10.1152/japplphysiol.01185.2002.
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Systemic hypoxia (SHx) produces microvascular inflammation in mesenteric, cremasteric, and pial microcirculations. In anesthetized rats, SHx lowers arterial blood pressure (MABP), which may alter microvascular blood flow and microvascular Po2(PmO2) and influence SHx-induced leukocyte-endothelial adherence (LEA). These experiments attempted to determine the individual contributions of the decreases in PmO2, venular blood flow and shear rate, and MABP to the hypoxia-induced increase in LEA. Cremaster microcirculation of anesthetized rats was visualized by intravital microscopy. PmO2was measured by a phosphorescence-quenching method. SHx [inspired Po2of 70 Torr for 10 min, MABP of 65 ± 3 mmHg, arterial Po2(PaO2) of 33 ± 1 Torr] and cremaster ischemia (MABP of 111 ± 7 mmHg, PaO2of 86 ± 3 Torr) produced similar PmO2: 7 ± 2 and 6 ± 2 Torr, respectively. However, LEA increased only in SHx (1.9 ± 0.9 vs. 11.2 ± 1.1 leukocytes/100 μm, control vs. SHx, P < 0.05). Phentolamine-induced hypotension (MABP of 55 ± 4 mmHg) in normoxia lowered PmO2to 26 ± 6 Torr but did not increase LEA. Cremaster equilibration with 95% N2-5% CO2during air breathing (PaO2of 80 ± 1 Torr) lowered PmO2to 6 ± 1 Torr but did not increase LEA. On the other hand, when cremaster PmO2was maintained at 60–70 Torr during SHx (PaO2of 35 ± 1 Torr), LEA increased from 2.1 ± 1.1 to 11.1 ± 1.5 leukocytes/100 μm ( P < 0.05). The results show a dissociation between PmO2and LEA and support the idea that SHx results in the release of a mediator responsible for the inflammatory response.
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Erickson, B. K., J. Seaman, K. Kubo, A. Hiraga, M. Kai, Y. Yamaya, and P. D. Wagner. "Mechanism of reduction in alveolar-arterial PO2 difference by helium breathing in the exercising horse." Journal of Applied Physiology 76, no. 6 (June 1, 1994): 2794–801. http://dx.doi.org/10.1152/jappl.1994.76.6.2794.
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Previous work has shown that replacing N2 in air with He at the same inspired O2 fraction reduces the exercise-induced alveolar-arterial PO2 difference (AaPO2) in horses but has provided no mechanism explaining this effect. We sought to distinguish among possible causes by using the multiple inert gas elimination technique. Six horses were studied on a high-speed treadmill while they breathed either ambient air or normoxic He-O2. O2 uptake reached 138.0 ml.min-1.kg-1 and was not affected by He-O2. Temperature-corrected arterial PO2 was 76.7 Torr (air) and 86.9 Torr (He-O2) (P < 0.01). Corresponding AaPO2 was 22.3 and 15.9 Torr, respectively (P < 0.01). Mean AaPO2 predicted from ventilation-perfusion inequality did not change with He-O2 (12.7 Torr with air and 11.9 Torr with He-O2). Mean arterial PCO2 was 50.1 Torr with air and 44.1 Torr with He-O2 (P < 0.01); minute ventilation and tidal volume were correspondingly higher by 140 l/min and 1.0 liter, respectively, with He-O2. Pulmonary O2 diffusing capacity, cardiac output, and all ventilation-perfusion dispersion indexes did not change with He-O2. Intrapulmonary shunt was insignificant. Higher ventilation with He-O2 explained only approximately 4 Torr of the 10-Torr rise observed in arterial PO2. The remainder (and the corresponding fall in AaPO2) was due to more complete diffusion equilibration as a consequence of the higher minute ventilation and thus alveolar PO2, which reduced the average slope of the O2 dissociation curve, thereby increasing the ratio of diffusive to perfusive conductance.
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Brower, R. G., J. Gottlieb, R. A. Wise, S. Permutt, and J. T. Sylvester. "Locus of hypoxic vasoconstriction in isolated ferret lungs." Journal of Applied Physiology 63, no. 1 (July 1, 1987): 58–65. http://dx.doi.org/10.1152/jappl.1987.63.1.58.
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To determine whether hypoxic pulmonary vasoconstriction (HPV) occurs mainly in alveolar or extra-alveolar vessels in ferrets, we used two groups of isolated lungs perfused with autologous blood and a constant left atrial pressure (-5 Torr). In the first group, flow (Q) was held constant at 50, 100, and 150 ml.kg-1 X min-1, and changes in pulmonary arterial pressure (Ppa) were recorded as alveolar pressure (Palv) was lowered from 25 to 0 Torr during control [inspired partial pressure of O2 (PIO2) = 200 Torr] and hypoxic (PIO2 = 25 Torr) conditions. From these data, pressure-flow relationships were constructed at several levels of Palv. In the control state, lung inflation did not affect the slope of the pressure-flow relationships (delta Ppa/delta Q), but caused the extrapolated pressure-axis intercept (Ppa0), representing the mean backpressure to flow, to increase when Palv was greater than or equal to 5 Torr. Hypoxia increased delta Ppa/delta Q and Ppa0 at all levels of Palv. In contrast to its effects under control condition, lung inflation during hypoxia caused a progressive decrease in delta Ppa/delta Q, and did not alter Ppa0 until Palv was greater than or equal to 10 Torr. In the second group of experiments flow was maintained at 100 ml.kg-1 X min-1, and changes in lung blood volume (LBV) were recorded as Palv was varied between 20 and 0 Torr. In the control state, inflation increased LBV over the entire range of Palv. In the hypoxic state inflation decreased LBV until Palv reached 8 Torr; at Palv 8–20 Torr, inflation increased LBV.(ABSTRACT TRUNCATED AT 250 WORDS)
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Johnson, Paul D., and Robert F. McMahon. "Effects of temperature and chronic hypoxia on survivorship of the zebra mussel (Dreissena polymorpha) and Asian clam (Corbicula fluminea)." Canadian Journal of Fisheries and Aquatic Sciences 55, no. 7 (July 1, 1998): 1564–72. http://dx.doi.org/10.1139/f98-030.
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We examined the effects of four levels of chronic hypoxic stress at three temperatures on the survivorship of Dreissena polymorpha and Corbicula fluminea to assess the efficacy of O2 deprivation as a macrofouling control treatment and examine if critical hypoxia limits support reported distribution patterns. At 25°C, the hypoxia tolerance was examined at Po2 = 7.9, 11.9, 15.9, 23.8, and 31.8 Torr (1 Torr = 133.322 Pa) or 5, 7.5, 10, 15, and 20% of full air O2 saturation (Po2 = 159 Torr). At 15°C, the hypoxia tolerance to 7.9, 11.9, and 15.9 Torr was tested and at 7.9 Torr for 5°C treatments. For both species, Po2 and temperature influenced survivorship dramatically with increasing survivorship at higher Po2 and decreasing temperatures. At 25°C, C. fluminea experienced mortality at 7.9, 11.9, and 15.9 Torr, with LT50 values of 144, 216, and 216 h, respectively, versus 288, 384, and 480 h for the 15°C exposures. Dreissena polymorpha treatments had LT50 values of 120, 216, and 216 h at 25°C for the 7.9-, 11.9-, and 15.9-Torr treatments versus 26% mortality after 600 h and 28% mortality after 720 h at 15°C. The 7.9-Torr treatments at 5°C had LT50 values of 480 h for C. fluminea and 1056 h for D. polymorpha. This study showed that both species displayed broad seasonal variation in hypoxia tolerance and that hypoxia limits may be used to assess infestation risk.
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Schaefer, S. L., and G. S. Mitchell. "Ventilatory control during exercise with peripheral chemoreceptor stimulation: hypoxia vs. domperidone." Journal of Applied Physiology 67, no. 6 (December 1, 1989): 2438–46. http://dx.doi.org/10.1152/jappl.1989.67.6.2438.
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Hypoxia potentiates the ventilatory response to exercise, eliciting a greater decrease in arterial PCO2 (PaCO2) from rest to exercise than in normoxia. The mechanism of this hypoxia-exercise interaction requires intact carotid chemoreceptors. To determine whether carotid chemoreceptor stimulation alone is sufficient to elicit the mechanism without whole body hypoxia, ventilatory responses to treadmill exercise were compared in goats during hyperoxic control conditions, moderate hypoxia (PaO2 = 38-44 Torr), and peripheral chemoreceptor stimulation with the peripheral dopamine D2-receptor antagonist, domperidone (Dom; 0.5 mg/kg iv). Measurements with Dom were made in both hyperoxia (Dom) and hypoxia (Dom/hypoxia). Finally, ventilatory responses to inspired CO2 at rest were compared in each experimental condition because enhanced CO2 chemoreception might be expected to blunt the PaCO2 decrease during exercise. At rest, PaCO2 decreased from control with Dom (-5.0 +/- 0.9 Torr), hypoxia (-4.1 +/- 0.5 Torr), and Dom/hypoxia (-11.1 +/- 1.2 Torr). The PaCO2 decrease from rest to exercise was not significantly different between control (-1.7 +/- 0.6 Torr) and Dom (-1.4 +/- 0.8 Torr) but was significantly greater in hypoxia (-4.3 +/- 0.7 Torr) and Dom/hypoxia (-3.5 +/- 0.9 Torr). The slope of the ventilation vs. CO2 production relationship in exercise increased with Dom (16%), hypoxia (18%), and Dom/hypoxia (68%). Ventilatory responses to inspired CO2 at rest increased from control to Dom (236%) and Dom/hypoxia (295%) and increased in four of five goats in hypoxia (mean 317%).(ABSTRACT TRUNCATED AT 250 WORDS)
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Lentini, A. C., R. S. McKelvie, N. McCartney, C. W. Tomlinson, and J. D. MacDougall. "Left ventricular response in healthy young men during heavy-intensity weight-lifting exercise." Journal of Applied Physiology 75, no. 6 (December 1, 1993): 2703–10. http://dx.doi.org/10.1152/jappl.1993.75.6.2703.
Full textAbstract:
We examined cardiac volumes (using echocardiography), intra-arterial blood pressure (BP), and intrathoracic pressure (ITP) in healthy males performing leg press exercise to failure at 95% of their maximum dynamic strength. Compared with preexercise, during the lifting phase of exercise, end-diastolic volume (EDV; 147 +/- 8 to 103 +/- 7 ml) and end-systolic volume (ESV; 54 +/- 5 to 27 +/- 4 ml) decreased (P < 0.05); heart rate (82 +/- 6 to 143 +/- 5 beats/min), systolic BP (160 +/- 6 to 270 +/- 21 Torr), diastolic BP (91 +/- 2 to 183 +/- 18 Torr), ITP (0.8 +/- 0.8 to 57.8 +/- 24 Torr), and peak systolic BP/ESV (SBP/ESV; 3.0 +/- 0.3 to 11.0 +/- 1.5 Torr/ml) increased (P < 0.05); and stroke volume decreased (94 +/- 3 to 77 +/- 4 ml; P > 0.05). Full knee extension was associated with most values returning to preexercise levels except for ESV (38 +/- 7 ml), heart rate (130 +/- 9 beats/min), and ITP (-12.5 +/- 2.1 Torr). During the lowering phase, significant decreases in EDV to 105 +/- 14 ml and ESV to 27 +/- 7 ml were observed with increases in systolic BP to 207 +/- 23 Torr, diastolic BP to 116 +/- 8 Torr, and SBP/ESV to 10.0 +/- 2.5 Torr/ml. Stroke volume decreased to 78 +/- 9 ml (P > 0.05). Thus rapid changes in cardiac volumes, contractility, and pressure occur during weight lifting that are related to different phases of the lift.
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Thornburg, K. L., and M. J. Morton. "Filling and arterial pressures as determinants of left ventricular stroke volume in fetal lambs." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 5 (November 1, 1986): H961—H968. http://dx.doi.org/10.1152/ajpheart.1986.251.5.h961.
Full textAbstract:
Left ventricular (LV) function was investigated in 16 fetal lambs (125-140 days gestation), each instrumented with an electromagnetic flow sensor on the ascending aorta and vascular catheters. Control arterial blood values were pH 7.38 +/- 0.02 (SD), PCO2 46.3 +/- 3.2 Torr, PO2 19.4 +/- 1.3 Torr, and hematocrit 34.8 +/- 4.3%. Control values for LV output (228 +/- 108 ml X min-1 X kg-1) and arterial pressure (AP, 47.4 +/- 6.5 Torr) were unchanged by administration of atropine and propranolol. LV function curves relating stroke volume (SV) to mean left atrial pressure (LAP) were generated by rapid withdrawal and reinfusion of fetal blood with or without concomitant infusion of nitroprusside (NP) or phenylephrine hydrochloride (PE) to lower or raise mean arterial pressure (AP). The control LV function curve was composed of a steep ascending limb of 0.39 +/- 0.34 ml X kg-1 X Torr-1 and a plateau of 0.04 +/- 0.04 ml X kg-1 X Torr-1. The breakpoint joining the limbs of the control curve was LAP 3.1 +/- 1.2 Torr and LVSV 1.3 +/- 0.5 ml/kg, and these values were not different from control LAP and SV. Function curve slopes were not affected by PE or NP treatment. Multiple linear regression of SV, LAP, and AP showed a small but significant coefficient for AP [-0.002 +/- 0.001 (SE) ml X kg-1 X Torr-1] and LAP [+0.053 +/- 0.004 (SE) ml X kg-1 X Torr-1] at LAP greater than breakpoint.(ABSTRACT TRUNCATED AT 250 WORDS)
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Khan, Akram, Mansour Qurashi, Kim Kwiatkowski, Don Cates, and Henrique Rigatto. "Measurement of the CO2 apneic threshold in newborn infants: possible relevance for periodic breathing and apnea." Journal of Applied Physiology 98, no. 4 (April 2005): 1171–76. http://dx.doi.org/10.1152/japplphysiol.00574.2003.
Full textAbstract:
We measured the Pco2 apneic threshold in preterm and term infants. We hypothesized that, compared with adult subjects, the Pco2 apneic threshold in neonates is very close to the eupneic Pco2, likely facilitating the appearance of periodic breathing and apnea. In contrast with adults, who need to be artificially hyperventilated to switch from regular to periodic breathing, neonates do this spontaneously. We therefore measured the apneic threshold as the average alveolar Pco2 (PaCO2) of the last three breaths of regular breathing preceding the first apnea of an epoch of periodic breathing. We also measured the PaCO2 of the first three breaths of regular breathing after the last apnea of the same periodic breathing epoch. In preterm infants, eupneic PaCO2 was 38.6 ± 1.4 Torr, the preperiodic PaCO2 apneic threshold was 37.3 ± 1.4 Torr, and the postperiodic PaCO2 was 37.2 ± 1.4 Torr. In term infants, the eupneic PaCO2 was 39.7 ± 1.1 Torr, the preperiodic PaCO2 apneic threshold was 38.7 ± 1.0 Torr, and the postperiodic value was 37.9 ± 1.2 Torr. This means that the PaCO2 apneic thresholds were 1.3 ± 0.1 and 1.0 ± 0.2 Torr below eupneic PaCO2 in preterm and term infants, respectively. The transition from eupneic PaCO2 to PaCO2 apneic threshold preceding periodic breathing was accompanied by a minor and nonsignificant increase in ventilation, primarily related to a slight increase in frequency. The findings suggest that neonates breathe very close to their Pco2 apneic threshold, the overall average eupneic Pco2 being only 1.15 ± 0.2 Torr (0.95–1.79, 95% confidence interval) above the apneic threshold. This value is much lower than that reported for adult subjects (3.5 ± 0.4 Torr). We speculate that this closeness of eupneic and apneic Pco2 thresholds confers great vulnerability to the respiratory control system in neonates, because minor oscillations in breathing may bring eupneic Pco2 below threshold, causing apnea.
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Tripathi, A., and E. R. Nadel. "Forearm skin and muscle vasoconstriction during lower body negative pressure." Journal of Applied Physiology 60, no. 5 (May 1, 1986): 1535–41. http://dx.doi.org/10.1152/jappl.1986.60.5.1535.
Full textAbstract:
In view of conflicting reports of skeletal muscle and skin blood flow participation in baroreceptor-mediated reflexes, we studied the effects of graded lower body negative pressure (LBNP) on cutaneous and muscular components of forearm blood flow (FBF) in seven male subjects at 28 degrees C. FBF was measured by venous occlusion plethysmography and cutaneous flow by laser-Doppler velocimetry, the difference being the muscular flow. Mean FBF decreased by 39 and 56% from control at LBNP of 20 and 50 Torr, respectively. Skin flow decreased linearly with graded LBNP contributing 32% of the decrease of total blood flow at 20 Torr and then 50% of total decrease of blood flow at 50 Torr. Conversely, the decrease in muscle flow represented 68% of the total decrease at LBNP of 20 Torr and then 50% of the total decrease at LBNP of 50 Torr. We concluded that both skin and muscle circulations participate in sustained peripheral vasoconstriction during LBNP, with muscle flow achieving near maximum vasoconstriction by 20 Torr and skin showing a graded vasoconstriction to decreases in LBNP.
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Geliebter, A., S. Westreich, R. N. Pierson, and T. B. Van Itallie. "Extra-abdominal pressure alters food intake, intragastric pressure, and gastric emptying rate." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 250, no. 4 (April 1, 1986): R549—R552. http://dx.doi.org/10.1152/ajpregu.1986.250.4.r549.
Full textAbstract:
Compression of the animal stomach gives rise to vagal discharges that could signal satiety. To test a noninvasive method of inducing compression of the human stomach, we first employed extra-abdominal pressure levels of 0, 10, and 20 Torr, counterbalanced for sequence, in six lean and obese subjects. A large blood pressure cuff was wrapped around the abdomen of the subject with the air bladder over the epigastrium. The bladder was inflated before ingestion of a liquid meal by the subject until satiated. Relative to 0 Torr, pressures of 10 and 20 Torr significantly reduced spontaneous food intake (P less than 0.03) without producing discomfort. In a second study, extra-abdominal pressure of 20 Torr also raised intragastric pressure by a mean of 5.5 Torr (P less than 0.03). In a third study, extra-abdominal pressure of 20 Torr did not alter gastric emptying rate during meal ingestion but ultimately enhanced emptying rate when this pressure was maintained for greater than 100 min after meal completion (P less than 0.01).
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Bickler, P. E., L. Litt, D. L. Banville, and J. W. Severinghaus. "Effects of acetazolamide on cerebral acid-base balance." Journal of Applied Physiology 65, no. 1 (July 1, 1988): 422–27. http://dx.doi.org/10.1152/jappl.1988.65.1.422.
Full textAbstract:
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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Cummings, Kevin J., and Richard J. A. Wilson. "Time-dependent modulation of carotid body afferent activity during and after intermittent hypoxia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 6 (June 2005): R1571—R1580. http://dx.doi.org/10.1152/ajpregu.00788.2004.
Full textAbstract:
The ventilatory response to several minutes of hypoxia consists of various time-dependent phenomena, some of which occur during hypoxia (e.g., short-term depression), whereas others appear on return to normoxia (e.g., posthypoxic frequency decline). Additional phenomena can be elicited by acute, intermittent hypoxia (e.g., progressive augmentation, long-term facilitation). Current data suggest that these phenomena originate centrally. We tested the hypothesis that carotid body afferent activity undergoes time-dependent modulation, consistent with a direct role in these ventilatory phenomena. Using an in vitro rat carotid body preparation, we found that 1) afferent activity declined during the first 5 min of severe (40 Torr Po2), moderate (60 Torr Po2), or mild (80 Torr Po2) hypoxia; 2) after return to normoxia (100 Torr Po2) and after several minutes of moderate or severe hypoxia, afferent activity was transiently reduced compared with prehypoxic levels; and 3) with successive 5-min bouts of mild, moderate, or severe hypoxia, afferent activity during bouts increased progressively. We call these phenomena sensory hypoxic decline, sensory posthypoxic decline, and sensory progressive augmentation, respectively. These phenomena were stimulus specific: similar phenomena were not seen with 5-min bouts of normoxic hypercapnia (100 Torr Po2 and 50–60 Torr Pco2) or hypoxic hypocapnia (60 Torr Po2 and 30 Torr Pco2). However, bouts of either normoxic hypercapnia or hypocapnic hypoxia resulted in sensory long-term facilitation. We suggest time-dependent carotid body activity acts in parallel with central mechanisms to shape the dynamics of ventilatory responses to respiratory chemostimuli.
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Walker, B. R., and B. L. Brizzee. "Renal vascular response to combined hypoxia and hypercapnia in conscious rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 254, no. 3 (March 1, 1988): R552—R558. http://dx.doi.org/10.1152/ajpregu.1988.254.3.r552.
Full textAbstract:
Experiments were performed to test for a possible role of arginine vasopressin (AVP) in the renal vascular responses to the combination of hypoxia and varying levels of CO2 in the conscious rat. Animals were instrumented with pulsed Doppler flow probes on the left renal artery and with arterial and venous catheters. Renal blood flow (RBF) and mean arterial blood pressure (MABP) were determined in conscious, unrestrained rats under the following conditions: 1) hypocapnic hypoxia [arterial PO2 (PaO2) = 26 Torr; arterial PCO2 (PaCO2) = 21 Torr]; 2) isocapnic hypoxia (PaO2 = 34 Torr; PaCO2 = 36 Torr); 3) hypercapnic hypoxia (PaO2 = 42 Torr; PaCO2 = 57 Torr); and 4) room air control (PaO2 = 93 Torr; PaCO2 = 38 Torr). MABP fell from 104 +/- 2 to 83 +/- 5 mmHg during hypocapnic hypoxia but was unaffected by the other stimuli. RBF was significantly reduced by both hypocapnic and hypercapnic hypoxia and unchanged in the other protocols, whereas renal vascular resistance (RVR) was elevated only in the hypercapnic hypoxia group. Additional experiments were performed to test whether activation of V1-vasopressinergic receptors during hypoxia might mediate the observed changes in renal hemodynamics. Experiments were performed as before except that at the midpoint of hypoxic or room air exposure, 10 micrograms/kg of the specific V1 vasopressinergic antagonist d(CH2)5Tyr(Me)AVP was administered. However, administration of the V1 antagonist had no effect on the observed renal hemodynamic responses to hypoxia. Therefore, although intense chemoreceptor stimulation by hypercapnic hypoxia may increase RVR and decrease renal perfusion, these renal hemodynamic responses do not appear to be mediated by increased circulating levels of AVP.
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Ferretti, G., M. Costa, M. Ferrigno, B. Grassi, C. Marconi, C. E. Lundgren, and P. Cerretelli. "Alveolar gas composition and exchange during deep breath-hold diving and dry breath holds in elite divers." Journal of Applied Physiology 70, no. 2 (February 1, 1991): 794–802. http://dx.doi.org/10.1152/jappl.1991.70.2.794.
Full textAbstract:
End tidal O2 and CO2 (PETCO2) pressures, expired volume, blood lactate concentration ([Lab]), and arterial blood O2 saturation [dry breath holds (BHs) only] were assessed in three elite breath-hold divers (ED) before and after deep dives and BH and in nine control subjects (C; BH only). After the dives (depth 40-70 m, duration 88-151 s), end-tidal O2 pressure decreased from approximately 140 Torr to a minimum of 30.6 Torr, PETCO2 increased from approximately 25 Torr to a maximum of 47.0 Torr, and expired volume (BTPS) ranged from 1.32 to 2.86 liters. Pulmonary O2 exchange was 455-1,006 ml. CO2 output approached zero. [Lab] increased from approximately 1.2 mM to at most 6.46 mM. Estimated power output during dives was 513-929 ml O2/min, i.e. approximately 20-30% of maximal O2 consumption. During BH, alveolar PO2 decreased from approximately 130 to less than 30 Torr in ED and from 125 to 45 Torr in C. PETCO2 increased from approximately 30 to approximately 50 Torr in both ED and C. Contrary to C, pulmonary O2 exchange in ED was less than resting O2 consumption, whereas CO2 output approached zero in both groups. [Lab] was unchanged. Arterial blood O2 saturation decreased more in ED than in C. ED are characterized by increased anaerobic metabolism likely due to the existence of a diving reflex.
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Wood, Chris M., and Junho Eom. "The internal CO 2 threat to fish: high P CO 2 in the digestive tract." Proceedings of the Royal Society B: Biological Sciences 286, no. 1907 (July 17, 2019): 20190832. http://dx.doi.org/10.1098/rspb.2019.0832.
Full textAbstract:
Our goal was to use novel fibreoptic sensors to make the first direct P CO 2 measurements in the digestive tracts of live freshwater fish (anaesthetized, artificially ventilated, 12°C). P CO 2 levels in gastrointestinal fluids were substantially higher than in blood, and were elevated after feeding. In the carnivorous, gastric rainbow trout, the mean P CO 2 in various parts of the tract increased from 7–13 torr (1 torr = 0.1333 kPa) during fasting to 20–41 torr after feeding, relative to arterial levels of 3.5–4 torr. In the agastric, omnivorous goldfish, the mean gut levels varied from 10–13 torr in fasted animals to 14–18 torr in fed animals, relative to arterial levels of 5–7 torr. These elevated P CO 2 values were associated with surprisingly high HC O 3 − concentrations (greater than 40 mmol l −1 ) in the intestinal chyme. Incubations of food pellets with acid or water revealed endogenous P CO 2 generation sufficient to explain gastric P CO 2 in fed trout and anterior intestine P CO 2 in fed goldfish. The impacts of possible equilibration with venous blood draining the tract are assessed. We conclude that fish are already coping with P CO 2 levels in the internal gastrointestinal environment many-fold greater than those of current concern in the external environment for climate change and aquacultural scenarios.
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Reeves, J. T., B. M. Groves, J. R. Sutton, P. D. Wagner, A. Cymerman, M. K. Malconian, P. B. Rock, P. M. Young, and C. S. Houston. "Operation Everest II: preservation of cardiac function at extreme altitude." Journal of Applied Physiology 63, no. 2 (August 1, 1987): 531–39. http://dx.doi.org/10.1152/jappl.1987.63.2.531.
Full textAbstract:
Hypoxia at high altitude could depress cardiac function and decrease exercise capacity. If so, impaired cardiac function should occur with the extreme, chronic hypoxemia of the 40-day simulated climb of Mt. Everest (8,840 m, barometric pressure of 240 Torr, inspiratory O2 pressure of 43 Torr). In the five of eight subjects having resting and exercise measurements at the barometric pressures of 760 Torr (sea level), 347 Torr (6,100 m), 282 Torr (7,620 m), and 240 Torr, heart rate for a given O2 uptake was higher with more severe hypoxia. Slight (6 beats/min) slowing of the heart rate occurred only during exercise at the lowest barometric pressure when arterial blood O2 saturations were less than 50%. O2 breathing reversed hypoxemia but never increased heart rate, suggesting that hypoxic depression of rate, if present, was slight. For a given O2 uptake, cardiac output was maintained. The decrease in stroke volume appeared to reflect decreased ventricular filling (i.e., decreased right atrial and wedge pressures). O2 breathing did not increase stroke volume for a given filling pressure. We concluded that extreme, chronic hypoxemia caused little or no impairment of cardiac rate and pump functions.
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Mulkey, Daniel K., Richard A. Henderson, James E. Olson, Robert W. Putnam, and Jay B. Dean. "Oxygen measurements in brain stem slices exposed to normobaric hyperoxia and hyperbaric oxygen." Journal of Applied Physiology 90, no. 5 (May 1, 2001): 1887–99. http://dx.doi.org/10.1152/jappl.2001.90.5.1887.
Full textAbstract:
We previously reported ( J Appl Physiol 89: 807–822, 2000) that ≤10 min of hyperbaric oxygen (HBO2; ≤2,468 Torr) stimulates solitary complex neurons. To better define the hyperoxic stimulus, we measured Po 2 in the solitary complex of 300-μm-thick rat medullary slices, using polarographic carbon fiber microelectrodes, during perfusion with media having Po 2 values ranging from 156 to 2,468 Torr. Under control conditions, slices equilibrated with 95% O2at barometric pressure of 1 atmospheres absolute had minimum Po 2 values at their centers (291 ± 20 Torr) that were ∼10-fold greater than Po 2values measured in the intact central nervous system (10–34 Torr). During HBO2, Po 2 increased at the center of the slice from 616 ± 16 to 1,517 ± 15 Torr. Tissue oxygen consumption tended to decrease at medium Po 2 ≥ 1,675 Torr to levels not different from values measured at Po 2 found in all media in metabolically poisoned slices (2-deoxy-d-glucose and antimycin A). We conclude that control medium used in most brain slice studies is hyperoxic at normobaric pressure. During HBO2, slice Po 2 increases to levels that appear to reduce metabolism.
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Straus, Christian, Richard JA Wilson, and John E. Remmers. "Oxygen sensitive chemoreceptors in the first gill arch of the tadpole,Rana catesbeiana." Canadian Journal of Physiology and Pharmacology 79, no. 11 (November 1, 2001): 959–62. http://dx.doi.org/10.1139/y01-077.
Full textAbstract:
Spike frequency was recorded in the nerve of the isolated superfused first gill arch of the bullfrog larva, Rana catesbeiana and the response to different superfusate [Formula: see text] was evaluated. In the metamorphic tadpole, spike frequency increased significantly when the superfusate [Formula: see text] was decreased (mean ± SEM): 8.5 ± 1.6 Hz at 650 Torr, 11.7 ± 1.9 Hz at 140 Torr, 13.3 ± 1.8 Hz at 65 Torr, 14.8 ± 2.4 Hz at 0 Torr (ANOVA, p = 0.0002). The O2sensitive chemoreceptor stimulants NaCN and almitrine also increased the spike frequency. This study demonstrates the presence of O2sensitive chemoreceptors in the first gill arch of the tadpole.Key words: tadpole, Rana catesbeiana, gill, chemoreceptor, oxygen.
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Xie, Ailiang, James B. Skatrud, Dominic S. Puleo, and Jerome A. Dempsey. "Influence of arterial O2 on the susceptibility to posthyperventilation apnea during sleep." Journal of Applied Physiology 100, no. 1 (January 2006): 171–77. http://dx.doi.org/10.1152/japplphysiol.00440.2005.
Full textAbstract:
To investigate the contribution of the peripheral chemoreceptors to the susceptibility to posthyperventilation apnea, we evaluated the time course and magnitude of hypocapnia required to produce apnea at different levels of peripheral chemoreceptor activation produced by exposure to three levels of inspired Po2. We measured the apneic threshold and the apnea latency in nine normal sleeping subjects in response to augmented breaths during normoxia (room air), hypoxia (arterial O2 saturation = 78–80%), and hyperoxia (inspired O2 fraction = 50–52%). Pressure support mechanical ventilation in the assist mode was employed to introduce a single or multiple numbers of consecutive, sighlike breaths to cause apnea. The apnea latency was measured from the end inspiration of the first augmented breath to the onset of apnea. It was 12.2 ± 1.1 s during normoxia, which was similar to the lung-to-ear circulation delay of 11.7 s in these subjects. Hypoxia shortened the apnea latency (6.3 ± 0.8 s; P < 0.05), whereas hyperoxia prolonged it (71.5 ± 13.8 s; P < 0.01). The apneic threshold end-tidal Pco2 (PetCO2) was defined as the PetCO2 at the onset of apnea. During hypoxia, the apneic threshold PetCO2 was higher (38.9 ± 1.7 Torr; P < 0.01) compared with normoxia (35.8 ± 1.1; Torr); during hyperoxia, it was lower (33.0 ± 0.8 Torr; P < 0.05). Furthermore, the difference between the eupneic PetCO2 and apneic threshold PetCO2 was smaller during hypoxia (3.0 ± 1.0 Torr P < 001) and greater during hyperoxia (10.6 ± 0.8 Torr; P < 0.05) compared with normoxia (8.0 ± 0.6 Torr). Correspondingly, the hypocapnic ventilatory response to CO2 below the eupneic PetCO2 was increased by hypoxia (3.44 ± 0.63 l·min−1·Torr−1; P < 0.05) and decreased by hyperoxia (0.63 ± 0.04 l·min−1·Torr−1; P < 0.05) compared with normoxia (0.79 ± 0.05 l·min−1·Torr−1). These findings indicate that posthyperventilation apnea is initiated by the peripheral chemoreceptors and that the varying susceptibility to apnea during hypoxia vs. hyperoxia is influenced by the relative activity of these receptors.
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Cymerman, A., J. T. Reeves, J. R. Sutton, P. B. Rock, B. M. Groves, M. K. Malconian, P. M. Young, P. D. Wagner, and C. S. Houston. "Operation Everest II: maximal oxygen uptake at extreme altitude." Journal of Applied Physiology 66, no. 5 (May 1, 1989): 2446–53. http://dx.doi.org/10.1152/jappl.1989.66.5.2446.
Full textAbstract:
Chronic exposure to high altitude reduces maximal O2 uptake (VO2max). At extreme altitudes approaching the summit of Mt. Everest [inspiratory PO2(PIO2) = 43 Torr], mean VO2max have been determined to be 15.3 ml.kg-1.min-1 in two subjects who breathed 14% O2 at 6,300 m on Mt. Everest (West et al., J. Appl. Physiol. 54: 1188–1194, 1983). To provide a more complete description of performance near the limits of human tolerance to chronic hypoxia, we measured VO2max in volunteers in an altitude chamber before, during, and after a 40-day decompression to a barometric pressure (PB) of 240 Torr (PIO2 = 43 Torr). In five of eight subjects studied at sea level and PB of 464, 347, 289, and 240 Torr, VO2max was reduced from 4.13 to 1.17 l/min (49.1–15.3 ml.kg-1.min-1) in agreement with the prior study. Although the range decreased, the rank order among the subjects was preserved. Arterial O2 saturation at maximum effort decreased (46% by ear oximetry), but minute ventilation, respiratory frequency, and tidal volume did not. The highest minute ventilation (201 l/min BTPS) was observed at PB of 464 Torr. Arterial PCO2 in three subjects at PB of 240 Torr, at rest, and with maximum effort, averaged 10.3 and 9.6 Torr, respectively. Sustained hyperventilation was crucial to exercise performance during chronic, severe hypoxemia. VO2max was lower after altitude exposure compared with initial sea level values, indicating that exposure had not improved sea level exercise capacity.
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Tolins, M., E. K. Weir, E. Chesler, D. P. Nelson, and A. H. From. "Pulmonary vascular tone is increased by a voltage-dependent calcium channel potentiator." Journal of Applied Physiology 60, no. 3 (March 1, 1986): 942–48. http://dx.doi.org/10.1152/jappl.1986.60.3.942.
Full textAbstract:
The mechanism of hypoxia-induced pulmonary vasoconstriction remains unknown. To explore the possible dependence of the hypoxic response on voltage-activated calcium (Ca2+) channels, the effects of BAY K 8644 (BAY), a voltage-dependent Ca2+ channel potentiator, were observed on the pulmonary vascular response to hypoxia of both the intact anesthetized dog and the perfused isolated rat lung. In six rat lungs given BAY (1 X 10(-6)M), hypoxia increased mean pulmonary arterial pressure (Ppa) to 30.5 +/- 1.7 (SEM) Torr compared with 14.8 +/- 1.2 Torr for six untreated rat lungs (P less than 0.01). After nifedipine, the maximum Ppa during hypoxia fell 14.1 +/- 2.4 Torr from the previous hypoxic challenge in the BAY-stimulated rats (P less than 0.01). BAY (1.2 X 10(-7) mol/kg) given during normoxia in seven dogs increased pulmonary vascular resistance 2.5 +/- 0.3 to 5.0 +/- 1.2 Torr X 1(-1) X min (P less than 0.05), and systemic vascular resistance 55 +/- 4.9 to 126 +/- 20.7 Torr X 1(-1) X min (P less than 0.05). Systemic mean arterial pressure rose 68 Torr, whereas Ppa remained unchanged. Administration of BAY during hypoxia produced an increase in Ppa: 28 +/- 1.5 to 33 +/- 1.9 Torr (P less than 0.05). Thus BAY, a Ca2+ channel potentiator, enhances the hypoxic pulmonary response in vitro and in vivo. This, together with the effect of nifedipine on BAY potentiation, suggests that increased Ca2+ channel activity may be important in the mechanism of hypoxic pulmonary vasoconstriction.
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Thompson, B. T., D. M. Steigman, C. L. Spence, S. P. Janssens, and C. A. Hales. "Chronic hypoxic pulmonary hypertension in the guinea pig: effect of three levels of hypoxia." Journal of Applied Physiology 74, no. 2 (February 1, 1993): 916–21. http://dx.doi.org/10.1152/jappl.1993.74.2.916.
Full textAbstract:
Chronic hypoxia [inspiratory PO2 (PIO2) = 76 Torr for 10 days] produces pulmonary hypertension and vascular remodeling in the guinea pig. Increasing the duration of hypoxia from 10 to 21 days does not increase further pulmonary arterial pressure or medial thickening. To see if increasing severity of hypoxia affects the magnitude of pulmonary hypertension and remodeling, we exposed three groups of male Hartley guinea pigs to three levels of normobaric hypoxia for 10 days: PIO2 = 90 (n = 6), 78 (n = 6), and 65 Torr (n = 5). Pulmonary arterial pressure increased from 14 +/- 1 (+/- SE, n = 7) in room air to 23 +/- 3 mmHg when PIO2 = 90 Torr (P < 0.05). Pulmonary arterial pressure was slightly higher when PIO2 = 78 or 65 Torr (25 +/- 1 and 26 +/- 1 mmHg, respectively) but did not reach statistical significance vs. PIO2 = 90 Torr. Total pulmonary vascular resistance increased from 0.049 +/- 0.004 in room air to between 0.084 +/- 0.006 and 0.101 +/- 0.003 mmHg.min.kg.ml-1 (P < 0.05) in the three hypoxic groups; again there was no difference in total pulmonary vascular resistance among hypoxic groups. Medial thickness of alveolar duct and terminal bronchiole arteries increased with hypoxia, but there was no significant difference among the hypoxic groups. The percentage of intra-acinar vessels with thick walls (a measure of muscular extension) increased when PIO2 = 78 Torr and nearly doubled when PIO2 = 65 Torr in comparison to control.(ABSTRACT TRUNCATED AT 250 WORDS)
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Pawelczyk, J. A., and P. B. Raven. "Reductions in central venous pressure improve carotid baroreflex responses in conscious men." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 5 (November 1, 1989): H1389—H1395. http://dx.doi.org/10.1152/ajpheart.1989.257.5.h1389.
Full textAbstract:
To test the hypothesis that unloading cardiopulmonary receptors improves human carotid baroreceptor responsiveness we measured heart rate (HR) and mean radial artery blood pressure (BP) responses elicited by trains of neck pressure and neck suction from +40 to -65 Torr during graded lower body negative pressure (LBNP) at -5, -10, -15, -20, -35, and -50 Torr in eight healthy men. Gain of the carotid baroreflexes was determined from logistic modeling of the HR [expressed as R-R interval (RRI)] and BP responses to neck pressure and neck suction. Central venous pressure (CVP) decreased progressively from control values of 6.2 +/- 0.6 (SE) Torr to -0.8 +/- 0.1 Torr at -50 Torr LBNP (P less than 0.001). HR changed little from control values of 62.7 +/- 2.1 beat/min to 65.9 +/- 2.8 beat/min at -15 Torr (P = NS), but increased significantly to 80.6 +/- 2.6 beats/min at -50 Torr (P less than 0.001). Maximum gain of the HR and BP stimulus-response curves was linearly and inversely related to decreases in CVP and could be described by the relationships Max RRI gain = -0.694 (CVP) + 11.6 [r2 = 0.94, standard error of estimate (SEE) = 0.45, P less than 0.001] and Max BP gain = -0.0292 (CVP) + 0.391 (r2 = 0.81, SEE = 0.038, P less than 0.001). We suggest that reductions in central venous pressure and/or central blood volume augment both HR and BP carotid baroreflex responses in man by reducing an inhibitory influence from cardiopulmonary receptors.
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Davidson, D. "Circulating vasoactive substances and hemodynamic adjustments at birth in lambs." Journal of Applied Physiology 63, no. 2 (August 1, 1987): 676–84. http://dx.doi.org/10.1152/jappl.1987.63.2.676.
Full textAbstract:
Circulating vasoactive substances and hemodynamics were examined in chronically instrumented unanesthetized lambs before, during, and after cesarean section (spontaneous respiration). One of three infusions were started 20 min before birth: saline control (n = 10), saralasin (n = 5), or captopril (n = 6). Control lambs exhibited peak (means +/- SE) increases above fetal base line at 5 min after birth in plasma renin activity (5.0 +/- 1.1 to 11.0 +/- 3.4 ng.ml-1.h-1), angiotensin II (ANG II, 37 +/- 6 to 141 +/- 45 pg/ml) and total catecholamines (318 +/- 35 to 3,821 +/- 580 pg/ml). Mean systemic arterial pressure (Psa) and arterial O2 partial pressure (PaO2) increased more rapidly and to a greater extent by 1 h after birth in control lambs (Psa, 65 +/- 1 Torr; PaO2, 45 +/- 3 Torr) compared with the captopril group (Psa, 53 +/- 2 Torr; PaO2, 31 +/- 4 Torr) and the saralasin group (Psa, 56 +/- 2 Torr; PaO2, 27 +/- 3 Torr). Intravenous infusions of ANG II in control lambs, 2 h after birth resulted in a preferential systemic vs. pulmonary pressor response. The results demonstrate that at birth ANG II formation fosters the postnatal rise in Psa and PaO2, and high levels of circulating catecholamines may support postnatal cardiac output and Psa.
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Curtis, S. E., B. P. Fuhrman, and D. F. Howland. "Airway and alveolar pressures during perfluorocarbon breathing in infant lambs." Journal of Applied Physiology 68, no. 6 (June 1, 1990): 2322–28. http://dx.doi.org/10.1152/jappl.1990.68.6.2322.
Full textAbstract:
Previous studies exploring the utility of liquid breathing using perfluorocarbon have reported proximal airway pressures (Paw) as high as 70 Torr during inspiration, generating concern about the safety of this form of mechanical ventilation. Effects on the pulmonary capillary bed are, however, more likely related to alveolar pressure (PA) than to Paw, and data on PA during liquid breathing are limited. In this study in infant lambs, we reconstructed the pressure waveforms of PA during liquid breathing by using an occlusion technique and compared these with Paw waveforms. Peak PA (18.6 +/- 10.4 Torr) was significantly less than peak Paw (31.5 +/- 10.5 Torr, P less than 0.001), indicating a large resistive pressure drop (14.4 +/- 4.5 Torr) across the bronchial tree. Mean PA (mPA) was very similar to mean Paw (mPaw) [bias = -2.0 Torr, standard error of the average difference = 0.27 Torr, predictive value of mPaw for mPA (r2) = 0.978], suggesting that mPaw, which is easily measured, may be used to estimate mPA during perfluorocarbon liquid breathing. These data show that alveoli do not experience the same large swings in pressure as the proximal airway does during liquid breathing and that simple measurements of mPaw can be used to approximate mPA during liquid breathing.
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Poulin, M. J., D. A. Cunningham, D. H. Paterson, J. M. Kowalchuk, and W. D. Smith. "Ventilatory sensitivity to CO2 in hyperoxia and hypoxia in older aged humans." Journal of Applied Physiology 75, no. 5 (November 1, 1993): 2209–16. http://dx.doi.org/10.1152/jappl.1993.75.5.2209.
Full textAbstract:
Findings from studies of the effects of aging on the human respiratory controller are equivocal. This study assessed the ventilatory response to CO2 in hyperoxia and hypoxia in groups of younger (YS) and older (OS) humans. Two protocols were used. In the first, end-tidal PCO2 (PETCO2) was clamped at 1–2 Torr above rest (eucapnia), and, in the second, PETCO2 was clamped at 7–8 torr above resting PETCO2 (moderate hypercapnia). End-tidal PO2 was clamped at 100 Torr throughout except for two 2-min periods at 500 and 50 Torr. The ventilatory responses for each subject at each PO2 were fitted to the linear equation, VE = S(PETCO2 - B), where VE is minute ventilation, S is the response curve slope, and B is the response curve threshold. In eucapnia, there were no differences in hypoxic and hyperoxic VE between YS and OS. In hypercapnia, hypoxic VE was 24% lower in OS [39.93 +/- 2.71 (SE) l/min] than in YS (52.16 +/- 3.17 l/min). In hypoxia, S was significantly lower in OS (3.25 +/- 0.38 l.min-1.Torr-1) than in YS (4.76 +/- 0.37 l.min-1.Torr-1). We conclude that, in older humans, VE is lower in hypoxia during moderate hypercapnia, resulting mainly from a decreased peripheral chemoreflex CO2 sensitivity.
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Maron, M. B. "A canine model of neurogenic pulmonary edema." Journal of Applied Physiology 59, no. 3 (September 1, 1985): 1019–25. http://dx.doi.org/10.1152/jappl.1985.59.3.1019.
Full textAbstract:
The purpose of this study was to evaluate the usefulness of the intracisternal administration of veratrine as a model of neurogenic pulmonary edema (NPE) in the alpha-chloralose-anesthetized dog. Veratrine (40–60 micrograms/kg) was injected into the cisterna magna of 17 animals, and systemic arterial, pulmonary arterial, and left ventricular end-diastolic (LVEDP) pressures were followed for 1 h. Eleven animals developed alveolar edema. In these animals, systemic arterial pressure increased to 273 +/- 9 (SE) Torr, pulmonary arterial pressure to 74.5 +/- 4.9 Torr, and LVEDP to 42.8 +/- 4.5 Torr, and large amounts of pink frothy fluid, with protein concentrations ranging from 48 to 93% of plasma, appeared in the airways. Postmortem extravascular lung water content (Qwl/dQl) averaged 7.30 +/- 0.46 g H2O/g dry lung wt. Six animals escaped developing this massive degree of edema after veratrine (Qwl/dQl = 4.45 +/- 0.24). These animals exhibited similar elevated systemic arterial pressures (268 +/- 15 Torr), but did not develop the degree of pulmonary hypertension (pulmonary arterial pressure = 52.5 +/- 6.7 Torr, LVEDP = 24.8 +/- 4.0 Torr) observed in the other group. These results suggest that both hemodynamic and permeability mechanisms may play a role in the development of this form of edema and that veratrine administration may provide a useful model of NPE.
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Rumsey, W. L., R. Iturriaga, D. Spergel, S. Lahiri, and D. F. Wilson. "Optical measurements of the dependence of chemoreception on oxygen pressure in the cat carotid body." American Journal of Physiology-Cell Physiology 261, no. 4 (October 1, 1991): C614—C622. http://dx.doi.org/10.1152/ajpcell.1991.261.4.c614.
Full textAbstract:
The relationship between oxygen pressure (PO2) in the carotid body and carotid sinus nerve discharge was evaluated in the isolated perfused/superfused cat carotid body using the oxygen-dependent quenching of phosphorescence. Images of phosphorescence intensity arising from Pd-coproporphyrin within the microcirculation of the carotid body provided measurements of intravascular PO2. These measurements were substantiated by determining phosphorescence life-time. The carotid body was perfused in the isolated state via the common carotid artery with N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered Tyrode solution, pH 7.4, at a constant pressure of 80 mmHg. Superfusion was maintained with similar media equilibrated with 100% argon. PO2 in the exchange vessels was markedly less than that in the perfusate entering the carotid artery, 23 +/- 3 and 45 +/- 3 Torr for normoxic (111 +/- 15 Torr) and hyperoxic (345 +/- 72 Torr) perfusates, respectively. Chemosensory discharge rose slowly in response to a brief interruption of perfusate flow as PO2 steadily declined from either of these capillary PO2 values to approximately 10 Torr. Between approximately 10 and 3 Torr, chemosensory discharge increased strikingly, concomitant with an enhanced rate of oxygen disappearance, from -36 +/- 4 to -69 +/- 13 (92% change) and -28 +/- 3 to -48 +/- 3 (71% change) Torr/s for normoxic and hyperoxic perfusates, respectively. As PO2 fell below approximately 3 Torr, oxygen disappearance slowed and neural activity decayed. Thus the relationships between microvascular PO2 and chemosensory discharge and between oxygen disappearance and neural discharge suggest that oxygen metabolism in the carotid body determines the expression of oxygen chemoreception.
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Robiolio, M., W. L. Rumsey, and D. F. Wilson. "Oxygen diffusion and mitochondrial respiration in neuroblastoma cells." American Journal of Physiology-Cell Physiology 256, no. 6 (June 1, 1989): C1207—C1213. http://dx.doi.org/10.1152/ajpcell.1989.256.6.c1207.
Full textAbstract:
Suspensions of human neuroblastoma cells consume oxygen at a constant rate when the oxygen pressure is greater than approximately 11 Torr. The rate of oxygen consumption, however, becomes dependent on the oxygen pressure below this level. The falling respiratory rate at the lower pressures gives rise to an oxygen pressure for half-maximal respiration (P50) of approximately 0.8 Torr, which is consistent with the 0.5 Torr value for suspensions of isolated mitochondria in the presence of ATP (J. Biol. Chem. 263: 2712-2718, 1988). When the cellular metabolic energy state is lowered by addition of an uncoupler of mitochondrial oxidative phosphorylation, the respiratory rate increases up to fivefold, but the P50 decreases to approximately 0.6 Torr. In the cells treated with uncoupler, the P50 decreases further when the mitochondrial respiratory rate is inhibited with amobarbital (amytal), an inhibitor of the respiratory chain. The additional decrease in P50 is proportional to the decrease in respiratory rate. Thus, for cells treated with uncoupler, the P50 appears to be limited by oxygen diffusion from the external medium to the mitochondria. When the respiratory rate of the uncoupled cells is inhibited to the level of coupled cells, the P50 for the former is less than 0.15 Torr. This indicates that for coupled cells the difference in oxygen pressure from the external medium to the mitochondria is less than 0.15 Torr at half-maximal respiratory rate and does not significantly affect the P50 for oxygen that occurs at 0.8 Torr.(ABSTRACT TRUNCATED AT 250 WORDS)
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Baron, J. F., E. Vicaut, X. Hou, and M. Duvelleroy. "Independent role of arterial O2 tension in local control of coronary blood flow." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 5 (May 1, 1990): H1388—H1394. http://dx.doi.org/10.1152/ajpheart.1990.258.5.h1388.
Full textAbstract:
The aim of this study of a blood-perfused isolated rabbit heart preparation was to differentiate the effects on coronary resistance of large changes in arterial O2 tension (arterial PO2 = 45-400 Torr) from the effects of variations in arterial O2 content or myocardial O2 delivery. Standard stored human blood was resuspended in Krebs-Henseleit buffer and was oxygenated to obtain normal PO2, high PO2, and low PO2. Hemoglobin concentrations were adjusted to obtain the same arterial O2 content (CaO2) for the three PO2s. In a first set of experiments, in which coronary blood flow (CBF) was free and adapted to a constant perfusion pressure, switching from control [138 +/- 17 (SE) Torr] to high PO2 blood (380 +/- 27 Torr) induced a significant decrease in CBF and myocardial O2 consumption (MVO2). Switching from control (125 +/- 3 Torr) to low PO2 blood (49 +/- 5 Torr) induced a significant increase in CBF and MVO2. In a second set of experiments, the switch from control (159 +/- 5 Torr) to high PO2 (389 +/- 32 Torr) was performed in a preparation in which CBF and consequently O2 delivery were constant. Under these conditions, the increase in perfusion pressure demonstrated that PO2 affected coronary resistance, even though the O2 delivery was constant. No significant change in myocardial performance was observed in any of these experimental procedures. These results show that arterial PO2 may affect coronary blood flow regulation independently of any mediation by the autonomic nervous system and of any associated changes in O2 content or O2 delivery.
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Schnader, J. Y., G. Juan, S. Howell, R. Fitzgerald, and C. Roussos. "Arterial CO2 partial pressure affects diaphragmatic function." Journal of Applied Physiology 58, no. 3 (March 1, 1985): 823–29. http://dx.doi.org/10.1152/jappl.1985.58.3.823.
Full textAbstract:
The purpose of this study was to examine in an in vivo preparation acute variations of PCO2 on diaphragmatic contractility. Plaster casts were snugly fit around the abdomen of six open-chested dogs, moving the abdominal contents rostrally. Diaphragmatic contractions against this very fixed load in response to phrenic nerve stimulation (supramaximal voltage at 1, 20, 50, and 80 Hz) or during spontaneous inspiratory efforts were virtually isometric (quasi-isometric). Transdiaphragmatic pressure (Pdi) measured by an abdominal balloon was used as an index of diaphragmatic contractility. Arterial PCO2 (PaCO2) was reduced by hyperventilation and raised by increasing PICO2. Pdi values in response to stimulation at 1, 20, 50, and 80 Hz in ranges I (PaCO2 = 0–19 Torr) and II (PaCO2 = 20–34 Torr) did not differ statistically from the control Pdi values (range III; PaCO2 = 35–45 Torr). In range IV (PaCO2 = 46–70 Torr) Pdi values for stimulations of 20, 50, and 80 Hz were significantly lower than control. In range V (PaCO2 = 71–90 Torr), VI (PaCO2 = 91–101 Torr), and VII (PaCO2 greater than or equal to 102 Torr) Pdi values were significantly less than those in range IV at all frequencies of stimulation. In the four dogs measured during spontaneous inspiratory efforts the integrated diaphragmatic electromyogram (Edi) was correlated with the Pdi. As PaCO2 rose (range III to VII), the Pdi values observed at 25, 50, 75, 100% of the maximum Edi (of range III) were significantly lower than the Pdi value of range III.(
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Jhong, Shih Bin, Sean Wu, and Maw Shung Lee. "Influence of Sputtering Pressure for Radio Frequency Magnetron Sputtering (103) Oriented AlN Films on (100) Silicon Substrate." Advanced Materials Research 538-541 (June 2012): 12–15. http://dx.doi.org/10.4028/www.scientific.net/amr.538-541.12.
Full textAbstract:
The thin film of (103)-oriented aluminum nitride (AlN) is an attractive piezoelectric material for the applications in film bulk acoustic wave resonator (FBAR) devices. Due to the bulk acoustic wave (BAW) properties of (103) oriented AlN films, it can excite a quasi-shear mode (velocity = 5,957 m/s, K2= 3.8%) that can be used for FBAR liquid sensor and even loss less than the FBAR device with (002) oriented AlN films. In this research, the (103) oriented AlN films were successfully deposited onto (100) silicon substrate by radio frequency (RF) magnetron sputtering. Different sputtering pressures (1m torr, 3m torr, 5m torr, and 7m torr) were discussed in this experiment process. Comparisons were made on their crystalline structures with X-ray diffraction (XRD) and the surface morphologies was investigated by the atomic force microscopy (AFM). The result exhibited the optimal sputtering pressure is 5m torr. The optimal (103) oriented AlN films have the strongest XRD intensity, the smallest full width at half maximum (FWHM) value (0.6°), the largest grain size (15.78nm) and the smooth surface roughness (Ra=3.259nm).
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Bebout, D. E., D. Story, J. Roca, M. C. Hogan, D. C. Poole, R. Gonzalez-Camarena, O. Ueno, P. Haab, and P. D. Wagner. "Effects of altitude acclimatization on pulmonary gas exchange during exercise." Journal of Applied Physiology 67, no. 6 (December 1, 1989): 2286–95. http://dx.doi.org/10.1152/jappl.1989.67.6.2286.
Full textAbstract:
Pulmonary gas exchange was studied in eight normal subjects both before and after 2 wk of altitude acclimatization at 3,800 m (12,470 ft, barometric pressure = 484 Torr). Respiratory and multiple inert gas tensions, ventilation, cardiac output (Q), and hemoglobin concentration were measured at rest and during three levels of constant-load cycle exercise during both normoxia [inspired PO2 (PIO2) = 148 Torr] and normobaric hypoxia (PIO2 = 91 Torr). After acclimatization, the measured alveolar-arterial PO2 difference (A-aPO2) for any given work rate decreased (P less than 0.02). The largest reductions were observed during the highest work rates and were 24.8 +/- 1.4 to 19.7 +/- 0.8 Torr (normoxia) and 22.0 +/- 1.1 to 19.4 +/- 0.7 Torr (hypoxia). This could not be explained by changes in ventilation-perfusion inequality or estimated O2 diffusing capacity, which were unaffected by acclimatization. However, Q for any given work rate was significantly decreased (P less than 0.001) after acclimatization. We suggest that the reduction in A-aPO2 after acclimatization is a result of more nearly complete alveolar/end-capillary diffusion equilibration on the basis of a longer pulmonary capillary transit time.
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Hutt, D. A., R. A. Parisi, T. V. Santiago, and N. H. Edelman. "Brain hypoxia preferentially stimulates genioglossal EMG responses to CO2." Journal of Applied Physiology 66, no. 1 (January 1, 1989): 51–56. http://dx.doi.org/10.1152/jappl.1989.66.1.51.
Full textAbstract:
Although the dominant respiratory response to hypoxia is stimulation of breathing via the peripheral chemoreflex, brain hypoxia may inhibit respiration. We studied the effects of two levels of brain hypoxia without carotid body stimulation, produced by inhalation of CO, on ventilatory (VI) and genioglossal (EMGgg) and diaphragmatic (EMGdi) responses to CO2 rebreathing in awake, unanesthetized goats. Neither delta VI/delta PCO2 nor VI at a PCO2 of 60 Torr was significantly different between the three conditions studied (0%, 25%, and 50% carboxyhemoglobin, HbCO). There were also no significant changes in delta EMGdi/delta PCO2 or EMGdi at a PCO2 of 60 Torr during progressive brain hypoxia. In contrast, delta EMGgg/delta PCO2 and EMGgg at a PCO2 of 60 Torr were significantly increased at 50% HbCO compared with either normoxia or 25% HbCO (P less than 0.05). The PCO2 threshold at which inspiratory EMGgg appeared was also decreased at 50% HbCO (45.6 +/- 2.6 Torr) compared with normoxia (55.0 +/- 1.4 Torr, P less than 0.02) or 25% HbCO (53.4 +/- 1.6 Torr, P less than 0.02). We conclude that moderate brain hypoxia (50% HbCO) in awake, unanesthetized animals results in disproportionate augmentation of EMGgg relative to EMGdi during CO2 rebreathing. This finding is most likely due to hypoxic cortical depression with consequent withdrawal of tonic inhibition of hypoglossal inspiratory activity.
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Gordon, J. B., R. C. Wetzel, M. L. McGeady, N. F. Adkinson, and J. T. Sylvester. "Effects of indomethacin on estradiol-induced attenuation of hypoxic vasoconstriction in lamb lungs." Journal of Applied Physiology 61, no. 6 (December 1, 1986): 2116–21. http://dx.doi.org/10.1152/jappl.1986.61.6.2116.
Full textAbstract:
To determine whether cyclooxygenase products mediated the attenuation of hypoxic pulmonary vasoconstriction induced by estradiol, we measured pulmonary arterial pressure at a flow of 50 ml X min-1 X kg-1 (Ppa50) during steady-state exposures to inspired O2 tensions (PIO2) between 0 and 200 Torr in isolated lungs of juvenile ewes. Intramuscular estradiol (10 mg) 44–60 h before study significantly decreased perfusate concentrations of 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), the stable metabolite of the pulmonary vasodilator, prostacyclin, but did not significantly affect the stimulus-response relationship between PIO2 and Ppa50. Estradiol (20 mg) 3–5 days before study increased 6-keto-PGF1 alpha concentrations and decreased Ppa50 at PIO2 of 10, 30, and 50 Torr. Indomethacin added to the perfusate of these lungs reduced 6-keto-PGF1 alpha to undetectable levels and altered the estradiol-induced attenuation, increasing Ppa50 at PIO2 of 10 and 30 Torr, but decreasing Ppa50 at PIO2 of 200 Torr. Despite these effects, Ppa50 remained lower than the values measured in lungs not treated with estradiol. These results suggest that the estradiol-induced attenuation of the hypoxic stimulus-response relationship was mediated only in part by cyclooxygenase products, the net effects of which were vasodilation at PIO2 of 10 and 30 Torr, but vasoconstriction at PIO2 of 200 Torr.