Breathing volumes and gas exchange during simulated rapid free ascent from 100 msw

1993 ◽  
Vol 74 (3) ◽  
pp. 1293-1298 ◽  
Author(s):  
D. Linnarsson ◽  
H. Ornhagen ◽  
M. Gennser ◽  
H. Berg
Keyword(s):  
Gas Exchange ◽  
Surface Pressure ◽  
Time Course ◽  
Decompression Sickness ◽  
Dilution Method ◽  
Gas Composition ◽  
Arterial Pco2 ◽  
End Tidal ◽  
Gas Expansion ◽  
The Brain

The crew of a disabled submarine can be rescued by means of free ascent through the water to the surface. Pulmonary gas exchange was studied during simulated rapid free ascent in subjects standing immersed to the neck in a pressure chamber. The pressure was rapidly increased to 1.1 MPa [100 meters seawater (msw)] followed by decompression at 0.03 MPa/s (3 msw/s). Effective inspired tidal volume, as estimated by an Ar dilution method, fell gradually to zero during decompression from 20 to 0 msw. Directly determined expired tidal volumes were increased up to two to three times at the time of return to surface pressure compared with pre- and postdecompression volumes. End-tidal PCO2 was increased on compression and fell to a nadir of 3.4 kPa (25 Torr) at the time of return to surface pressure. Thus, intrapulmonary gas expansion caused simultaneous inspiratory hypoventilation and expiratory hyperventilation. If O2-enriched gas is to be used to reduce the risk of decompression sickness, it should be administered early during decompression to alter the intrapulmonary gas composition. The time course of arterial PCO2 changes as reflected by end-tidal values during short-lasting compression/decompression would act to promote inert gas supersaturation in the brain.

Evaluation of estimates of alveolar gas exchange by using a tidally ventilated nonhomogenous lung model

1997 ◽  
Vol 82 (6) ◽  
pp. 1963-1971 ◽  
Author(s):  
Thierry Busso ◽  
Peter A. Robbins
Keyword(s):  
Gas Exchange ◽  
Lung Model ◽  
Gas Composition ◽  
Breathing Patterns ◽  
Alveolar Volume ◽  
Gas Concentration ◽  
Pulmonary Capillaries ◽  
Partial Pressures ◽  
End Tidal ◽  
Alveolar Gas Exchange

Busso, Thierry, and Peter A. Robbins. Evaluation of estimates of alveolar gas exchange by using a tidally ventilated nonhomogenous lung model. J. Appl. Physiol. 82(6): 1963–1971, 1997.—The purpose of this study was to evaluate algorithms for estimating O2 and CO2 transfer at the pulmonary capillaries by use of a nine-compartment tidally ventilated lung model that incorporated inhomogeneities in ventilation-to-volume and ventilation-to-perfusion ratios. Breath-to-breath O2 and CO2 exchange at the capillary level and at the mouth were simulated by using realistic cyclical breathing patterns to drive the model, derived from 40-min recordings in six resting subjects. The SD of the breath-by-breath gas exchange at the mouth around the value at the pulmonary capillaries was 59.7 ± 25.5% for O2 and 22.3 ± 10.4% for CO2. Algorithms including corrections for changes in alveolar volume and for changes in alveolar gas composition improved the estimates of pulmonary exchange, reducing the SD to 20.8 ± 10.4% for O2 and 15.2 ± 5.8% for CO2. The remaining imprecision of the estimates arose almost entirely from using end-tidal measurements to estimate the breath-to-breath changes in end-expiratory alveolar gas concentration. The results led us to suggest an alternative method that does not use changes in end-tidal partial pressures as explicit estimates of the changes in alveolar gas concentration. The proposed method yielded significant improvements in estimation for the model data of this study.

Change in time course of posthyperventilation hyperpnea during menstrual cycle

1988 ◽  
Vol 64 (6) ◽  
pp. 2631-2635 ◽  
Author(s):  
N. Takano
Keyword(s):  
Menstrual Cycle ◽  
Time Course ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Inverse Correlation ◽  
Decay Process ◽  
Slow Recovery ◽  
Voluntary Hyperventilation ◽  
End Tidal ◽  
The Brain

Ventilatory response after 1 min of voluntary hyperventilation (HV) was studied in 10 healthy women. Before, during, and after HV, end-tidal PCO2 (PETCO2) was maintained at a given level between resting and 60 Torr. After cessation of HV, hyperpnea was seen in 179 out of a total of 195 runs but in the remaining 16 runs in 3 subjects hypopnea occurred, both ventilatory changes being followed by slow recovery to the pre-HV level. The time constant (tau) of the decay process of post-HV hyperpnea was calculated and compared between the follicular (F) and luteal (L) phases of menstruation. For post-HV hypopnea, tau was assumed to be zero. There was an inverse correlation between tau and PETCO2 during the test, the relation being similar in F and L. With a phase change from F to L, tau value at resting PETCO2 increased from 17.7 to 23.7 s. Resting PETCO2 decreased from 40.8 to 37.7 Torr, and minute ventilation (VE) increased by 10%. The increased tau in L was ascribable to the decrease in resting PETCO2 but not to the increased ventilatory activity during the pre-HV period (corresponding to the resting VE) that was probably produced by ventilatory stimulation with progesterone in L. From these results, it is inferred that the ventilatory influence of progesterone might not be exerted on the brain stem, which has been implicated as a locus of the afterdischarge mechanism.

Morphological Changes in the Brain of Acutely Ill and Weight-Recovered Patients with Anorexia Nervosa

2014 ◽  
Vol 42 (1) ◽  
pp. 7-18 ◽  
Author(s):  
Jochen Seitz ◽  
Katharina Bühren ◽  
Georg G. von Polier ◽  
Nicole Heussen ◽  
Beate Herpertz-Dahlmann ◽  
...  
Keyword(s):  
Anorexia Nervosa ◽  
Cognitive Deficits ◽  
Time Course ◽  
Morphological Changes ◽  
Meta Analysis ◽  
Short Term ◽  
Clinical Prognosis ◽  
Qualitative Review ◽  
Brain Changes ◽  
The Brain

Objective: Acute anorexia nervosa (AN) leads to reduced gray (GM) and white matter (WM) volume in the brain, which however improves again upon restoration of weight. Yet little is known about the extent and clinical correlates of these brain changes, nor do we know much about the time-course and completeness of their recovery. Methods: We conducted a meta-analysis and a qualitative review of all magnetic resonance imaging studies involving volume analyses of the brain in both acute and recovered AN. Results: We identified structural neuroimaging studies with a total of 214 acute AN patients and 177 weight-recovered AN patients. In acute AN, GM was reduced by 5.6% and WM by 3.8% compared to healthy controls (HC). Short-term weight recovery 2–5 months after admission resulted in restitution of about half of the GM aberrations and almost full WM recovery. After 2–8 years of remission GM and WM were nearly normalized, and differences to HC (GM: –1.0%, WM: –0.7%) were no longer significant, although small residual changes could not be ruled out. In the qualitative review some studies found GM volume loss to be associated with cognitive deficits and clinical prognosis. Conclusions: GM and WM were strongly reduced in acute AN. The completeness of brain volume rehabilitation remained equivocal.

scholarly journals Conceptual and Practical Issues in the Pharmacological Treatment of Brain Injury

1993 ◽  
Vol 4 (3) ◽  
pp. 227-237 ◽  
Author(s):  
Donald G. Stein ◽  
Marylou M. Glasier ◽  
Stuart W. Hoffman
Keyword(s):  
Central Nervous System ◽  
Brain Injury ◽  
Time Course ◽  
Chemical Activity ◽  
Behavioral Testing ◽  
Naturally Occurring ◽  
New Information ◽  
Definition Of ◽  
Injury And Repair ◽  
The Brain

It is only within the last ten years that research on treatment for central nervous system (CNS) recovery after injury has become more focused on the complexities involved in promoting recovery from brain injury when the CNS is viewed as an integrated and dynamic system. There have been major advances in research in recovery over the last decade, including new information on the mechanics and genetics of metabolism and chemical activity, the definition of excitotoxic effects and the discovery that the brain itself secretes complex proteins, peptides and hormones which are capable of directly stimulating the repair of damaged neurons or blocking some of the degenerative processes caused by the injury cascade. Many of these agents, plus other nontoxic naturally occurring substances, are being tested as treatment for brain injury. Further work is needed to determine appropriate combinations of treatments and optimum times of administration with respect to the time course of the CNS disorder. In order to understand the mechanisms that mediate traumatic brain injury and repair, there must be a merging of findings from neurochemical studies with data from intensive behavioral testing.

Direct effect of PaCO2 on respiratory sinus arrhythmia in conscious humans

2002 ◽  
Vol 282 (3) ◽  
pp. H973-H976 ◽  
Author(s):  
Nobuko Sasano ◽  
Alex E. Vesely ◽  
Junichiro Hayano ◽  
Hiroshi Sasano ◽  
Ron Somogyi ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Direct Effect ◽  
Respiratory Sinus Arrhythmia ◽  
Random Order ◽  
Mean Amplitude ◽  
Frequency Component ◽  
Pulmonary Gas Exchange ◽  
High Frequency Component ◽  
Sinus Arrhythmia ◽  
End Tidal

Respiratory sinus arrhythmia (RSA) may improve the efficiency of pulmonary gas exchange by matching the pulmonary blood flow to lung volume during each respiratory cycle. If so, an increased demand for pulmonary gas exchange may enhance RSA magnitude. We therefore tested the hypothesis that CO2directly affects RSA in conscious humans even when changes in tidal volume (VT) and breathing frequency ( F B), which indirectly affect RSA, are prevented. In seven healthy subjects, we adjusted end-tidal Pco 2 (Pet CO2 ) to 30, 40, or 50 mmHg in random order at constant VT and F B. The mean amplitude of the high-frequency component of R-R interval variation was used as a quantitative assessment of RSA magnitude. RSA magnitude increased progressively with Pet CO2 ( P < 0.001). Mean R-R interval did not differ at Pet CO2 of 40 and 50 mmHg but was less at 30 mmHg ( P < 0.05). Because VT and F B were constant, these results support our hypothesis that increased CO2directly increases RSA magnitude, probably via a direct effect on medullary mechanisms generating RSA.

Gas exchange in dogs in the prone and supine positions

1992 ◽  
Vol 72 (6) ◽  
pp. 2292-2297 ◽  
Author(s):  
K. C. Beck ◽  
J. Vettermann ◽  
K. Rehder
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Prone Position ◽  
Pulmonary Blood Flow ◽  
Random Order ◽  
Arterial Pco2 ◽  
Supine Posture ◽  
Pulmonary Shunting ◽  
The Difference ◽  
Arterial Po2

To determine the cause of the difference in gas exchange between the prone and supine postures in dogs, gas exchange was assessed by the multiple inert gas elimination technique (MIGET) and distribution of pulmonary blood flow was determined using radioactively labeled microspheres in seven anesthetized paralyzed dogs. Each animal was studied in the prone and supine positions in random order while tidal volume and respiratory frequency were kept constant with mechanical ventilation. Mean arterial PO2 was significantly lower (P less than 0.01) in the supine [96 +/- 10 (SD) Torr] than in the prone (107 +/- 6 Torr) position, whereas arterial PCO2 was constant (38 Torr). The distribution of blood flow (Q) vs. ventilation-to-perfusion ratio obtained from MIGET was significantly wider (P less than 0.01) in the supine [ln SD(Q) = 0.75 +/- 0.26] than in the prone position [ln SD (Q) = 0.34 +/- 0.05]. Right-to-left pulmonary shunting was not significantly altered. The distribution of microspheres was more heterogeneous in the supine than in the prone position. The larger heterogeneity was due in part to dorsal-to-ventral gradients in Q in the supine position that were not present in the prone position (P less than 0.01). The decreased efficiency of oxygenation in the supine posture is caused by an increased ventilation-to-perfusion mismatch that accompanies an increase in the heterogeneity of Q distribution.

Sensation of dyspnea during hypercapnia, exercise, and voluntary hyperventilation

1990 ◽  
Vol 68 (5) ◽  
pp. 2100-2106 ◽  
Author(s):  
T. Chonan ◽  
M. B. Mulholland ◽  
J. Leitner ◽  
M. D. Altose ◽  
N. S. Cherniack
Keyword(s):  
Visual Analog Scale ◽  
Line Intensity ◽  
Time Course ◽  
Normal Subjects ◽  
Cycle Ergometer ◽  
Base Line ◽  
Analog Scale ◽  
Voluntary Hyperventilation ◽  
The Difference ◽  
End Tidal

To determine whether the intensity of dyspnea at a given level of respiratory motor output depends on the nature of the stimulus to ventilation, we compared the sensation of difficulty in breathing during progressive hypercapnia (HC) induced by rebreathing, during incremental exercise (E) on a cycle ergometer, and during isocapnic voluntary hyperventilation (IVH) in 16 normal subjects. The sensation of difficulty in breathing was rated at 30-s intervals by use of a visual analog scale. There were no differences in the level of ventilation or the base-line intensity of dyspnea before any of the interventions. The intensity of dyspnea grew linearly with increases in ventilation during HC [r = 0.98 +/- 0.02 (SD)], E (0.95 +/- 0.03), and IVH (0.95 +/- 0.06). The change in intensity of dyspnea produced by a given change in ventilation was significantly greater during HC [0.27 +/- 0.04 (SE)] than during E (0.12 +/- 0.02, P less than 0.01) and during HC (0.30 +/- 0.04) than during IVH (0.16 +/- 0.03, P less than 0.01). The difference in intensity of dyspnea between HC and E or HC and IVH increased as the difference in end-tidal PCO2 widened, even though the time course of the increase in ventilation was similar. No significant differences were measured in the intensity of dyspnea that occurred with changes in ventilation between E and IVH. These results indicate that under nearisocapnic conditions the sensation of dyspnea produced by a given level of ventilation seems not to depend on the method used to produce that level of ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Ceramide and Related-Sphingolipid Levels Are Not Altered in Disease-Associated Brain Regions of APPSLand APPSL/PS1M146LMouse Models of Alzheimer's Disease: Relationship with the Lack of Neurodegeneration?

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Laurence Barrier ◽  
Bernard Fauconneau ◽  
Anastasia Noël ◽  
Sabrina Ingrand
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Models ◽  
Neuronal Death ◽  
Time Course ◽  
Neuronal Loss ◽  
Brain Regions ◽  
App Processing ◽  
Ceramide Accumulation ◽  
The Brain

There is evidence linking sphingolipid abnormalities, APP processing, and neuronal death in Alzheimer's disease (AD). We previously reported a strong elevation of ceramide levels in the brain of the APPSL/PS1Ki mouse model of AD, preceding the neuronal death. To extend these findings, we analyzed ceramide and related-sphingolipid contents in brain from two other mouse models (i.e., APPSLand APPSL/PS1M146L) in which the time-course of pathology is closer to that seen in most currently available models. Conversely to our previous work, ceramides did not accumulate in disease-associated brain regions (cortex and hippocampus) from both models. However, the APPSL/PS1Ki model is unique for its drastic neuronal loss coinciding with strong accumulation of neurotoxic Aβisoforms, not observed in other animal models of AD. Since there are neither neuronal loss nor toxic Aβspecies accumulation in APPSLmice, we hypothesized that it might explain the lack of ceramide accumulation, at least in this model.

Effects of hypercapnia on ECoG and oxidative metabolism in neonatal dog brain

1995 ◽  
Vol 78 (6) ◽  
pp. 2272-2278 ◽  
Author(s):  
H. Yoshioka ◽  
H. Miyake ◽  
D. S. Smith ◽  
B. Chance ◽  
T. Sawada ◽  
...  
Keyword(s):  
Electrical Activity ◽  
Resonance Spectroscopy ◽  
Respiratory Enzymes ◽  
Arterial Pco2 ◽  
A Value ◽  
Electrocorticogram Ecog ◽  
The Brain ◽  
Mitochondrial Respiratory

The effects of hypercapnia on cerebral electrical activity and mitochondrial oxidative phosphorylation were studied in the anesthetized neonatal dog by using the electrocorticogram (ECoG) and 31P-magnetic resonance spectroscopy. Three levels of hypercapnia with arterial PCO2 values of approximately 70, 100, and 140 Torr reduced the intracellular pH of the brain from 7.11 to 6.99, 6.87, and 6.76, respectively. These levels of hypercapnia also reduced ADP concentration ([ADP]) from 21.5 to 18.1, 14.8, and 12.9 microM as well as the average ECoG power output by 20, 30, and 40%. A Michaelis-Menten relationship for the mitochondrial respiratory enzymes was fitted with [ADP] and the change in the average ECoG. The result suggests that mitochondrial respiration is regulated by [ADP] and that the in vivo Michaelis-Menten constant for ADP was 21 microM, a value close to the in vitro value. The mitochondrial maximal reaction velocity was reduced by only 10% during hypercapnia and showed no relationship with the degree of acidosis, suggesting that mitochondrial respiratory enzymes are not responsible for the inhibition of the brain electrical activity.

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