Computer simulation of experiments in responses to intravenous and inhaled CO2

1981 ◽  
Vol 50 (4) ◽  
pp. 835-843 ◽  
Author(s):  
W. S. Yamamoto
Keyword(s):  
Venous Return ◽  
Neural Signal ◽  
Set Point ◽  
Ventilatory Responses ◽  
Operating Level ◽  
Excitatory State ◽  
Co2 Level ◽  
Neural Excitation ◽  
Low Levels ◽  
Hypercapnic Response

A simulation of ventilatory responses to infused and inhaled CO2 at controlled cardiac output and high and low levels of neural excitation mimics comparable experiments in animals. The model suggests that at low levels of endogenous and exogenous CO2 load the alert quiescent animal will show hyperpnea to both test states associated with hypercapnia. The nonalert quiescent animal simulated will show an isocapnic response to endogenous load and hypercapnic response to exogenous load. The explanation of this behavior lies in the model formulation, which allows the neural signal from metabolically active sources to drive the proportional component of the controller below an operating level established by its set point. By this reasoning the excited but metabolically inactive animal should be paradoxically less sensitive to small changes in CO2, whether exogenous or endogenous, than the quiescent animal. The model demonstrates further that a neural "exercise" signal in proportion to venous return better simulates observations in which CO2 load and venous return are dissociated than one in which the neural signal is computed from metabolism. The use of delta V/delta P slopes as estimates of sensitivity go awry in experiment and simulation when blood flow, CO2 level, and neural excitatory state are dissociated. This is particularly true when the organism is operating at and below the hypothesized set point.

Sexual influence on the control of breathing

1983 ◽  
Vol 54 (4) ◽  
pp. 874-879 ◽  
Author(s):  
D. P. White ◽  
N. J. Douglas ◽  
C. K. Pickett ◽  
J. V. Weil ◽  
C. W. Zwillich
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Premenopausal Women ◽  
Co2 Production ◽  
Menstrual Phase ◽  
Co2 Partial Pressure ◽  
Ventilatory Responses ◽  
Chemical Stimuli ◽  
Low Levels ◽  
Normal Women

Previous investigation has demonstrated that progesterone, a hormone found in premenopausal women, is a ventilatory stimulant. However, fragmentary data suggest that normal women may have lower ventilatory responses to chemical stimuli than men, in whom progesterone is found at low levels. As male-female differences have not been carefully studied, we undertook a systematic comparison of resting ventilation and ventilatory responses to chemical stimuli in men and women. Resting ventilation was found to correlate closely with CO2 production in all subjects (r = 0.71, P less than 0.001), but women tended to have a greater minute ventilation per milliliter of CO2 produced (P less than 0.05) and consequently a lower CO2 partial pressure (PCO2) (men 35.1 +/- 0.5 Torr, women 33.2 +/- 0.5 Torr; P less than 0.02). Women were also found to have lower tidal volumes, even when corrected from body surface area (BSA), and greater respiratory frequency than comparable males. The hypoxic ventilatory response (HVR) quantitated by the shape parameter A was significantly greater in men [167 +/- 22 (SE)] than in women (109 +/- 13; P less than 0.05). In men this hypoxic response was found to correlate closely with O2 consumption (r = 0.75, P less than 0.001) but with no measure of size or metabolic rate in women. The hypercapnic ventilatory response, expressed as the slope of ventilation vs. PCO2, was also greater in men (2.30 +/- 0.23) than in women (1.58 +/- 0.19, P less than 0.05). Finally women tended to have higher ventilatory responses in the luteal than in the follicular menstrual phase, but this was significant only for HVR (P less than 0.05). Women, with relatively higher resting ventilation, have lower responses to hypoxia and hypercapnia.

Ventilatory responses to carbon dioxide at low and high levels of oxygen are elevated after episodic hypoxia in men compared with women

2004 ◽  
Vol 97 (5) ◽  
pp. 1673-1680 ◽  
Author(s):  
Chris Morelli ◽  
M. Safwan Badr ◽  
Jason H. Mateika
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
High Oxygen ◽  
Set Point ◽  
Ventilatory Responses ◽  
Episodic Hypoxia ◽  
Before And After ◽  
Oxygen Gas ◽  
End Tidal

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.

Time course of augmentation and depression of hypoxic ventilatory responses at altitude

1994 ◽  
Vol 77 (1) ◽  
pp. 313-316 ◽  
Author(s):  
M. Sato ◽  
J. W. Severinghaus ◽  
P. Bickler
Keyword(s):  
Pulse Oximetry ◽  
Sea Level ◽  
Time Course ◽  
Ventilatory Response ◽  
Barometric Pressure ◽  
Hypoxic Ventilatory Response ◽  
Set Point ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Arterial O2 Saturation

Hypoxic ventilatory response (HVR) and hypoxic ventilatory depression (HVD) were measured in six subjects before, during, and after 12 days at 3,810-m altitude (barometric pressure approximately 488 Torr) with and without 15 min of preoxygenation. HVR was tested by 5-min isocapnic steps to 75% arterial O2 saturation measured by pulse oximetry (Spo2) at an isocapnic PCO2 (P*CO2) chosen to set hyperoxic resting ventilation to 140 ml.kg-1.min-1. Hypercapnic ventilatory response (HCVR, 1.min-1.Torr-1) was tested at ambient and high SPO2 6–8 min after a 6- to 10-Torr step increase of end-tidal PCO2 (PETCO2) above P*CO2. HCVR was independent of preoxygenation and was not significantly increased at altitude (when corrected to delta logPCO2). Preoxygenated HVR rose from -1.13 +/- 0.23 (SE) l.min-1.%SPO2(-1) at sea level to -2.17 +/- 0.13 by altitude day 12, without reaching a plateau, and returned to control after return to sea level for 4 days. Ambient HVR was measured at P*CO2 by step reduction of SPO2 from its ambient value (86–91%) to approximately 75%. Ambient HVR slope was not significantly less, but ventilation at equal levels of SPO2 and PCO2 was lower by 13.3 +/- 2.4 l/min on day 2 (SPO2 = 86.2 +/- 2.3) and by 5.9 +/- 3.5 l/min on day 12 (SPO2 = 91.0 +/- 1.5; P < 0.05). This lower ventilation was estimated (from HCVR) to be equivalent to an elevation of the central chemoreceptor PCO2 set point of 9.2 +/- 2.1 Torr on day 2 and 4.5 +/- 1.3 on day 12.(ABSTRACT TRUNCATED AT 250 WORDS)

The control of denitrification time in full scale by the automatic detection of the low nitrate bend in the redox curve

2008 ◽  
Vol 57 (7) ◽  
pp. 1095-1101 ◽  
Author(s):  
David Cecil
Keyword(s):  
Nitrogen Removal ◽  
Nitrate Concentration ◽  
Electricity Consumption ◽  
Full Scale ◽  
Practical Application ◽  
Third Order ◽  
Set Point ◽  
Fixed Set ◽  
Order Polynomial ◽  
Low Levels

A practical problem with using redox potential to control nitrogen removal in activated sludge is detecting the bend in the redox curve that occurs when the nitrate concentration is reduced to low levels. In this paper, a method for detecting the bend is proposed. The method is based on fitting a third-order polynomial to the whole redox curve during a denitrification period. The bend is then the point of inflection on this curve. This is the potential when the second derivative of the polynomial is zero. The practical application of the method is demonstrated in full scale. The method successfully detected the bend in about 90% of aeration denitrification cycles. However, this method gave no significant improvement in nitrogen removal and less than 4% reduction in electricity consumption when compared with control based on a fixed redox set point. Therefore, it is recommended that a fixed set point be used, as this is a much simpler and more robust method.

scholarly journals Evidence from high-altitude acclimatization for an integrated cerebrovascular and ventilatory hypercapnic response but different responses to hypoxia

2017 ◽  
Vol 123 (6) ◽  
pp. 1477-1486 ◽  
Author(s):  
Zachary M. Smith ◽  
Erin Krizay ◽  
Rui Carlos Sá ◽  
Ethan T. Li ◽  
Miriam Scadeng ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Control Mechanism ◽  
Integrated Control ◽  
Acute Hypoxia ◽  
Absolute Value ◽  
Ventilatory Responses ◽  
Two Systems ◽  
Hypercapnic Response ◽  
Sustained Hypoxia

Ventilation and cerebral blood flow (CBF) are both sensitive to hypoxia and hypercapnia. To compare chemosensitivity in these two systems, we made simultaneous measurements of ventilatory and cerebrovascular responses to hypoxia and hypercapnia in 35 normal human subjects before and after acclimatization to hypoxia. Ventilation and CBF were measured during stepwise changes in isocapnic hypoxia and iso-oxic hypercapnia. We used MRI to quantify actual cerebral perfusion. Measurements were repeated after 2 days of acclimatization to hypoxia at 3,800 m altitude (partial pressure of inspired O2 = 90 Torr) to compare plasticity in the chemosensitivity of these two systems. Potential effects of hypoxic and hypercapnic responses on acute mountain sickness (AMS) were assessed also. The pattern of CBF and ventilatory responses to hypercapnia were almost identical. CO2 responses were augmented to a similar degree in both systems by concomitant acute hypoxia or acclimatization to sustained hypoxia. Conversely, the pattern of CBF and ventilatory responses to hypoxia were markedly different. Ventilation showed the well-known increase with acute hypoxia and a progressive decline in absolute value over 25 min of sustained hypoxia. With acclimatization to hypoxia for 2 days, the absolute values of ventilation and O2 sensitivity increased. By contrast, O2 sensitivity of CBF or its absolute value did not change during sustained hypoxia for up to 2 days. The results suggest a common or integrated control mechanism for CBF and ventilation by CO2 but different mechanisms of O2 sensitivity and plasticity between the systems. Ventilatory and cerebrovascular responses were the same for all subjects irrespective of AMS symptoms. NEW & NOTEWORTHY Ventilatory and cerebrovascular hypercapnic response patterns show similar plasticity in CO2 sensitivity following hypoxic acclimatization, suggesting an integrated control mechanism. Conversely, ventilatory and cerebrovascular hypoxic responses differ. Ventilation initially increases but adapts with prolonged hypoxia (hypoxic ventilatory decline), and ventilatory sensitivity increases following acclimatization. In contrast, cerebral blood flow hypoxic sensitivity remains constant over a range of hypoxic stimuli, with no cerebrovascular acclimatization to sustained hypoxia, suggesting different mechanisms for O2 sensitivity in the two systems.

Somatostatin inhibits the ventilatory response to hypoxia in humans

1986 ◽  
Vol 60 (3) ◽  
pp. 997-1002 ◽  
Author(s):  
D. L. Maxwell ◽  
P. Chahal ◽  
K. B. Nolop ◽  
J. M. Hughes
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Open Circuit ◽  
Co2 Production ◽  
Adult Males ◽  
Hypoxic Response ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Hypercapnic Response ◽  
Ventilatory Response To Hypoxia

The effects of a 90-min infusion of somatostatin (1 mg/h) on ventilation and the ventilatory responses to hypoxia and hypercapnia were studied in six normal adult males. Minute ventilation (VE) was measured with inductance plethysmography, arterial 02 saturation (SaO2) was measured with ear oximetry, and arterial PCO2 (Paco2) was estimated with a transcutaneous CO2 electrode. The steady-state ventilatory response to hypoxia (delta VE/delta SaO2) was measured in subjects breathing 10.5% O2 in an open circuit while isocapnia was maintained by the addition of CO2. The hypercapnic response (delta VE/delta PaCO2) was measured in subjects breathing first 5% and then 7.5% CO2 (in 52–55% O2). Somatostatin greatly attenuated the hypoxic response (control mean -790 ml x min-1.%SaO2 -1, somatostatin mean -120 ml x min-1.%SaO2 -1; P less than 0.01), caused a small fall in resting ventilation (mean % fall - 11%), but did not affect the hypercapnic response. In three of the subjects progressive ventilatory responses (using rebreathing techniques, dry gas meter, and end-tidal Pco2 analysis) and overall metabolism were measured. Somatostatin caused similar changes (mean fall in hypoxic response -73%; no change in hypercapnic response) and did not alter overall O2 consumption nor CO2 production. These results show an hitherto-unsuspected inhibitory potential of this neuropeptide on the control of breathing; the sparing of the hypercapnic response is suggestive of an action on the carotid body but does not exclude a central effect.

Ventilatory responses to low levels of CO2 inhalation in the cat

1984 ◽  
Vol 55 (1) ◽  
pp. 81-94 ◽  
Author(s):  
Wayne E. Fordyce ◽  
Susan L. Knuth ◽  
Donald Bartlett
Keyword(s):  
Ventilatory Responses ◽  
Low Levels

scholarly journals Habituation of the cardiac response to involuntary diving in diving and dabbling ducks

1987 ◽  
Vol 131 (1) ◽  
pp. 403-415 ◽  
Author(s):  
G. R. Gabbott ◽  
D. R. Jones
Keyword(s):  
Blood Gases ◽  
Cardiac Response ◽  
Dabbling Ducks ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Aythya Americana ◽  
Habituation Training ◽  
Before And After ◽  
The Central Nervous System ◽  
Low Levels

1. Bradycardia in response to forced submergence was habituated in dabbling (Anas platyrhynchos, Linnaeus) and diving (Aythya americana, Eyton) ducks by repetitively submerging the animals, each day for several days, for periods of 40 and 20 s, respectively. The onset of pronounced bradycardia was delayed with each successive trial, until little or no bradycardia occurred during submergence. Diving bradycardia is driven by chemoreceptors in the dabbler and caused by stimulation of narial receptors in the diver. 2. Mean arterial blood pressure in dives was unchanged from pre-dive levels in both naive and trained dabbling ducks. PaO2, PaCO2 and pHa at the end of a dive were similar before and after habituation training. 3. Bradycardia occurred in dives by habituated dabbling ducks if the animal breathed 15% O2 before submergence. The ventilatory responses to breathing high and low levels of oxygen were unaffected by habituation training. 4. The changes in blood gases during dives by naive and habituated dabbling ducks were the same: therefore, in the absence of a demonstrated decrement in receptor chemosensitivity or efferent potency, the locus of habituation must reside in the central nervous system.

MECHANISMS OF HEMOCONCENTRATION IN THE DOG DURING ACUTE ENDRIN INSECTICIDE POISONING

1965 ◽  
Vol 43 (5) ◽  
pp. 793-800 ◽  
Author(s):  
Thomas E. Emerson Jr.
Keyword(s):  
Pulmonary Artery ◽  
Venous Return ◽  
Venous Pressure ◽  
Lung Weight ◽  
Vascular Volume ◽  
Isolated Perfused Lung ◽  
Blood Ph ◽  
Early Increase ◽  
Perfused Lung ◽  
Low Levels

Hemoconcentration following intravenous administration of the chlorinated hydrocarbon insecticide endrin was investigated in sham-operated, splenectomized, and abdominal-eviscerated dogs. Isolated perfused lung preparations and those in which total venous return to the heart was monitored were also utilized. By 30 minutes after endrin the hematocrit had increased 14% in sham-operated animals but only 8% in splenectomized and eviscerated dogs. Blood pH fell to low levels in all groups. Pulmonary artery pressure increased in the constant flow perfused lungs after endrin; an early increase preceded a loss of lung weight. Pulmonary vascular resistance and left atrial and pulmonary artery pressures increased after endrin in the venous return studies. Hemoconcentration appears to result in part from addition of cell-rich blood from the spleen, and an increase in mean corpuscular volume secondary to the severe acidemia as observed in several experiments may also be involved. Loss of plasma fluid in the hepatosplanchnic area does not seem to occur, but pulmonary venous pressure was elevated, and loss of vascular volume from the lungs cannot be excluded.

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