Ventilatory response to 8 h of isocapnic and poikilocapnic hypoxia in humans

1995 ◽  
Vol 78 (3) ◽  
pp. 1092-1097 ◽  
Author(s):  
L. S. Howard ◽  
P. A. Robbins
Keyword(s):  
Analysis Of Variance ◽  
Ventilatory Response ◽  
Progressive Increase ◽  
Nasal Catheter ◽  
Partial Pressures ◽  
End Tidal ◽  
Almost All ◽  
And Control

Almost all studies of the effects of prolonged hypoxia on ventilation (VE) in humans have been performed with the end-tidal PCO2 (PETCO2) left uncontrolled. The purpose of this study was to compare the effects of 8 h of hypoxia with PETCO2 held constant with 8 h of hypoxia with PETCO2 left uncontrolled. Ten subjects completed the study. Each was seated inside a chamber in which the inspired gas could be controlled so as to maintain the desired partial pressures of end-tidal gases (sampled via nasal catheter) constant (see L.S.G.E. Howard et al. J. Appl. Physiol. 78:1088–1091, 1995.). Three 8-h protocols were employed: 1) isocapnic hypoxia, at an end-tidal PO2 of 55 Torr with PETCO2 held at the subject's resting value; 2) poikilocapnic hypoxia, at the same end-tidal PO2; and 3) control, where the inspired gas was air. VE was measured (over 3 min) at 0 and 20 min and at hourly intervals between 1.5 and 7.5 h. There was a rise in VE during isocapnic hypoxia [from an initial VE of 16.2 +/- 1.3 (SE) l/min to a final VE of 24.8 +/- 1.6 l/min], which was significant compared with poikilocapnic hypoxia and control values (P < 0.001, analysis of variance). There was no significant progressive rise in VE during poikilocapnic hypoxia compared with control values. These results show that isocapnic hypoxia produces a progressive increase in VE when sustained over an 8-h period. The onset of this response is faster than has been noted in studies of the progressive rise in VE associated with the poikilocapnic hypoxia of altitude.

Alterations in respiratory control during 8 h of isocapnic and poikilocapnic hypoxia in humans

1995 ◽  
Vol 78 (3) ◽  
pp. 1098-1107 ◽  
Author(s):  
L. S. Howard ◽  
P. A. Robbins
Keyword(s):  
Analysis Of Variance ◽  
Ventilatory Response ◽  
Acute Hypoxia ◽  
Respiratory Control ◽  
Companion Paper ◽  
Tidal Forcing ◽  
Nasal Catheter ◽  
The Subject ◽  
Per Se ◽  
End Tidal

In the preceding companion paper (L. S. G. E. Howard and P.A. Robbins, J. Appl. Physiol. 78: 1092–1097, 1995), we showed that ventilation rises during 8 h of isocapnic hypoxia. In the present study we report the changes that occur in the ventilatory response to acute hypoxia (AHVR) over 8 h of both isocapnic and poikilocapnic hypoxia. Ten subjects completed the study. Each was seated inside a chamber in which the inspired gas could be controlled so as to maintain the desired end-tidal gases (sampled via nasal catheter) constant. Three 8-h protocols were compared: 1) isocapnic hypoxia, at an end-tidal PO2 of 55 Torr with the end-tidal PCO2 held at the subject's resting value; 2) poikilocapnic hypoxia, at the same end-tidal PO2; and 3) control, where the inspired gas was air. AHVR was measured before and at 20 min and 4 and 8 h after the start of the experiment. A sequence of hypoxic square waves and sawtooth inputs was imposed by an end-tidal forcing system, with the subject breathing through a mouthpiece. End-tidal PCO2 was held constant at 1–1.5 Torr above resting. Values for hypoxic sensitivity (Gp; 1.min-1.%-1) and hypoxia-independent ventilation (Vc; l/min) were calculated for each test of AHVR. Both Gp and Vc increased significantly during both hypoxic exposures in relation to control (P < 0.001, analysis of variance). Over the 8-h period, increases in Gp were 87% in isocapnic hypoxia and 44% in poikilocapnic hypoxia, and increases in Vc were 89% in isocapnic hypoxia and 84% in poikilocapnic hypoxia. There were no significant differences between the isocapnic and poikilocapnic exposures. We conclude that Gp and Vc rise mainly as result of hypoxia per se and not the associated alkalosis.

Ventilatory response to exercise in diabetic subjects with autonomic neuropathy

1996 ◽  
Vol 81 (5) ◽  
pp. 1978-1986 ◽  
Author(s):  
C. Tantucci ◽  
P. Bottini ◽  
M. L. Dottorini ◽  
E. Puxeddu ◽  
G. Casucci ◽  
...  
Keyword(s):  
Respiratory Rate ◽  
Autonomic Neuropathy ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Control Subjects ◽  
Inhibitory Modulation ◽  
End Tidal ◽  
And Control ◽  
Response To Exercise ◽  
Maximal Voluntary Ventilation

Tantucci, C., P. Bottini, M. L. Dottorini, E. Puxeddu, G. Casucci, L. Scionti, and C. A. Sorbini. Ventilatory response to exercise in diabetic subjects with autonomic neuropathy. J. Appl. Physiol. 81(5): 1978–1986, 1996.—We have used diabetic autonomic neuropathy as a model of chronic pulmonary denervation to study the ventilatory response to incremental exercise in 20 diabetic subjects, 10 with (Dan+) and 10 without (Dan−) autonomic dysfunction, and in 10 normal control subjects. Although both Dan+ and Dan− subjects achieved lower O2 consumption and CO2 production (V˙co 2) than control subjects at peak of exercise, they attained similar values of either minute ventilation (V˙e) or adjusted ventilation (V˙e/maximal voluntary ventilation). The increment of respiratory rate with increasing adjusted ventilation was much higher in Dan+ than in Dan− and control subjects ( P < 0.05). The slope of the linearV˙e/V˙co 2relationship was 0.032 ± 0.002, 0.027 ± 0.001 ( P < 0.05), and 0.025 ± 0.001 ( P < 0.001) ml/min in Dan+, Dan−, and control subjects, respectively. Both neuromuscular and ventilatory outputs in relation to increasingV˙co 2 were progressively higher in Dan+ than in Dan− and control subjects. At peak of exercise, end-tidal [Formula: see text] was much lower in Dan+ (35.9 ± 1.6 Torr) than in Dan− (42.1 ± 1.7 Torr; P < 0.02) and control (42.1 ± 0.9 Torr; P < 0.005) subjects. We conclude that pulmonary autonomic denervation affects ventilatory response to stressful exercise by excessively increasing respiratory rate and alveolar ventilation. Reduced neural inhibitory modulation from sympathetic pulmonary afferents and/or increased chemosensitivity may be responsible for the higher inspiratory output.

Respiratory control in humans after 8 h of lowered arterial Po 2, hemodilution, or carboxyhemoglobinemia

2001 ◽  
Vol 90 (4) ◽  
pp. 1189-1195 ◽  
Author(s):  
Xiaohui Ren ◽  
Keith L. Dorrington ◽  
Peter A. Robbins
Keyword(s):  
Oxygen Content ◽  
Ventilatory Response ◽  
Acute Hypoxia ◽  
Venous Blood ◽  
Respiratory Control ◽  
Progressive Increase ◽  
Arterial Oxygen ◽  
Hypoxic Ventilatory Response ◽  
Arterial Oxygen Content ◽  
End Tidal

In humans exposed to 8 h of isocapnic hypoxia, there is a progressive increase in ventilation that is associated with an increase in the ventilatory sensitivity to acute hypoxia. To determine the relative roles of lowered arterial Po 2 and oxygen content in generating these changes, the acute hypoxic ventilatory response was determined in 11 subjects after four 8-h exposures: 1) protocol IH (isocapnic hypoxia), in which end-tidal Po 2 was held at 55 Torr and end-tidal Pco 2 was maintained at the preexposure value; 2) protocol PB (phlebotomy), in which 500 ml of venous blood were withdrawn; 3) protocol CO, in which carboxyhemoglobin was maintained at 10% by controlled carbon monoxide inhalation; and 4) protocol C as a control. Both hypoxic sensitivity and ventilation in the absence of hypoxia increased significantly after protocol IH ( P < 0.001 and P < 0.005, respectively, ANOVA) but not after the other three protocols. This indicates that it is the reduction in arterial Po 2 that is primarily important in generating the increase in the acute hypoxic ventilatory response in prolonged hypoxia. The associated reduction in arterial oxygen content is unlikely to play an important role.

The Ventilatory Response to Hypoxia Below the Carbon Dioxide Threshold

1997 ◽  
Vol 22 (1) ◽  
pp. 23-36 ◽  
Author(s):  
Theodore Rapanos ◽  
James Duffin
Keyword(s):  
Carbon Dioxide ◽  
Partial Pressure ◽  
Ventilatory Response ◽  
Pressure Threshold ◽  
Partial Pressures ◽  
Progressive Hypoxia ◽  
End Tidal ◽  
Peripheral Chemoreflex ◽  
Ventilatory Response To Hypoxia ◽  
Lower Carbon

The ventilatory response to acute progressive hypoxia below the carbon dioxide threshold using rebreathing was investigated. Nine subjects rebreathed after 5 min of hyperventilation to lower carbon dioxide stores. The rebreathing bag initially contained enough carbon dioxide to equilibrate alveolar and arterial partial pressures of carbon dioxide to the lowered mixed venous partial pressure (≈ 30 mmHg), and enough oxygen to establish a chosen end-tidal partial pressure (50-70 mmHg), within one circulation time. During rebreathing, end-tidal partial pressure of carbon dioxide increased while end-tidal partial pressure of oxygen fell. Ventilation increased linearly with end-tidal carbon dioxide above a mean end-tidal partial pressure threshold of 39 ± 2.7 mmHg. Below this peripheral-chemoreflex threshold, ventilation did not increase, despite a progressive fall in end-tidal oxygen partial pressure to a mean of 37 ± 4.1 mmHg. In Conclusion, hypoxia does not stimulate ventilation when carbon dioxide is below its peripheral-chemoreflex threshold. Key words: peripheral chemoreflex, rebreathing technique, hyperventilation

Human ventilatory response to 8 h of euoxic hypercapnia

1998 ◽  
Vol 84 (2) ◽  
pp. 431-434 ◽  
Author(s):  
John G. Tansley ◽  
Michala E. F. Pedersen ◽  
Christine Clar ◽  
Peter A. Robbins
Keyword(s):  
Steady State ◽  
Analysis Of Variance ◽  
Ventilatory Response ◽  
End Tidal

Tansley, John G., Michala E. F. Pedersen, Christine Clar, and Peter A. Robbins. Human ventilatory response to 8 h of euoxic hypercapnia. J. Appl. Physiol. 84(2): 431–434, 1998.—Ventilation (V˙e) rises throughout 40 min of constant elevated end-tidal[Formula: see text] without reaching steady state (S. Khamnei and P. A. Robbins. Respir. Physiol. 81: 117–134, 1990). The present study investigates 8 h of euoxic hypercapnia to determine whetherV˙e reaches steady state within this time. Two protocols were employed: 1) 8-h euoxic hypercapnia (end-tidal[Formula: see text] = 6.5 Torr above prestudy value, end-tidal [Formula: see text] = 100 Torr) followed by 8-h poikilocapnic euoxia; and 2) control, where the inspired gas was air. V˙ewas measured over a 5-min period before the experiment and then hourly over a 16-h period. In the hypercapnia protocol,V˙e had not reached a steady state by the first hour ( P < 0.001, analysis of variance), but there were no further significant differences inV˙eover hours 2–8 (analysis of variance). V˙efell promptly on return to eucapnic conditions. We conclude that, whereas there is a component of theV˙e response to hypercapnia that is slow, there is no progressive rise inV˙e throughout the 8-h period.

Effects of haloperidol on ventilation during isocapnic hypoxia in humans

1997 ◽  
Vol 83 (4) ◽  
pp. 1110-1115 ◽  
Author(s):  
Michala E. F. Pedersen ◽  
Keith L. Dorrington ◽  
Peter A. Robbins
Keyword(s):  
Dopamine Receptor ◽  
Analysis Of Variance ◽  
Similar Pattern ◽  
Ventilatory Response ◽  
Placebo Control ◽  
Hypoxic Ventilatory Response ◽  
Abrupt Increase ◽  
Receptor Antagonism ◽  
Ventilatory Responses ◽  
End Tidal

Pedersen, Michala E. F., Keith L. Dorrington, and Peter A. Robbins. Effects of haloperidol on ventilation during isocapnic hypoxia in humans. J. Appl. Physiol.83(4): 1110–1115, 1997.—Exposure to isocapnic hypoxia produces an abrupt increase in ventilation [acute hypoxic ventilatory response (AHVR)], which is followed by a subsequent decline [hypoxic ventilatory depression or decline (HVD)]. In cats, both anesthetized and awake, haloperidol has been reported to increase AHVR and almost entirely abolish HVD. To investigate whether this occurs in humans, the ventilatory responses of 15 healthy young volunteers to 20 min of isocapnic hypoxia (end-tidal [Formula: see text] = 50 Torr) were assessed at 1, 2, and 4.5 h after placebo (control) and after oral haloperidol (Seranace, 0.05 mg/kg) on different days. Three subjects were unable to complete the study because of akathisia. AHVR was significantly greater with haloperidol compared with control ( P < 0.01, analysis of variance). However, no significant change in HVD was found [control HVD = 9.3 ± 1.6 (SD) l/min, haloperidol HVD = 9.9 ± 2.1 l/min; P = not significant, analysis of variance]. We conclude that combined central and peripheral dopamine-receptor antagonism in humans with haloperidol produces a similar pattern of change to that reported previously with the peripheral antagonist domperidone. We have been unable to show in humans a decrease in HVD by the centrally acting drug as observed in cats.

Human ventilatory response to acute hyperoxia during and after 8 h of both isocapnic and poikilocapnic hypoxia

1997 ◽  
Vol 82 (2) ◽  
pp. 513-519 ◽  
Author(s):  
J. G. Tansley ◽  
C. Clar ◽  
M. E. F. Pedersen ◽  
P. A. Robbins
Keyword(s):  
Analysis Of Variance ◽  
Ventilatory Response ◽  
Significant Rise ◽  
Acid Base ◽  
Air Breathing ◽  
Breathing Control ◽  
End Tidal

Tansley, J. G., C. Clar, M. E. F. Pedersen, and P. A. Robbins. Human ventilatory response to acute hyperoxia during and after 8 h of both isocapnic and poikilocapnic hypoxia. J. Appl. Physiol. 82(2): 513–519, 1997.—During 8 h of either isocapnic or poikilocapnic hypoxia, there may be a rise in ventilation (V˙e) that cannot be rapidly reversed with a return to higher[Formula: see text] (L. S. G. E. Howard and P. A. Robbins. J. Appl. Physiol. 78: 1098–1107, 1995). To investigate this further, three protocols were compared: 1) 8-h isocapnic hypoxia [end-tidal[Formula: see text]([Formula: see text] ) held at prestudy value, end-tidal [Formula: see text]([Formula: see text]) = 55 Torr], followed by 8-h isocapnic euoxia[Formula: see text] = 100 Torr); 2) 8-h poikilocapnic hypoxia followed by 8-h poikilocapnic euoxia; and 3) 16-h air-breathing control. Before and at intervals throughout each protocol, theV˙e response to eucapnic hyperoxia [Formula: see text] held 1–2 Torr above prestudy value,[Formula: see text] = 300 Torr) was determined. There was a significant rise in hyperoxicV˙e over 8 h during both forms of hypoxia ( P < 0.05, analysis of variance) that persisted during the subsequent 8-h euoxic period ( P < 0.05, analysis of variance). These results support the notion that an 8-h period of hypoxia increases subsequent hyperoxic V˙e, even if acid-base changes have been minimized through maintenance of isocapnia during the hypoxic period.

Effects of airway anesthesia on ventilatory responses to graded dead spaces and CO2

1988 ◽  
Vol 64 (5) ◽  
pp. 1885-1892 ◽  
Author(s):  
C. Shindoh ◽  
W. Hida ◽  
Y. Kikuchi ◽  
T. Chonan ◽  
H. Inoue ◽  
...  
Keyword(s):  
Steady State ◽  
Dead Space ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Co2 Response ◽  
Co2 Gas ◽  
Ventilatory Responses ◽  
Before And After ◽  
End Tidal ◽  
And Control

Ventilatory response to graded external dead space (0.5, 1.0, 2.0, and 2.5 liters) with hyperoxia and CO2 steady-state inhalation (3, 5, 7, and 8% CO2 in O2) was studied before and after 4% lidocaine aerosol inhalation in nine healthy males. The mean ventilatory response (delta VE/delta PETCO2, where VE is minute ventilation and PETCO2 is end-tidal PCO2) to graded dead space before airway anesthesia was 10.2 +/- 4.6 (SD) l.min-1.Torr-1, which was significantly greater than the steady-state CO2 response (1.4 +/- 0.6 l.min-1.Torr-1, P less than 0.001). Dead-space loading produced greater oscillation in airway PCO2 than did CO2 gas loading. After airway anesthesia, ventilatory response to graded dead space decreased significantly, to 2.1 +/- 0.6 l.min-1.Torr-1 (P less than 0.01) but was still greater than that to CO2. The response to CO2 did not significantly differ (1.3 +/- 0.5 l.min-1.Torr-1). Tidal volume, mean inspiratory flow, respiratory frequency, inspiratory time, and expiratory time during dead-space breathing were also depressed after airway anesthesia, particularly during large dead-space loading. On the other hand, during CO2 inhalation, these respiratory variables did not significantly differ before and after airway anesthesia. These results suggest that in conscious humans vagal airway receptors play a role in the ventilatory response to graded dead space and control of the breathing pattern during dead-space loading by detecting the oscillation in airway PCO2. These receptors do not appear to contribute to the ventilatory response to inhaled CO2.

Ventilation in exercise studied with circulatory occlusion

1981 ◽  
Vol 50 (4) ◽  
pp. 718-723 ◽  
Author(s):  
A. J. Sargeant ◽  
M. Y. Rouleau ◽  
J. R. Sutton ◽  
N. L. Jones
Keyword(s):  
Ventilatory Response ◽  
Initial Period ◽  
Cycle Ergometer ◽  
Similar Degree ◽  
Oxygen Intake ◽  
Venous Pco2 ◽  
End Tidal ◽  
And Control ◽  
Response To Exercise ◽  
Male Subjects

Five male subjects exercised on a cycle ergometer (100 W) for 8 min; circulation to the legs was occluded by cuffs during the first 2 and last 2 min. Ventilation (VE), oxygen intake (VO2), and carbon dioxide output (VCO2) were measured breath by breath. Repeat studies were used to follow arterial PCO2 (PaCO2) and rebreathing mixed venous PCO2 (PVCO2). The results were compared to studies without cuffing, but which were otherwise identical. The initial period of cuffing was associated with marked hyperpnea, high VE/VCO2 ratio, and low PaCO2 and PVCO2. Following release of occlusion at the end of the first 2 min, there was an immediate fall in VE, followed by an increase after an average of 12 s. VE/VCO2 fell and end-tidal PCO2 rose after 4-5 s and reached control values after 12 s. Studies during rebreathing established that CO2 reached the lungs from the legs 4-5 s after release of occlusion, and control PVCO2 was reached after 12 s. Repeated occlusion for the final 2 min of exercise was associated with hyperpnea of similar degree to the initial occlusion. An identical study performed in a patient with absent ventilatory response to CO2 and reduced ventilatory response to exercise showed normal hyperventilatory response to cuffing but did not show an increase in ventilation associated with the arrival of CO2 in the lungs, following release of occlusion. The studies confirmed the importance of CO2 in mediating rapid changes in ventilation during exercise.

Convergence in norming and control of modern wireless technologies electromagnetic fields

2020 ◽  
Vol 60 (9) ◽  
pp. 610-613
Author(s):  
Michail Yu. Maslov ◽  
Yuri M. Spodobaev
Keyword(s):  
Wireless Communication ◽  
Electromagnetic Fields ◽  
Communication Systems ◽  
Communication Technologies ◽  
Telecommunications Industry ◽  
High Tech ◽  
Wireless Technologies ◽  
Almost All ◽  
Network Technologies ◽  
And Control

Telecommunications industry evolution shows the highest rates of transition to high-tech systems and is accompanied by a trend of deep mutual penetration of technologies - convergence. The dominant telecommunication technologies have become wireless communication systems. The widespread use of modern wireless technologies has led to the saturation of the environment with technological electromagnetic fields and the actualization of the problems of protecting the population from them. This fundamental restructuring has led to a uniform dense placement of radiating fragments of network technologies in the mudflow areas. The changed parameters of the emitted fields became the reason for the revision of the regulatory and methodological support of electromagnetic safety. A fragmented structural, functional and parametric analysis of the problem of protecting the population from the technological fields of network technologies revealed uncertainty in the interpretation of real situations, vulnerability, weakness and groundlessness of the methodological basis of sanitary-hygienic approaches. It is shown that this applies to all stages of the electromagnetic examination of the emitting fragments of network technologies. Distrust arises on the part of specialists and the population in not only the system of sanitary-hygienic control, but also the safety of modern network technologies is being called into question. Growing social tensions and radio phobia are everywhere accompanying the development of wireless communication technologies. The basis for solving almost all problems of protecting the population can be the transfer of subjective methods and means of monitoring and sanitary-hygienic control of electromagnetic fields into the field of IT.

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