[Human experiments of metabolism, blood alkalization and oxygen effect on control and regulation of breathing. II: room air exercise test after blood alkalization].
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Basis on the dynamic changes of the ventilation and arterial blood gas parameters to symptom-limited maximum cardiopulmonary exercise testing (CPET), we further investigate the effect of alkalized blood by drinking 5% NaHCO3 on ventilation during exercise.After drinking 5% NaHCO3 75 ml (3.75 g) every 5 min, total dosage of 0.3 g/Kg, 5 volunteers repeated CPET. All CPET and ABG data changes were analyzed and calculated. At the same time, CPET and ABG parameters after alkalized blood were compared with those before alkalized blood (control) used paired t test.After alkalized blood, CPET response patterns of parameters of ventilation, gas exchange and arterial blood gas were very similar (P > 0.05). All minute ventilation, tidal volume, respiratory rate, oxygen uptake and carbon dioxide elimination were gradually increased from resting stage (P < 0.05-0.001), according to the increase of power loading. During CPET after alkalized blood, ABG parameters were compared with those of control: hemoglobin concentrations were lower, CaCO2 and pHa were increased at all stages (P < 0.05). The PaCO2 increased trend was clear, however only significantly at warm-up from 42 to 45 mmHg (P < 0.05). Compared with those of control, only the minute ventilation was decreased from 13 to 11 L/min at resting (P < 0.05).Even with higher mean CaCO2, PaCO2 and pHa, lower Hba and [H+]a, the CPET response patterns of ventilatory parameters after alkalized blood were similar.Keywords:
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In human subjects at rest changes in heart rate pulmonary ventilation, tidal volume, respiratory rate, and end-tidal carbon dioxide tension were examined at increases in deep body temperature of 1 degrees C and 2 degrees C. Each of these latter target temperatures was achieved at two different rates of temperature increase. The increase in deep body temperature was associated with a rise in heart rate and tidal volume and a reduction in respiratory rate. An increase in pulmonary ventilation associated with a reduction in end-tidal carbon dioxide tension occurred only when deep body temperature increase reached 1.5 degrees C. The apparently greater change in both pulmonary ventilation and end-tidal carbon dioxide tension during the more rapid increase in deep body temperature by 2 degrees C was not significant.
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Basis on the dynamic changes of the ventilation and arterial blood gas parameters to symptom-limited maximum cardiopulmonary exercise testing (CPET), we further investigate the effect of alkalized blood by drinking 5% NaHCO3 on ventilation during exercise.After drinking 5% NaHCO3 75 ml (3.75 g) every 5 min, total dosage of 0.3 g/Kg, 5 volunteers repeated CPET. All CPET and ABG data changes were analyzed and calculated. At the same time, CPET and ABG parameters after alkalized blood were compared with those before alkalized blood (control) used paired t test.After alkalized blood, CPET response patterns of parameters of ventilation, gas exchange and arterial blood gas were very similar (P > 0.05). All minute ventilation, tidal volume, respiratory rate, oxygen uptake and carbon dioxide elimination were gradually increased from resting stage (P < 0.05-0.001), according to the increase of power loading. During CPET after alkalized blood, ABG parameters were compared with those of control: hemoglobin concentrations were lower, CaCO2 and pHa were increased at all stages (P < 0.05). The PaCO2 increased trend was clear, however only significantly at warm-up from 42 to 45 mmHg (P < 0.05). Compared with those of control, only the minute ventilation was decreased from 13 to 11 L/min at resting (P < 0.05).Even with higher mean CaCO2, PaCO2 and pHa, lower Hba and [H+]a, the CPET response patterns of ventilatory parameters after alkalized blood were similar.
Respiratory minute volume
Arterial blood
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Respiratory exchange ratio
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Thermoregulatory benefits of cold-induced changes in breathing pattern and mechanism(s) by which cold induces hypoventilation were investigated using male Holstein calves (1-3 mo old). Effects of ambient temperatures (Ta) between 4 and 18 degrees C on ventilatory parameters and respiratory heat loss (RHL) were determined in four calves. As Ta decreased, respiratory frequency decreased 29%, tidal volume increased 35%, total ventilation and RHL did not change, and the percentage of metabolic rate attributed to RHL decreased 26%. Total ventilation was stimulated by increasing inspired CO2 in six calves (Ta 4-6 degrees C), and a positive relationship existed between respiratory frequency and expired air temperature. Therefore, cold-exposed calves conserve respiratory heat by decreasing expired air temperature and dead space ventilation. Compared with thermoneutral exposure (16-18 degrees C), hypoventilation was induced by airway cold exposure (4-6 degrees C) alone and by exposing the body but not the airways to cold. Blocking nasal thermoreceptors with topical lidocaine during airway cold exposure prevented the ventilatory response but did not lower hypothalamic temperature. Hypothalamic cooling (Ta 16-18 degrees C) did not produce a ventilatory response. Thus, airway temperature but not hypothalamic temperature appears to control ventilation in cold-exposed calves.
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Arterial blood gas tensions, pulmonary mechanics, and lung volumes were measured in 4 sedated ponies every hour for 6 hours and in 5 ponies 4 times at 2-month intervals to assess the short- and long-term reproducibility of pulmonary function measurements. Variability in blood gas tensions was small over the short- and long-term measurement periods, whereas the variability in total respiratory resistance and functional residual capacity was small over the short term but larger over the long term. The variability in tidal volume, minute ventilation, respiratory rate, and dynamic and quasistatic compliance was relatively large over the short and long term. When data from 5 ponies were pooled, significant change did not occur in any of the variables over a 6-month period. Vagal blockade increased tidal volume and decreased respiratory rate and total respiratory resistance, but arterial blood gas tensions, minute ventilation, dynamic compliance, quasistatic compliance, functional residual capacity, and lung and thoracic cage pressure-volume curves were unaffected. Total respiratory resistance decreased with increasing lung volume, with the vagus intact. After vagal blockade, the decrease in total respiratory resistance with lung volume was minimal. Dynamic compliance was frequency independent over a range of 15 to 60 breaths/min-1, suggesting that measurable inhomogeneity of peripheral time constants did not exist in our clinically normal ponies.
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Background: The study of gas exchange and ventilation was previously carried out on a group of healthy subjects, where the response to the use of respiratory devices consisted of a decrease in respiratory rate, oxygen consumption, and carbon dioxide emission, as well as an increase in respiratory volume.
Aim: To assess the impact of respiratory devices on ventilation and gas exchange parameters in patients with COPD.
Methods: The study included patients with COPD (n= 21) of both sexes with the mean age of 59. The values of VE, f, Vt, VO2, VCO2, RER, VE/VO2 were recorded on a spirometabolic complex at the initial state and after connecting respiratory devices (Valve 22F-22V and Y - piece 22M, 22M/15F, Intersurgical). Each record was conducted successively over five minutes, while the subject was sitting ar rest and breathing ambient air.
Results: It was found that the ventilation parameters did not significantly change during the study, while there was an 18% decrease in oxygen consumption (VO2) and 17% decrease in carbon dioxide elimination (VCO2); the ventilatory equivalent of oxygen (VE/VO2) increased by 15.5%, and the respiratory exchange ratio (RER) did not change.
Conclusions: The observed decrease in gas exchange parameters is manifested in both healthy subjects and in patients with COPD. Yet, as opposed to healthy subjects, the patients with COPD show no changes in ventilation values. Thus, during the examination of patients, the impact of respiratory devices should be taken into account, which can vary depending on the respiratory system function.
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1. A study has been made of the effects of resistance to respiration in the inspiratory and expiratory phases. 2. Resistance to inspiration caused an increase in respiratory rate, a decrease in tidal air, and in most instances a severe limitation of the minute volume of pulmonary ventilation. Anoxemia and acidosis accompanied these changes. 3. When resistance was removed the respiratory rate continued to be rapid, but the tidal air and minute volume increased. As a result of this there was a fall in pCO(2), a rise in pH, and in some cases a complete disappearance of anoxemia. 3. Resistance to expiration slowed the respiratory rate and produced a constant decrease in the minute volume of pulmonary ventilation. Anoxemia and carbon dioxide retention occurred, but were less pronounced than in the inspiratory experiments. Release of resistance to expiration resulted in a return of all functions to their normal, or approximately normal, levels. 4. A difference in the gross pulmonary pathology found at autopsy in these two types of experiments has been described, and an attempt has been made to correlate changes in function with changes in structure. 5. No direct evidence has been supplied for the liability to fatigue of the respiratory center.
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