[Mechanical properties of the lung and distribution of ventilation].
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Biomedical subjects
Publications and source records attributed to J Milic-Emili.
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The effects of doxapram infusion (0.25 mg.kg-1. min-1) were studied in cats anaesthetized with pentobarbitone (35 mg . kg-1 intraperitoneally). Cats were studied breathing 50 per cent oxygen and the responses to two concentrations of inspired carbon dioxide were measured. Doxapram infusion increased pulmonary ventilation by increasing both tidal volume and respiratory frequency, and also caused increases in the volume inspired in the first 0.5 second after the onset of an inspiration (V0.5) and the pressure generated in the airway 0.5 second after the onset of an inspiration when the airway had been occluded (P degrees 0.5). V 0.5, P degrees 0.5 and the mean inspiratory flow rate (VT/VI) were essentially equivalent indices of inspiratory drive. Doxapram infusion did not alter the effective impedance of the respiratory system (P degrees 0.5/V 0.5). Doxapram infusion increased the ventilatory response to carbon dioxide. The slope of the ventilatory response to carbon dioxide was increased and the response line was shifted to the left. We conclude that the increase in pulmonary ventilation caused by doxapram infusion is due almost entirely to increased inspiratory neuromuscular drive (P degrees 0.5).
Tidal volume (VT), minute ventilation (VE), the duration of inspiratats anaesthetized with 0.7%, 1% and 1.5% (inspired) trichloroethylene (TCE). The tracheal cannula was occluded at intervals at the start of inspiration and the tracheal pressure was measured to assess the force of contraction of the respiratory muscles. Anaesthesia with TCE 0.7% was associated with an increase in VE, a reduction in VT, and a marked increase in respiratory frequency and mean inspiratory flow rate, but PaCO2 values did not differ significantly from those in conscious animals. Ventilation was also greater than in conscious animals during anaesthesia with TCE 1%. TCE 1.5% caused a significantly greater PaCO2 than in conscious animals. All concentrations of TCE caused a reduction in the ventilatory response to carbon dioxide, measured by the steady-state method. Cervical vagal section did not abolish the tachypnoea caused by TCE.
Ventilatory patterns during rest, CO2 inhalation (2, 3, and 4%) and three levels of exercise were analyzed in supine men using a canopy system for noninvasive measurements. Changes in tidal volume (VT) and breathing frequency (f) with equal increases in minute ventilation (VE) differed significantly during exercise and CO2 inhalation. Increases in VE during exercise was accompanied by increases in VT and f. During CO2 inhalation, the change in frequency was less than during exercise. However, when analyzed in terms of inspiratory flow (VT/TI) and inspiratory duty cycle (TI/Ttot), the response to both stimuli was similar. With increases to twice control VE both TI/Ttot and VT/VI increased. Thereafter only VTTI increased with increasing VE. At rest, inspiratory time on a breath by breath basis increased minimally with VT, while changes in inspiratory flow accounted for the variability in VT. These two respiratory stimulants appear to increase ventilation through different mechanisms when analyzed in terms of VT and f. However, changes in inspiratory flow and duty cycle are similar in both.
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1. Using the mouth occlusion pressure technique, we have studied the control of breathing in seven hypercapnic and eight non-hypercapnic patients with chronic obstructive lung disease. 2. When breathing room air, pulmonary ventilation, mean inspiratory flow and P0.1 (mouth occlusion pressure developed 0.1 s after the onset of occluded inspiration at functional residual capacity) were not significantly different between the two groups of patients. Tidal volume, however, was significantly lower in the hypercapnic than in the non-hypercapnic patients, as a result of a significantly lower duration of inspiration. 3. The lower tidal volume in the hypercapnic patients leads to decreased alveolar ventilation, and appears to be the main cause of retention of carbon dioxide.
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The maturation of control of breathing was studied in unanesthetized rabbit pups breathing room air in a body plethysmograph during the first 8 postnatal days. Measurements include pulmonary ventilation (VE), tidal volume (VT), inspiratory (TI) and total breathing cycle (Ttot) durations, TI/Ttot, mean inspiratory flow (VT/TI), and tracheal pressure developed by the inspiratory muscles 0.1 and 0.2 s after the onset of inspirations with airways occluded at functional residual capacity (P0.1 and P0.2). All of the above variables increased progressively from the 1st to the 8th day, except for P0.1, P0.2, and TI/Ttot which remained constant. The constancy of TI/Ttot implies that the increase in VE with age was due entirely to increased VT/TI. The constancy of P0.1 and P0.2 implies that the increase in VT/TI with age was due to decreased "effective" impedance of the respiratory system. The latter probably mainly reflects increased compliance and decreased flow resistance with growth. The results also show that during the first 8 days of life there is a progressive shift to the right in the VT vs. TI relationship.
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Using the airway occlusion pressure technique, control of breathing was studied in unanesthetized and anesthetized newborn rabbits breathing various gas mixtures under steady-state conditions. Independent of the gas mixture breathed, barbiturate anesthesia resulted in a reduction of ventilation. This was not due to a change in inspiratory drive since for each gas mixture breathed the pressure generated by the inspiratory muscles 0.3 s after the onset of the occluded inspiration (P0.3) remained virtually unchanged, nor could this be attributed to changes in respiratory mechanics as indicated by the fact that the relation between P0.3 and V0.3 (the volume generated 0.3 s after onset of the immediately preceding unoccluded inspiration) did not change. On the other hand, during anesthesia inspiratory time was slightly shortened as a result of a change in both central (bulbopontine) and peripheral (volume-related vagal reflex) modulation, while expiratory duration was markedly prolonged. This disproportionate increase in expiratory duration with respect to inspiratory duration was responsible for most of the depression of ventilation found in the newborn rabbits during barbiturate anesthesia.
The present investigation was undertaken to study the interaction of CO2 and body temperature on phrenic activity (moving average) and tracheal occlusion pressure. Studies were performed on spontaneously ventilated cats anesthetized with pentobarbital sodium at different body temperatures (32-41 degrees C) while breathing room air, 2 and 4% CO2 in 50% O2. At any given chemical drive, increased body temperature caused a similar increase in rate of phrenic activity and tracheal occlusion pressure, while their peak values remained virtually unchanged. At any given body temperature, increased chemical drive caused an increase in both rate of rise and peak values of phrenic activity and tracheal occlusion pressure. These results confirm previous findings that body temperature affects the rate of rise of the central inspiratory activity (CIA), but not the inspiratory "off-switch" threshold, while CO2 increases both the rate of rise of CIA and off-switch threshold. In addition the results indicate that tracheal occlusion pressure provides a similar index of CIA as "integrated" phrenic activity.
In seven anesthetized tracheotomized cats we studied the acute respiratory effects of SO2 inhalation at different steady-state levels of arterial CO2 tension (Paco2). During room air breathing, SO2 (0.05%) addition caused a progressive reduction in tidal volume (VT) and increases in both respiratory frequency (f) and pulmonary resistance (RL). Atropine sulfate abolished the bronchoconstriction response to SO2 and thus permitted the study of the influence of SO2 on VT and f in the absence of constricted airways. Despite marked reductions in the VT VS. PaCO2 relationships with SO2 exposure after atropine, the relationship between pulmonary ventilation (VE) and PaCO2 was not signifcantly altered. This was the case since SO2 caused solely a reduction in inspiratory duration (Ti), affecting neither the mean rate of rise of inspiratory activity (i.e., VT/Ti) nor the relationship between Ti and breath duration. Thus, airways irritation with SO2 produced rapid, shallow breathing characterized by a shortening of inspiratory and total respiratory cycle times with no change in the rate of development of inspiratory activity. The findings suggest an influence exclusively concerned with the timing of inspiration. Perhaps premature onset of inspiratory activity accounts for the observed effects.