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Biomedical subjects

J Milic-Emili

Publications and source records attributed to J Milic-Emili.

At least 235 records · Page 13Linked to original sources
PubMed1977

Vagal contribution to the inspiratory 'off-switch' mechanism.

It has been suggested that vagal contribution to the inspiratory inhibition can be estimated from the difference between the amplitudes of the 'integrated' phrenic activity with and without phasic vagal feedback. At any given body temperature, there is a linear relationship between estimated vagal contribution to the 'off-switch' mechanism and the 'integrated' vagal activity recorded directly. The temperature displaces this relationship to facilitate vagal central effect. There are evidences that a temperature related activity, which is mediated from hypothalamic thermosensitive structures, may directly influence the vagal input to the R beta neurons of the dorsal group of respiratory neurons in the medulla. An increase in Paco2 results in an increase in the peak 'integrated' vagal activity and in the estimated vagal central effect. However, the inhibitory effect of CO2 on pulmonary stretch receptors seems to be enhanced by an increase in body temperature.

Anesthesia↗
PubMed1976

Respiratory regulation after elastic loading and CO2 rebreathing in normal term infants.

Studies of airway pressure, tidal volume, respiratory duration, and total breath duration before and after elastic loading airway occlusions were carried out on ten full-term, normal infants on two occassions in the first week of life. Using these noninvasive techniques we infer that static compliance and the Hering-Breuer reflex are unchanged during the first week; that infants may increase sensitivity to chemical drive toward the end of the first week; and that there may be a volume related threshold for vagal inhibition of inspiration in some infants.

Carbon Dioxide↗
PubMed1976

Effect of ether on control of rate and depth of breathing in newborn rabbits.

The effect of ether anesthesia on Hering-Breuer inflation reflexes of newborn rabbit pups was investigated. Studies were done at a level of anesthesia at which an apneustic pattern of respiration is seen in vagotomized animals. The hypothesis that increase in vagal influence on respiratory frequency is accompanied by increase in influence on contractile force of the inspiratory muscles was tested. Two aspects of the Hering-Breuer reflex, breath duration and airway pressure developed with an elastic load, were evaluated simultaneously. This was done by performing airway occlusions at FRC--the results expressed as percent slowing on occlusion and as effective elastance (E'rs). The animals were studied with and without anesthesia, before and after vagotomy. Anesthesia resulted in a marked increase in vagal influence on inspiratory duration (34% increase) and on total breath duration (36% increase). In contrast E'rs was decreased (20%) after anesthesia whereas passive elastance was slightly increased. The vagal contribution to E'rs was essentially the same before and after anesthesia (36-38%). Thus ether anesthesia increases one aspect of the Hering-Breuer reflex without changing the other. These findings are likely due to depression of the central nervous system rather than due to peripheral effects of ether.

Airway Obstruction↗
PubMed1976

Occlusion pressures in men rebreathing CO2 under methoxyflurane anesthesia.

The effect of general anesthesia on control of breathing was studied by CO2 rebreathing and occlusion pressure measurements in six normal human subjects under methoxyflurane anesthesia. CO2 was found to increase the amplitude of the occlusion pressure wave without changing its shape, so that CO2 responses in terms of the occlusion pressure developed 100 ms after the onset of inspiration (Po/0.1) gave results equivalent to the responses in terms of Po/1.o or any other parameter of the pressure wave. Methoxyflurane depressed the ventilatory response to CO2 but not the occlusion pressure response, implying that the most important action of the anesthetic was to increase the effective elastance of the respiratory system rather than to depress the respiratory centers. The elastance was further increased by CO2, and this mechanical change had the effect of shifting the "apneic threshold" extrapolated from the ventilatory response curve to a lower PAco2. Frequency of breathing, inspiratory and expiratory times were not altered by CO2 in anesthetized subjects.

Adult↗
PubMed1976

Influence of lung volume and electrode position on electromyography of the diaphragm.

In cats anesthetized with Nembutal, electromyograms of the diaphragm (Edi) were recorded from an anchored esophageal electrode, a pair of silver hooks inserted in the paratendinous region, and a pair of silver hooks and a pair of clips of small surface inserted in the costal region of the diaphragm facing the rib cage at FRC but covered with lung tissue at FRC + 80 ml. When single supramaximal electrical stimuli were applied to an isolated phrenic nerve, changes in lung volume from RV to near TLC had a negligible effect on muscle potentials from esophageal or paratendinous hooks, but increased the amplitude of potentials recorded from peripheral hooks and clips. In addition, it was found that small displacements of the esophageal electrode caused substantial changes in the amplitude of the recorded muscle potentials. The integration of the Edi spontaneously generated during occluded inspirations, recorded from paratendinous hooks and the esophageal electrode was linearly related to transdiaphragmatic pressure up to 50 cmH2O at all lung volumes. Above that level, esophageal electrode recordings showed a curvilinear Edi/Pdi relationship, while hook recordings showed a rectilinear relationship.

Animals↗
PubMed1976

Effect of mechanical factors on the relation between rate and depth of breathing in cats.

In anesthetized tracheotomized cats we compared the time sequence of ventilatory events with neurological events (electrical activity of the diaphragm) during the breathing cycle. We found that under control conditions a phase shift existed between the neurological and the spirometric duration of inspiration, amounting to about 150 ms. This phase shift was increased by increasing the time constant of the respiratory system (resistive loading) and decreased by decreasing it (elastic loading). These phase shifts resulted in a difference in the appreciation of the volume responsible for the termination of inspiration (Hering-Breuer inhibition) because the volume corresponding to the end of the neurological event was somewhat smaller than the final tidal volume reached.

Animals↗
PubMed1976

Adaptation of anesthetized men to breathing through an inspiratory resistor.

Normal men anesthetized with methoxyflurane rebreathed carbon dioxide under two conditions. In one case they breathed most of the time through a low-resistance circuit and an inspiratory resistor of 40.4 cmH2O/1-s-1 was applied at intervals. In another case they breathed most of the time through the resistor and were allowed occasional free breaths. There were no differences between the two types of runs in tidal volume, respiratory frequency, duration of inspiration of loaded or unloaded breaths, or in amplitude or shape of occlusion pressure waves. It is concluded that the reaction of conscious men to an inspiratory resistive load, consisting of a compensatory augmentation of neural drive to respiratory muscles that does not depend on a chemical stimulus, is absent in anesthetized men.

Adult↗
PubMed1975

The progressive response of the newborn infant to added respiratory loads.

The responses of 10 normal full-term infants to 10-sec airway occlusions at functional residual capacity were studied. The responses were quantified by measuring the pressure generated on successive inspiratory efforts following occlusions in room air and 100% oxygen. The response after oxygen breathing was 30-40% less than after air breathing, indicating that hypoxia accounted for part of the response. There was an increase in the response in air from the first to the fourth day of life. Endtidal carbon dioxide tension was shown to increase during the occlusion, but the response remaining after hypoxia was eliminated may not have been due entirely to hypercapnea. We conclude that the compensatory response of the infant to added respiratory loads is in part due to hypoxia, and that the hypoxic response increases over the first week of life.

Airway Obstruction↗
PubMed1975

Occlusion pressure as a measure of respiratory center output in conscious man.

The output of the "respiratory centers" has been estimated by measuring ventilation, inspiratory muscle power, EMG of the diaphragm, and by various other means, each of which has serious disadvantages. The static pressure generated by the inspiratory muscles at FRC against an obstructed airway is here suggested as a useful alternative. Ten conscious, normal, sitting human subjects were subjected to CO2 rebreathing (Read, 1967) and their airways were occluded at end-expiration at intervals without the subjects being aware in advance. The inspiratory pressure waves so generated were found to be distorted by conscious or unconscious responses to the occlusion which had a minimum latency of 0.15 sec. The pressure generated at 0.1 sec after the onset of inspiration (P0.1) was nevertheless easy to measure and was reproducible in each subject. The CO2 response obtained by plotting P0.1 against PCO2, was curvilinear, the P0.1 increasing more rapidly at high PCO2. The P0.1 is independent of pulmonary mechanics. Since it measures the rate of rise of inspiratory activity and not the peak activity it is also independent of mechanisms that alter the respiratory pattern by affecting inspiratory duration, in particular the vagal volume-related inspiratory-inhibitory reflex. It is concluded that measurements of P0.1 represent a useful index of the output of the respiratory centers.

Airway Obstruction↗
PubMed1975

Effect of added elastances on the first loaded breath in man.

Tidal volume together with end-inspiratory pressure was measured in four seated healthy men, during normal breathing and during single inspirations taken from a series of rigid containers which provided added elastances (range: 5-70 cmH2O/l). Experiments were performed both during quiet breathing and during ventilation increased by added dead space. Added elastic loads always resulted in a decreased tidal volume. This decrease was partly compensated by increased pressure developed by the inspiratory muscles; being more so with greater added elastance, control ventilation, or both. Analysis of our results indicates that the load-compensatory response may be attributed to changes in mechanical impedance of the ventilatory pump, due to the mechanical arrangement and the intrinsic properties of the inspiratory muscles (force-length and force-velocity relationships), changes in respiratory frequency with increasing ventilation, and to vagally mediated load compensation.

Adult↗
PubMed1975

A method for the assessment of phasic vagal influence on tidal volume.

Vagal influence related to lung volume changes results in reduction in tidal volume during spontaneous breathing due primarily to premature termination of inspiration. The strength of this vagal influence was traditionally assessed by the duration of apnea following lung inflation, a method recently shown to be inadequate and potentially misleading. An alternate method is described utilizing analysis of the volume tracing of spontaneous breaths and the tracheal pressure tracing during the first breath following airway occlusion at FRC. A formula was devised which, on the basis of previous observations, should predict the tidal volume to be obtained in the absence of phasic vagal influence. The formula was tested in four pentobarbital-anesthetized rabbits using a technique of vagal cooling which rapidly eliminated the vagal influence under study. It was found that the tidal volume obtained following vagal block could be accurately predicted provided allowances were made for the vagally mediated terminal inhibition during spontaneous breathing and the relative stiffness of the respiratory system at high lung volumes.

Action Potentials↗
PubMed1975

Regulation of frequency and depth of breathing during expiratory threshold loading in cats.

In six spontaneously breathing anesthetized cats, intermittently subjected to inspiratory elastic loads, we have studied the relationships between tidal volume (VT) and the durations of inspiration (Ti) and breath duration (Ttot) obtained during spontaneous ventilation from resting lung volume (FRCc) and from elevated end-expiratory levels. The latter was elevated by submerging the expiratory breathing line into a column of water, representing the addition of an expiratory threshold load (ETL). The VT vs. Ti relationships obtained at different end-expiratory levels were similar, indicating that during ETL the vagal mechanism regulating Ti responds only to lung volume changes above the new end-expiratory level and is independent of the absolute end-expiratory lung volume. Single vagal fiber recordings suggest that this effect on Ti control may be explained on the basis of adaptation occurring at the level of the pulmonary stretch receptors. The control of Ttot, on the other hand, was found to depend both on the Ti of the preceding breath (phasic component) and on a separate vagal mechanism specifically affecting the duration of expiration (Te) in response to changes in the absolute end-expiratory lung volume. The latter mechanism is functionally inoperative at FRCc.

Animals↗
PubMed1975

Control of depth and frequency of breathing during baroreceptor stimulation in cats.

In 10 tracheotomized anesthetized cats during steady-state inhalation of various concentrations of CO2 and O2, the acute respiratory response to baroreceptor stimulation produced by transient inflation of a balloon placed in the descending aorta was studied. The latter induced a sudden rise in mean arterial pressure, ranging from 62 to 95 mmHg. At all PACO2 levels above 30 mmHg, elevation in arterial pressure was accompanied by an immediate drop in tidal volume (VT) and prolongation of the durations of inspiration (Ti) and total breath (Ttot). Breaths obtained during baroreceptor stimulation fell along the same VT vs. Ti and VT vs. Ttot relationships obtained in the normotensive state, suggesting that the lung volume-related vagal control of Ti and Ttot is unaffected by changes in arterial pressure. Since, for a given change in arterial pressure, a constant reduction in VT was obtained at all PACO2 levels above 30 mmHg, it can be concluded that the interaction between PACO2 and arterial pressure is additive. In three cats, at PACO2 levels below 30 mmHg, aortic obstruction resulted in brief periods of apnea. Following apnea, the control of Ti and Ttot was transiently offset, describing hysteresis pathways on the VT vs. Ti and VT vs. Ttot relationships.

Abdominal Muscles↗
PubMed1975

Regional distribution of a 133Xe labelled gas volume inspired at constant flow rates.

We measured the regional distribution of 480 ml of 133Xe labelled gases inspired from FRC at constant inspiratory flow rates ranging from 0.1 to 6 litres/s. The gases used were air and 20% O2 in helium. At low inspiratory flow rates the gas was preferentially delivered to the dependent region of the lung. At maximal inspiratory flows, all regions of the lung were more evenly ventilated. The rate of redistribution was found to be slower and more even than in previous studies using smaller volumes of inspired gas. Assuming equal and synchronous changes of pleural surface pressure, these results can be reasonably predicted by the mechanical time constant theory applied to a simple two-compartment lung model based on equal regional resistances. Breathing the HeO2 mixture did not significantly change ventilation distribution at any flow rate.

Functional Residual Capacity↗