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Biomedical subjects

M D Altose

Publications and source records attributed to M D Altose.

At least 91 records · Page 5Linked to original sources
PubMed1977

Effects of hypercapnia and inspiratory flow-resistive loading on respiratory activity in chronic airways obstruction.

The respiratory responses to hypercapnia alone and to hypercapnia and flow-resistive loading during inspiration were studied in normal individuals and in eucapnic and hypercapnic patients with chronic airways obstruction. Responses were assessed in terms of minute ventilation and occlusion pressure (mouth pressure during airway occlusion 100 ms after the onset of inspiration). Ventilatory responses to CO2 (deltaV/deltaPCO2) were distinctly subnormal in both groups of patients with airways obstruction. The two groups of patients, however, showed different occlusion pressure responses to CO2 (deltaP100/deltaPCO2): deltaP100/deltaPCO2 was normal in the eucapnic patients but subnormal in the hypercapnic patients. Flow-resistive loading during inspiration reduced deltaV/deltaPCO2 both in normal subjects and in patients with airways obstruction. The occlusion pressure response to CO2 increased in normal subjects during flow-resistive loading but remained unchanged in both groups of patients with chronic airways obstruction. These results indicate that while chemosensitivity as determined by deltaP100/deltaPCO2 is impaired only in hypercapnic patients with chronic airways obstruction, an acute increase in flow resistance elicits a subnormal increase in respiratory efferent activity in both eucapnic and hypercapnic patients.

Adult↗
PubMed1976

Extracorporeal membrane oxygenation during bronchopulmonary lavage.

Extracorporeal membrane oxygenation (ECMO) in a venoarterial perfusion circuit was used to provide support of gas exchange during bronchopulmonary lavage in a 32-year-old man with pulmonary alveolar proteinosis and severe arterial hypoxemia. Prior to the lavage, Pao2 during mechanical ventilation with 100% oxygen and positive end-expiratory pressure was only 125 mm Hg. Extracorporeal perfusion at a flow rate of 3 liters/min, with oxygen delivery of 244 ml/min, increased the Pao2 to 227 mmHg and lowered the mean pulmonary artery pressure from 28 to 24 mm Hg. During bronchopulmonary lavage and ECMO, the Pao2 ranged between 46 and 96 mm Hg. After the procedure, pulmonary performance decidely improved. By reducing the chances of fatal hypoxemia, ECMO allowed treatment to be instituted for this potentially reversible disorder and proved helpful as a form of support during the management of pulmonary alveolar proteinosis when severe hypoxemia may have other wise precluded bronchopulmonary lavage.

Adult↗
PubMed1976

Airway occlusion pressures in awake and anesthetized goats.

The pressures generated by the inspiratory muscles as they contract isometrically during airway occlusion seem to be a measure of respiratory neuron efferent activity. The ventilatory and occlusion pressure responses to increasing levels of CO2 were studied in goats, awake and anesthetized, with and without inspiratory flow resistance. Hypercapnia was produced by rebreathing. Randomly, during rebreathing, inspiratory airflow was prevented on single breaths. Ventilation and pressures developed during the first 100, 200, 300 and 400 milliseconds of an inspiratory effort against a complete occlusion increased linearly with CO2 in both awake and anesthetized animals. Anesthesia reduced both the ventilatory and occlusion pressure responses to CO2. Inspiratory resistance increased occlusion pressure responses in awake goats but not in the same animals when anesthetized. Inspiratory airflow resistance seems to augment respiratory efferent activity as reflected in the pressure responses only in conscious goats. Thus the response to an inspiratory resistance seems to depend on the state of consciousness.

Airway Resistance↗
PubMed1976

Electromyographic response of respiratory muscles during elastic loading.

The response of respiratory motor neurons to graded elastic loading was assessed in anesthetized dogs by recording the electromyogram (EMG) from the diaphragm (ED) and the intercostal muscle (EIC). Elastic loads were applied for 1-20 breaths. The effects of changes in PCO2 on respiratory motor neuron output was assessed by applying loads during the course of CO2 rebreathing. On the first loaded breath, ED and EIC increased reflexly due chiefly to prolongation of inspiration. Vagotomy or vagal cooling to block the Hering-Breuer reflex eliminated the increase in ED and diminished the increase in EIC. During the second to fifth breath, the level of EMG activity was disproportionately high for the level of PCO2, suggesting an additional reflex component over and above the reflex activity present on the first loaded breath.

Animals↗
PubMed1976

Effects of hypercapnia on mouth pressure during airway occlusion in conscious man.

The effects of hypercapnia and inspiratory flow-resistive loading on mouth pressure during periods of arrested airflow were studied in conscious human subjects to determine the usefulness of inspiratory muscle force in the assessment of respiratory neural efferent activity. Hypercapnia increased the peak end-inspiratory mouth pressure (Ppeak) during complete airway occlusion and the pressures at 100, 200, and 300 ms after the onset of inspiration (P100, P200, P300). During rebreathing without added mechanical loads, P100 and Ppeak increased linearly with the electrical activity of the diaphragm and changes in P100 and Ppeak during hypercapnia correlated well with ventilatory responses to PCO2 (DELTA V/DELTA PCO2) suggesting that occluded mouth pressures are reliable measures of respiratory activity. In individuals with the greatest reduction in delta V/DELTA PCO2 during inspiratory flow-resistive loading, changes in P100 and Ppeak with PCO2 increased only minimally. In contrast, there was a much greater increase in occluded mouth pressures with hypercapnia in the presence of mechanical loading when inspiratory flow-resistive loading failed to depress delta V/DELTA PCO2. In all subjects, occluded mouth pressures were greater at any given PCO2 during mechanical loading than during free breathing. Mechanical loading resulted in augmented respiratory neural efferent activity unexplained by alterations in chemical stimulation.

Adult↗
PubMed1976

Effects of hypercapnia and flow-resistive loading on tracheal pressure during airway occlusion.

To determine whether the isometric force of concentration of the inspiratory muscles could be used to assess respiratory efferent neural activity, the tracheal pressure generated by the inspiratory muscles during airway occlusion (occluded tracheal pressure) was measured during progressive hypercapnia in anesthetized dogs breathing normally and breathing against added flow-resistive loads. Hypercapnia increased the peak end-inspiratory tracheal pressure and the occluded tracheal pressures generated 100, 200, and 300 ms after the onset of inspiration. The duration of the occluded inspiratory effort generally remained unchanged and the configuration of the pressure tracing was not affected. During normal breathing occluded tracheal pressures increased linearly with tidal volume and with the electrical activity of the diaphragm and the external intercostal muscles both before and after vagotomy. Inspiratory flow-resistive loading reduced the ventilatory response to CO2 but did not affect occluded tracheal pressures at any given PCO2 or the change in pressures with hypercapnia both before and after vagotomy. Similarly, expiratory flow-resistive loading failed to affect occluded tracheal pressures. These results suggest that occluded tracheal pressures measure respiratory efferent neural activity and can be used as indices of CO2 responsivity even during mechanical loading in anesthetized animals.

Airway Obstruction↗
PubMed1976

Effect of hypoxia on the pressure developed by inspiratory muscles during airway occlusion.

The effect of progressive isocapnic hypoxia on the pressure generated by the inspiratory muscle during airway occlusion was studied in 10 awake subjects during normal and obstructed breathing. Isocapnic hypoxia was produced by rebreathing a gas mixture of 6% CO2 in air while the expired gas was passed through a CO2 scrubber so as to maintain PACO2 constant (42.6 mmHg +/- 2.2 SE). Occlusion of the airway was performed randomly for a single breath at FRC. In all 10 subjects maximal pressure (Ppeak) and the pressures measured 100, 200, 300, and 400 ms after the onset of inspiration increased during hypoxia. Furthermore, good correlation was noted between the occlusion pressure response to hypoxia (delta P/DELTA[1/PO2-32]) and simultaneous changes in ventilatory response to hypoxia (delta VI/DELTA[1/PO2-32]). The occlusion pressure response to hypoxia therefore seems to be a reliable measure of respiratory center output. When rebreathing was repeated during inspiratory resistive loading, the occlusion pressure at any given PO2 and delta P/DELTA(1PO2-32) measured in the first 400 ms of inspiration increased in 9 of 10 subjects. Since PACO2 and PAO2 during both control and loaded experiments were the same, the increase in occlusion pressure in the presence of flow-resistive loading appeared to represent a neurally mediated increase in inspiratory motoneuron activity.

Adult↗
PubMed1975

Evaluation of breath holding in hypercapnia as a simple clinical test of respiratory chemosensitivity.

Breath holding was used as the basis of a simple test of respiratory chemosensitivity. Breath holding was begun at selected degrees of hypercapnia produced by CO2 rebreathing. In 16 healthy control subjects there was a linear regression of the log of breath-holding time on the PCO2 at the start of breath holding. Breath-holding time (BHT) and the slope of a log BHT/Pco2 plot were closely correlated with the ventilatory response to CO2. In five cases of the idiopathic hypoventilation syndrome, CO2 retention and reduced ventilatory response to CO2 were accompanied by prolonged breath-holding time and the regression of log BHT on Pco2 was abnormally flat. However, in 17 patients with chronic airways obstruction, breath-holding time was never prolonged and the log BHT/Pco2 relationship was normal, even though 13 had a diminished ventilatory response to CO2 and four had chronic CO2 retention. It is concluded that the BHT/Pco2 relationship provides a useful index of respiratory chemosensitivity which is not influenced by airways obstruction. This may be helpful in the detection of impaired chemosensitivity as a cause of CO2 retention even when the ventilation CO2 response is reduced non-specifically by coexisting airways obstruction.

Airway Obstruction↗
PubMed1975

Effect of fiberoptic bronchoscopy on respiratory performance in patients with chronic airways obstruction.

Lung volumes, airway resistance, expiratory flow rates, distribution of ventilation, and arterial blood gases were measured before and after fiberoptic bronchoscopy in 13 patients with moderately severe chronic airways obstruction and in 10 healthy non-smoking controls. Arterial blood gases were also monitored serially during the procedure. Arterial oxygen tension (Pao2) fell during fiberoptic bronchoscopy in both patients and controls whereas arterial carbon dioxide tension and pH remained unchanged. Control subjects had no change in lung mechanics after fiberoptic bronchoscopy. However, the patients consistently developed increased airway obstruction after fiberoptic bronchoscopy. Within 24 hours after bronchoscopy lung function in the patients returned to baseline values, except for the residual volume which remained abnormally high. The topical application of lignocaine (Lidocaine) for local anesthesia before fiberoptic bronchoscopy produced no effect on lung mechanics in nine patients and 10 controls, but Pao2 decreased in both the patient and control groups. These results indicate that fiberoptic bronchoscopy consistently inpairs lung mechanics and gas exchange in patients with chronic airways obstruction but that the impairment is mild and reversible. Lignocaine administration as well as the intubation procedure contribute to the fall in Pao2 which occurs both in the patients and in subjects without pre-existing lung disease.

Adult↗
PubMed1975

Effects of mechanical loading and hypercapnia on inspiratory muscle EMG.

The electromyograms of the diaphragm and an external intercostal muscle were analyzed to see if the effects of hypercapnia on inspiratory muscle electrical activity could be distinguished from those of mechanical loading and to determine whether changes in inspiratory muscle electrical activity were a sueful measure of CO2 response during mechanical loading. Anesthetized dogs were studied: 1) during progressive hypercapnia without mechanical loading, 2) during flow-resistive and elastic loading at constant PCO2, and 3) during progressive hypercapnia and mechanical loading. Both mechanical loading and hypercapnia increased total inspiratory diaphragmatic and intercostal muscle electrical activity. However, inspiratory duration was increased by mechanical loads but reduced by hypercapnia. Because of these changes in inspiratory duration, the average rate of diaphragmatic electrical activity remained unaffected by mechanical loading before and after vagotomy but was increased by hypercapnia. In contrast, both hypercapnia and mechanical loading increased the average rate of intercostal muscle electrical activity. There was a greater increase in both total and average rate of intercostal muscle electrical activity during hypercapnia in the presence of mechanical loading than during unloaded breathing. However, the change in total and average rate of diaphragmatic electrical activity with PCO2 was unaffected by added mechanical loads. These results suggest that diaphragmatic but not intercostal muscle electrical activity can be used as an index of CO2 response even during mechanical loading.

Airway Resistance↗
PubMed1975

Changes in strength of lung inflation reflex during prolonged inflation.

Recovery from respiratory inhibition produced by the lung inflation reflex was studied in anesthetized dogs, paralyzed and ventilated with a respiratory pump. During constant ventilation the lungs were periodically inflated using positive end-expiratory pressure, while the respiratory motor output was monitored in the phrenic nerve. Inhibition of the phrenic discharge was followed by gradual recovery throughout 8-min inflation periods despite constant blood gases. Recording afferent potentials in a vagus nerve indicated that adaptation of pulmonary stretch receptors contributed to the initial recovery of the phrenic discharge, but this recovery continued after the receptor discharge had stabilized. The phrenic discharge also recovered after initial inhibition in two situations which avoided stretch receptor adaptation: a) when the stretch receptor discharge from the separate lungs was alternated in an overlapping manner by asynchronous pulmonary ventilation, and b) during continuous electrical stimulation of a vagus nerve. Phrenic activity was temporarily increased above its control value after periods of lung inflation, asynchronous ventilation and vagal stimulation. It is concluded that the lung inflation reflex gradually attenuates during prolonged stimulation due to both stretch receptor adaptation and changes within the central pathways.

Adaptation, Physiological↗
PubMed1975

Changing effect of lung volume on respiratory drive in man.

Experiments were conducted on human subjects to study the effect of lung inflation during breath holding on respiratory drive. Two series of experiments were performed: the first to examine respiratory drive during a single breath hold, the second designed to examine the sustained effect of lung inflation on subsequent breath holds. The experiments involved breath holding begun either at the end of a normal expiration or after a maximum inspiration. When breath holding was repeated at 10-min intervals, the increase in BHT produced by lung inflation was greater in short breath holds (after CO2 rebreathing) than in long breath holds (after hyperventilation). If breath holds were made in rapid succession, the first breath hold was much longer when made at total lung capacity than at functional residual capacity, but this effect of lung inflation diminished in subsequent breath holds. It is concluded that the inhibitory effect of lung inflation decays during breath holding and is regained remarkably slowly during the period of breathing immediately after breath holding.

Adult↗
PubMed1975

Immunocompetent cells from the lower respiratory tract of normal human lungs.

Subpopulations of lymphocytes in the broncho-alveolar air spaces of normal human lungs were compared with those in peripheral blood. Bone marrow-derived (bursal-equivalent) cells (B cells) were identified by complement receptors (EAC rosettes) and by surface immunoglobulin. Thymus-derived lymphocytes (T cells) were identified by their proliferative response to mitogens and the E rosette technique. Cells in lung air spaces were recovered from eight healthy nonsmoking volunteers by segmental lavage with the flexible bronchofiberscope. On the average, macrophages constituted 78% and lymphocytes 17% of the cells in the aspirates. B cells detected by surface immunoglobulin and complement receptors equaled 22% and 15% of lung lymphocytes, respectively. The distribution of lung B cells into heavy chain immunoglobulin classes revealed IgM and IgG to be the predominant classes, with mean values of 14.5% and 9.3%, respectively; the corresponding value for IgA was 5%. A comparable order of frequency (IgM greater than IgG greater than IgA) was observed for purified peripheral blood lymphocytes in the same and other control subjects. T cells comprised the majority (47%) of identifiable lung lymphocytes by the E rosette method. The presence of lung T cells was also corroborated by their proliferative response to mitogens (phytohemagglutinin and concanavallin A), but the response was less than that of equal numbers of peripheral blood lymphocytes from the same subjects. The B/T cell ratio for lung lymphocytes was comparable to results with peripheral blood lymphocytes in the same subjects, but a higher proportion of lung lymphocytes could not be identified as either T or B cells. It is postulated that lung lymphocytes participate in the local immune defenses of the lung.

Adult↗