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Biomedical subjects

A C Bryan

Publications and source records attributed to A C Bryan.

At least 109 records · Page 6Linked to original sources
PubMed1976

Respiratory load compensation in infants.

We have studied the respiratory compensation for elastic loads in 15 term and preterm infants. Elastic loads, approximately equal to the infant's effective elastance, were applied to the airway for five breaths while tidal volume and mask pressure were monitored. Motion of the rib cage and abdomen were monitored simultaneously with magnetometers. The studies were done both in active or REM sleep and in quiet or non-REM sleep. During quiet sleep the load immediately reduced the tidal volume by about 50% but a progressive increase in tidal volume occurred over the next four loaded breaths. During active sleep load compensation was disorganized with respect to both tidal volume and frequency, and compensation was significantly less. Active sleep was also characterized by marked rib cage distortion. We suggest that during active sleep there is tonic inhibition of the intercostal muscles, allowing the diaphragm to distort the rib cage. This distortion impairs load compensation by a direct mechanical effect and indirectly by initiating an intercostal-phrenic reflex.

Abdomen↗
PubMed1976

Effect of increased gas density on pulmonary gas exchange in man.

Pulmonary gas exchange was measured in seven resting supine subjects breathing air or a dense gas mixture containing 21% O2 in sulfur hexafluoride (SF6). The mean value of the alveolar-arterial oxygen difference (AaDO2) decreased from 12.4 on air to 7.0 on SF6 (P less than 0.01), and increased again to 13.4 when air breathing resumed (P less than 0.01). No differences occurred between gas mixtures for O2 consumption, respiratory quotient, minute ventilation, breathing frequency, heart rate, or blood pressure, and the improved oxygen transfer could not be attributed to changes in cardiac output or mixed venous oxygen content in the one subject in which they were measured. These results are best explained by an altered distribution of ventilation during dense gas breathing, so that the ventilation-perfusion ratio (VA/Q) variance was reduced. Of several considered mechanisms, we favor one in which SF6 promotes cardiogenic gas mixing between peripheral parallel units having different alveolar gas concentrations. This mechanism allows for observed increases in arterial carbon dioxide tension and dead space-to-tidal volume ratio during dense gas breathing, and suggests that intraregional VA/Q variance accounts for at least one-half of the resting AaDO2 in healthy supine young men.

Blood Gas Analysis↗
PubMed1976

Pulmonary gas exchange in acute mountain sickness.

The severity of acute mountain sickness (AMS) was investigated in healthy volunteers, airlifted to high altitude (5,360 m). Blood gases were measured at 2,990 m and 5,360 m. Symptoms of AMS were found in all subjects, but ranged from malaise to vomiting with intractable headache. The clinical severity of AMS was directly related to the arterial PCO2 and inversely to pH, but unrelated to the PO2 on arrival at high altitude. However, PO2 fell and was lowest 48 h after arrival at high altitude in those subjects with the most severe AMS. These were the only subjects to show an increase in the alveolar-arterial PO2 difference and in the venous admixture ratio during the first 48 h. These abnormalities in gas exchange, which developed in the subjects with the most marked cerebral symptoms, suggest that the manifestations of cerebral and pulmonary dysfunction at altitude develop simultaneously, a finding that suggests coexisting cerebral and pulmonary edema.

Acute Disease↗
PubMed1975

Mucociliary tracheal transport rates in man.

A new method for measuring mucociliary tracheal transport rates (MTTR's) is described. An aqueous aerosol containing albumin microspheres labeled with 99mTc was inhaled in such a manner that it was deposited in local concentrations in the large airways. These boli of microspheres were transported up the trachea and their MTTR's measured using a gamma camera. MTTR's were measured in 42 healthy nonsmoking adults (32 men and 10 women, mean age 28 yr). The mean MTTR's appeared to be log normally distributed with a geometric mean of 3.6 mm/min and a coefficient of variation of 75%. The MTTR's of men and women were similar. Each individual's short-term coefficient of variation was 25%. Twenty-two repeat studies 1 wk to 15 mo apart showed the variation within individuals was less than between individuals. The parasympatholytic drug, atropine (0.6 mg iv) decreased MTTR's for at least 3 h. Inhalation of the sympathomimetic drug, Th1165a increased MTTR's. Chronic and acute smoking did not appreciably change the MTTR'S.

Adrenergic beta-Agonists↗
PubMed1975

Effect of altitude exposure on platelets.

Since decompression from depth is known to produce a fall in platelet count, the effect of altitude decompression and high-altitude exposure on platelets was investigated. Sixteen subjects decompressed without hypoxia to 20,000 ft simulated altitude for two hours showed a significant (P less than 0.01) drop in circulating platelet count of approximately 10% for three days following decompression. Four of five subjects similarly exposed had a shortened autologous platelet survival compared to that prior to exposure. Subjects exposed to 9,800 ft and then 17,600 ft in a mountain environment showed a significant mean decrease in platelet count on day 2 of 7% and 25% respectively, which had returned to control by day 5. Nonhypoxic and hypoxic decompressed rabbits which received homologous chromium-51-labeled platelets had an increase in lung radioactivity compared with sea-level controls. It is postulated that altitude decompression produces platelet reductions similar to these seen after decompression from depth, and that platelets sequester in the pulmonary vascular bed.

Altitude↗
PubMed1975

A new method of evaluating the chemosensitivity of the respiratory center in children.

Decreased ventilatory response to carbon dioxide is often present in lung disease. This can be due to a reduction in the output of the respiratory center or an inability of the respiratory pump to respond to a normal output because of the size or impedence of the pump. To separate these mechanisms we have measured the isometric force developed by the respiratory muscle during brief airway occlusion, by measuring the pressure generated at 100 msec (Pm100). We studied 43 subjects ranging in age from 6 to 50 years, and nine neonates. We found a linear rise of Pm100 with rising PAco2 during carbon dioxide rebreathing maneuvers. Our results also show that although there are wide variations in slopes of Pm100 to carbon dioxide tension (SPm100/PAco2) between individuals, in a given subject this slope remains constant even following repeated studies. It also remains constant for age and size, indicating that the neuromechanical output of the respiratory apparatus does not change with growth. In contrast the ventilatory response either assessed as Ve/PAco2 or Vt/PAco2 depended on age and lung size. The results suggest that throughout growth, comparison of Pm100/PAco2 and Ve/PAco2 can distinguish between abnormalities of neuromuscular output from other causes of ventilatory impairment.

Adolescent↗