Search PubMed⌕ Search

Biomedical subjects

J R Stradling

Publications and source records attributed to J R Stradling.

At least 109 records · Page 6Linked to original sources
PubMed1987

Evaluation of the Ohmeda 3700 pulse oximeter.

Arterial oxygen saturation values (Sao2) from 60% to 98% were measured by the Ohmeda 3700 pulse oximeter with the three types of probe available and compared with values of oxygen saturation estimated from direct arterial sampling (arterial oxygen and carbon dioxide tensions and pH) on 65 occasions. The response time of the oximeter was measured after a sudden rise in inspired oxygen concentration. Artefact rejection was assessed by arterial compression proximal to the probe site, and by simultaneous recordings of overnight Sao2 on opposite hands. The ability to recreate patterns of oscillating Sao2 from the data stored in the oximeter was also investigated. With the best probe system the oximeter measured Sao2, relative to arterial values estimated from Pao2, with a mean (SD) difference of -0.4% (1.8%). The response time was comparable with those of previous oximeters. It was not possible to generate artefactual dips in excess of 2% Sao2, and the dual overnight recordings rarely showed even small dips on one tracing alone. The stored data can recreate oscillating Sao2 signals with wavelengths down to about 35 seconds, but not below. The Ohmeda 3700 pulse oximeter appears to be suitable for unattended overnight recordings of Sao2.

Evaluation Studies as Topic↗
PubMed1987

Role of upper airway in ventilatory control in awake and sleeping dogs.

We examined the role of the upper airway in the regulation of the pattern of breathing in six adult dogs during wakefulness and sleep. The dogs breathed through a fenestrated endotracheal tube inserted through a tracheostomy. The tube was modified to allow airflow to be directed either through the nose or through the tracheostomy. When airflow was diverted from nose to tracheostomy there was an abrupt increase in the rate of expiratory airflow, resulting in prolongation of the end-expiratory pause but no change in overall expiratory duration or respiratory frequency. Furthermore, electromyogram recordings from implanted diaphragmatic and laryngeal muscle electrodes did not show any changes that could be interpreted as an attempt to delay expiratory airflow or increase end-expiratory lung volume. The effects of switching from nose to tracheostomy breathing could be reversed by adding a resistance to the endotracheal tube so as to approximate upper airway resistance. The findings indicate that under normal conditions in the adult dog upper airway receptors play little role in regulation of respiratory pattern and that the upper airway exerts little influence on the maintenance of end-expiratory lung volume.

Animals↗
PubMed1987

Effect of acute diaphragm paralysis on ventilation in awake and sleeping dogs.

The mechanisms responsible for hypoventilation during rapid-eye-movement (REM) sleep in patients with diaphragmatic weakness are not clear. Therefore, we studied the effects of unilateral (UDP) and bilateral (BDP) diaphragmatic paralysis on ventilation during wakefulness (W), slow-wave sleep (SWS), and REM sleep. Studies were performed in 3 trained dogs in which small silicone cuffs had been implanted surgically around the phrenic nerves. Reversible diaphragmatic paralysis was induced during wakefulness or sleep by bathing the phrenic nerves in local anesthetic injected through a catheter attached to the phrenic cuffs. The UDP reduced abdominal expansion and increased rib cage expansion, but had no effect on minute volume of ventilation (VI) or end-tidal PCO2 (PACO2). The BDP produced marked abdominal paradox, but did not reduce VI during W or SWS and had no effect on tidal volume or respiratory frequency. In contrast, during REM sleep, VI was decreased by an average of 21% mainly because of a fall in tidal volume, and PACO2 increased by 2.4 mm Hg compared with that during the intact state. Furthermore, addition of extra dead space to the breathing circuit, which was well tolerated in intact dogs, led to a progressive increase in PACO2 during BDP and to arousal from sleep. The findings indicate that acute BDP does not impair ventilation during quiet W or SWS, but reduces ventilation during REM sleep, supporting the concept that during REM sleep maintenance of ventilation is critically dependent on diaphragmatic compensation for intercostal and accessory muscle inhibition.

Animals↗
PubMed1986

Respiratory activity of laryngeal muscles in awake and sleeping dogs.

Experiments were conducted in adult dogs to determine the respiratory activity of laryngeal muscles during wakefulness and sleep. We studied the EMG activity of three laryngeal muscles in five trained dogs, two of which were completely intact, and three of which had a previously-formed side-hole tracheal stoma. Pairs of electrodes were implanted chronically into the posterior cricoarytenoid muscle (PCA), a laryngeal dilator, cricothyroid (CT), and thyroarytenoid (TA), a laryngeal adductor. EMG electrodes were also inserted into the costal portion of the diaphragm. In wakefulness (W), slow wave sleep (SWS) and rapid eye movement (REM) sleep the EMGs of the PCA and CT muscles increased in intensity during diaphragm activation, with varying levels of basal activity during expiration. However, the greatest levels of inspiratory activity in PCA and CT during sleep were found in REM sleep, usually in the absence of augmented diaphragm EMG activity. This laryngeal muscle activity was associated with laryngeal dilation. There were also marked state-related changes in the level of activity of CT during expiration, suggestive of changes in the degree of expiratory adduction of the larynx. The adductor muscles (TA) were not active during expiration, except during alert W. There were no consistent differences in respiratory activity of the laryngeal muscles between the two intact dogs and those with a tracheal stoma (whether or not an endotracheal tube was in place), nor was laryngeal muscle activity affected by the subsequent creation of a tracheal stoma in the two intact dogs. The findings indicate that sleep-wakefulness state exerts important influences on the respiratory activity of laryngeal muscles in the adult dog.

Airway Resistance↗
PubMed1986

Laryngeal muscle activities during progressive hypercapnia and hypoxia in awake and sleeping dogs.

Laryngeal, intercostal and diaphragmatic muscle activities were recorded during progressive hypercapnia and hypoxia in dogs with chronically implanted electrodes. As ventilation increased during progressive chemoreceptor stimulation, inspiratory activity of the posterior cricoarytenoid muscle, a laryngeal abductor, and of the cricothyroid muscle were augmented. When expiratory flow rates reached 2-3 times resting levels, both of these muscles were also active during expiration and recruitment of the internal intercostal muscles was observed. The thyroarytenoid muscle, a laryngeal adductor, was active only rarely and no consistent activation of this muscle was observed with either hypercapnia or hypoxia. The patterns of muscle activation in response to respiratory stimulation were not different during wakefulness, slow wave sleep, and rapid eye movement sleep. The results indicate that the laryngeal muscles are activated during hypercapnia and hypoxia in a manner which reduces both inspiratory and expiratory airflow resistance regardless of sleep-wakefulness state.

Animals↗
PubMed1985

Changes in ventilation and its components in normal subjects during sleep.

Non-invasive measurements were made of ventilation, its derivatives, the contributions of abdomen and rib cage and arterial oxygen saturation in six healthy normal men whilst awake and during sleep. Minute ventilation fell significantly during slow wave (SW) sleep and rapid eye movement (REM) sleep (awake = 6.3 1 min-1, SW sleep = 5.7 1 min-1, REM sleep = 5.4 1 min-1; p less than 0.04). Mean inspiratory flow also fell significantly but timing was unchanged. The abdominal (diaphragmatic) contribution to ventilation fell very significantly during SW sleep but returned to awake levels during REM sleep (awake 54%, SW sleep 38%, REM sleep 56%; p less than 0.007). There were also significant falls in arterial oxygen saturation during SW and REM sleep (awake 97.3%, SW sleep 96.5%, REM sleep 96.2%; p less than 0.002). These falls represent reductions in arterial oxygen tension similar to those seen in patients with chronic airways obstruction and can be accounted for entirely by the associated reduction in ventilation.

Abdomen↗
PubMed1984

The effects of oral almitrine on pattern of breathing and gas exchange in patients with chronic obstructive pulmonary disease.

Almitrine at a low dose of 100 mg orally significantly raises PaO2 and lowers PaCO2 in patients with chronic obstructive pulmonary disease, compared with placebo, when they were breathing air or 28% oxygen. The estimated ideal alveolar-arterial PO2 difference was less after almitrine compared with placebo, when patients were breathing either air or 28% oxygen. After almitrine overall ventilation breathing air increased by 10% but this did not reach statistical significance. During 28% oxygen breathing almitrine hardly altered overall ventilation but the inspiratory duty cycle (Ti/Ttot.) decreased and mean inspiratory flow rate (VT/Ti) increased compared with placebo. These changes were significant on a paired t-test (P less than 0.05). Changes in both volume and pattern of breathing may explain the improved gas exchange in the lung after almitrine.

Administration, Oral↗
PubMed1983

Nocturnal hypoxaemia in chronic obstructive pulmonary disease.

1. Day and night arterial oxygen saturation (Sao2) has been measured in forty-one patients with chronic obstructive pulmonary disease (COPD), mean FEV1 0.84 (range 0.4-1.4)litres, and with a range of daytime Sao2 values of 67-95%. 2. The mean and biggest falls in Sao2 at night were much greater in the patients with lower daytime saturations. However, when falls in arterial oxygen tension (Pao2) were estimated from the decreases in Sao2, there was no correlation between the estimated biggest fall in Pao2 and daytime Sao2 and only a weak correlation between estimated mean fall in Pao2 and daytime Sao2. 3. Measurement of ventilation in four hypoxaemic patients with COPD (range 60-90% Sao2) by respiratory inductance plethysmography showed that nocturnal hypoxaemic dips were accompanied by diminished ventilation, which was not always shown by nasal thermistors. 4. Because nocturnal hypoxaemic dips are transient the ideal alveolar-arterial oxygen difference, which assumes a constant respiratory exchange ratio, cannot be used to assess the mechanism of hypoxaemia. 5. Erythrocyte mass was strongly correlated with daytime Sao2 but this correlation was not significantly improved by including nocturnal hypoxaemia in the regression. 6. The results suggest that greater falls in Sao2 at night are related to lower initial Sao2 values and that the cause may be a reduction in ventilation.

Circadian Rhythm↗
PubMed1983

Quantitative measurement of intrapulmonary and extrapulmonary right-to-left shunt.

We have developed a new technique that enables the shunting of blood from the right to the left side of the circulation to be partitioned into a cardiac and a lung component. The effects of recirculation are minimal, and the method does not require on-line data analysis. Quantitative estimates of these components have been made in two normal dogs and in five patients with raised pulmonary arterial pressures, some of whom were known to have a patent foramen ovale. The results were compared with oxygen shunt measured during air breathing. A poorly soluble gas, nitrogen, radiolabelled with 13N in solution is injected first into a central vein while matched samples of blood are drawn from the pulmonary artery and the aorta. A second solution containing 13N is injected into the right ventricle and sampled from the aorta only. Standardized gamma-counting techniques were used to analyze both the injected radioactivity and the radioactivity in the samples. These two measurements enable us to calculate the total right-to-left shunt, the pulmonary shunt, and by subtraction the extrapulmonary cardiac shunt.

Animals↗
PubMed1983

Pattern of breathing and gas exchange following oral almitrine bismesylate in patients with chronic obstructive pulmonary disease.

Almitrine bismesylate (100 mg orally) significantly raised PaO2 and lowered PaCO2 in six patients with chronic obstructive pulmonary disease, compared to placebo, when they were breathing air or 28% oxygen. The estimated ideal alveolar arterial PO2 difference (AaDO2) was less after almitrine bismesylate compared to placebo, when patients were breathing either air or 28% oxygen. After almitrine bismesylate overall ventilation breathing air increased by 10% but this did not reach statistical significance. During 28% oxygen breathing, almitrine bismesylate hardly altered overall ventilation but the inspiratory duty cycle (TI/TTOT) decreased and mean inspiratory flow rate (VT/TI) increased compared to placebo. These changes were significant on a paired T test (P less than 0.05). The improvement in AaDO2 correlated with the rise in VT/TI (r = 0.67, P = 0.02) and thus we suggest that changes in both volume and pattern of breathing might explain the improved gas exchange in the lung after almitrine bismesylate .

Administration, Oral↗
PubMed1982

The effects of almitrine on the ventilatory response to hypoxia and hypercapnia in normal subjects.

1. Almitrine at a dose of 0.5 mg h-1 kg-1 given intravenously over 2 h had no effect on resting ventilation in normal males. 2. There was a small, but insignificant, rise in the hypercapnic drive to breathe as compared with placebo. 3. A large rise in the hypoxic drive to breathe was seen in response to almitrine. 4. These findings support the claim that almitrine has its action on ventilation via the peripheral chemoreceptors. 5. No correlation between blood levels of almitrine and the rise in hypoxic response was seen.

Adult↗