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Biomedical subjects

K Gleeson

Publications and source records attributed to K Gleeson.

At least 19 recordsLinked to original sources
PubMed2001

Transbronchial biopsy with virtual CT bronchoscopy and nodal highlighting.

Transbronchial biopsy to sample lymph nodes and tumors that are not visible at endoscopy has a poor (<50%) success rate. These nodes can be highlighted easily at virtual computed tomographic (CT) bronchoscopy to provide a guide. This study was performed to evaluate if the addition of this information to the bronchoscopist improved the success rate of transbronchial biopsy of subcarinal and aortopulmonary lymph nodes. The addition of virtual CT bronchoscopy with lymph node highlighting significantly (P < .5) increased biopsy success rates for pretracheal, hilar, and high pretracheal adenopathy.

Adult↗
PubMed2001

Contribution of perfusion pressure to vascular resistance response during head-up tilt.

We measured brachial and femoral artery flow velocity in eight subjects and peroneal and median muscle sympathetic nerve activity (MSNA) in five subjects during tilt testing to 40 degrees. Tilt caused similar increases in MSNA in the peroneal and median nerves. Tilt caused a fall in femoral artery flow velocity, whereas no changes in flow velocity were seen in the brachial artery. Moreover, with tilt, the increase in the vascular resistance employed (blood pressure/flow velocity) was greater and more sustained in the leg than in the arm. The ratio of the percent increase in vascular resistance in leg to arm was 2.5:1. We suggest that the greater vascular resistance effects in the leg were due to an interaction between sympathetic nerve activity and the myogenic response.

Adult↗
PubMed2000

The control of breathing in clinical practice.

The control of breathing results from a complex interaction involving the respiratory centers, which feed signals to a central control mechanism that, in turn, provides output to the effector muscles. In this review, we describe the individual elements of this system, and what is known about their function in man. We outline clinically relevant aspects of the integration of human ventilatory control system, and describe altered function in response to special circumstances, disorders, and medications. We emphasize the clinical relevance of this topic by employing case presentations of active patients from our practice.

Animals↗
PubMed1999

Volatile organic compounds in breath as markers of lung cancer: a cross-sectional study.

BACKGROUND: Many volatile organic compounds (VOCs), principally alkanes and benzene derivatives, have been identified in breath from patients with lung cancer. We investigated whether a combination of VOCs could identify such patients. METHODS: We collected breath samples from 108 patients with an abnormal chest radiograph who were scheduled for bronchoscopy. The samples were collected with a portable apparatus, then assayed by gas chromatography and mass spectroscopy. The alveolar gradient of each breath VOC, the difference between the amount in breath and in air, was calculated. Forward stepwise discriminant analysis was used to identify VOCs that discriminated between patients with and without lung cancer. FINDINGS: Lung cancer was confirmed histologically in 60 patients. A combination of 22 breath VOCs, predominantly alkanes, alkane derivatives, and benzene derivatives, discriminated between patients with and without lung cancer, regardless of stage (all p<0.0003). For stage 1 lung cancer, the 22 VOCs had 100% sensitivity and 81.3% specificity. Cross-validation of the combination correctly predicted the diagnosis in 71.7% patients with lung cancer and 66.7% of those without lung cancer. INTERPRETATION: In patients with an abnormal chest radiograph, a combination of 22 VOCs in breath samples distinguished between patients with and without lung cancer. Prospective studies are needed to confirm the usefulness of breath VOCs for detecting lung cancer in the general population.

Aged↗
PubMed1997

Respiratory arousal from sleep: mechanisms and significance.

The mechanisms by which respiratory stimuli induce arousal from sleep and the clinical significance of these arousals have been explored by numerous studies in the last two decades. Evidence to date suggests that the arousal stimulus in nonrapid eye movement sleep (NREM) is related to the level of inspiratory effort rather than the individual stimuli that contribute to ventilatory drive. A component of the arousal stimulus proportional to the level of inspiratory effort may originate in mechanoreceptors either in the upper airway or respiratory pump. Medullary centers responsible for ventilatory drive may also send a signal proportionate to the level of drive to higher centers in the brain which are responsible for arousal. Thus, the arousal stimulus may consist of multiple components, each increasing as inspiratory effort increases. The level of effort triggering arousal is an index of the arousability of the brain (arousal threshold). A deeper stage of sleep, central nervous system depressants, prior sleep fragmentation, and the presence of obstructive sleep apnea (OSA) have been observed to increase the arousal threshold to airway occlusion. Less information is available concerning the mechanisms of arousal from rapid eye movement (REM) sleep. While REM sleep is associated with the longest obstructive apneas in patients with OSA, normal human subjects appear to have a similar or lower arousal threshold to respiratory stimuli in REM compared to NREM sleep. Recent studies have challenged the assumption that the termination of all obstructive apnea is dependent on arousal from sleep. Improvements in methods to detect and quantitate changes in the cortical electroencephalogram (EEG) may better define the relationship between arousal and apnea termination. This may result in improved criteria for identifying EEG changes of clinical significance. While little is known concerning the mechanisms of arousal in central sleep apnea, arousal may play an important role in inducing this type of apnea in some patients.

Arousal↗
PubMed1997

Quantitative aspiration during sleep in normal subjects.

STUDY OBJECTIVE: To determine the within-subject variability and to estimate the quantity of occult aspiration of nasopharyngeal secretions during sleep in normal humans. DESIGN: Prospective duplicate full-night sleep studies. SETTING: Pulmonary sleep laboratory, university hospital. PARTICIPANTS: Ten normal male volunteers aged 22 to 55 years. INTERVENTIONS: Two full-night polysomnographic recordings with infusion of 2 mL/h radioactive 99mTc tracer into the nasopharynx through a small catheter during EEG-documented sleep. Standard lung scans were conducted immediately following final awakening. Aspiration was defined as the presence of radioactivity in the pulmonary parenchyma on two separate views. RESULTS: A mean sleep efficiency of 85.7 +/- 2.6% was found with no difference between the two study nights. A total of 5 of the 10 subjects studied had tracer evident in the pulmonary parenchyma following final awakening. Three had the tracer apparent following the first-night study and four had tracer apparent following the second-night study. Thus, two subjects aspirated on both nights. Comparing the subjects who aspirated with those who did not, no significant difference could be found for age, time spent in bed, sleep efficiency, apnea-hypopnea index, arousal plus awakening index, or percent of sleep time spent in a supine position. The quantities of tracer aspirated were on the order of magnitude of 0.01 to 0.2 mL. CONCLUSIONS: Aspiration measured by this technique occurs commonly in healthy young men during sleep, is unrelated to sleep quality, and is variable within subjects studied on more than one occasion. The quantity aspirated is of an order of magnitude likely to contain bacterial organisms in physiologically significant quantities.

Adult↗
PubMed1995

Diagnostic flexible fiberoptic pleuroscopy in suspected malignant pleural effusions.

Up to 25% of malignant pleural effusions can remain undiagnosed following history, physical examination, thoracentesis, and percutaneous closed pleural biopsy. The next diagnostic procedure is often rigid thoracoscopy, an invasive procedure requiring an operating suite and usually a postprocedure chest tube. We performed flexible fiberoptic pleuroscopy using a fiberoptic bronchoscope in conjunction with a closed pleural biopsy on 12 patients with exudative pleural effusions that remained undiagnosed despite extensive clinical evaluation. A sterile 4.8-mm outside diameter flexible fiberoptic bronchoscope was placed into the pleural space during the course of a routine closed pleural biopsy. Pneumothorax was induced to allow visualization. Brush or forceps biopsy specimens of suspicious parietal pleural lesions were taken. Eight pleural spaces appeared smooth while four were diffusely studded on the parietal surface. Of these four, three were proven to have diffuse pleural adenocarcinoma using this procedure; the fourth proved ultimately to have pleural mesothelioma. On long-term follow-up (mean = 17.7 +/- 11.4 months), no false-negative studies or unexpected morbidity was noted. Flexible fiberoptic pleuroscopy may provide a diagnosis in exudative pleural effusions when other less invasive procedures fail to do so and is well tolerated with minimal discomfort and risk.

Aged↗
PubMed1994

Exercise induced asthma: a clinical perspective.

Exercise is a very common precipitant of asthma. Inflammation and edema are felt to be important components of the asthmatic response. Heat and water loss from the airway mucosa are most likely important in its pathogenesis, although the exact etiology remains unknown. A good history combined with proper diagnostic testing can usually determine the diagnosis, and prevention is the key to effective management. Although modified training techniques are often helpful, medications are usually needed for both prevention and treatment. While antiinflammatory agents are gaining therapeutic importance, inhaled beta-agonists remain the treatment of choice. With appropriate diagnosis and management, exercise-induced asthma should not limit participation nor performance in athletics for the great majority of the population.

Administration, Inhalation↗
PubMed1994

Life-threatening pneumonia.

Severe pneumonia can be acquired by previously healthy patients, those with pre-existing illness, or those hospitalized for an unrelated illness. Because diagnosis is frequently difficult or delayed, treatment is usually empirically tailored to the most probable offending organisms and the patient's condition. This article reviews the pathogenesis of community- and hospital-acquired pneumonia, clinical features, and diagnostic techniques. An approach to selecting an antibiotic regimen is suggested.

Anti-Bacterial Agents↗
PubMed1993

Ventilatory pattern after hypoxic stimulation during wakefulness and NREM sleep.

The ventilatory after-discharge mechanism (VAD) may stabilize ventilation (VE) after hyperventilation but has not been studied in detail in humans. Several studies conducted during wakefulness suggest that VAD is present, although none has been conducted during sleep, when disordered ventilation is most common. We conducted two experiments during wakefulness and non-rapid-eye-movement (NREM) sleep in 14 healthy young men to characterize the ventilatory response after termination of a 45- to 60-s 10-12% O2 hypoxic stimulus. Eight subjects had triplicate hypoxic trials terminated by 100% O2 during wakefulness and NREM sleep. Hypoxia caused a drop in arterial O2 saturation to 78.5 +/- 0.5%, an increase in VE of 4.4 +/- 0.6 l/min, and a decrease in end-tidal PCO2 of 4.4 +/- 0.4 Torr during wakefulness, with no significant differences during sleep. When the hypoxia was terminated with 100% O2, VE was variable within and between subjects during wakefulness. During sleep, all subjects developed hypopnea (VE < 67% baseline) with a mean decrease of 65.5 +/- 7.8% at the onset of hyperoxia (P < 0.05 compared with baseline VE). We hypothesized that this uniform decrease in VE might be due to the nonphysiological hyperoxia employed. We therefore studied six additional subjects, all during NREM sleep, with identical hypoxic stimulation of breathing terminated by 100% O2 or room air. We again found that termination of hypoxia with 100% O2 produced uniform hypoventilation. However, when the identical stimulus was terminated with room air, no hypoventilation occurred.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Adenosine infusion and periodic breathing during sleep.

Intravenously administered adenosine may increase ventilation (VI) and the ventilatory response to CO2 (HCVR). Inasmuch as we have previously hypothesized that those with higher HCVR may be more prone to periodic breathing during sleep, we measured VI and HCVR and monitored ventilatory pattern in seven healthy subjects before and during an infusion of adenosine (80 micrograms.kg-1.min-1) during uninterrupted sleep. Adenosine increased the mean sleeping VI (7.6 +/- 0.4 vs. 6.5 +/- 0.4 l/min, P less than 0.05) and decreased mean end-tidal CO2 values (42.4 +/- 1.2 vs. 43.7 +/- 1.0 Torr, P = 0.06, paired t test) during stable breathing. In six of seven subjects, periodic breathing occurred during this infusion. The amplitude (maximum VI--mean VI) and period length of this periodic breathing was variable among subjects and not predicted by baseline HCVR [correlation coefficients (r) = 0.64, P = 0.17 and r = -0.1, P = 0.9, respectively]. Attempts to measure HCVR during adenosine infusion were unsuccessful because of frequent arousals and continued periodic breathing despite hyperoxic hypercapnia. We conclude that adenosine infusion increases VI and produces periodic breathing during sleep in most normal subjects studied.

Adenosine↗
PubMed1992

Adenosine stimulation, ventilation, and arousal from sleep.

The mechanism for arousal from sleep resulting from respiratory stimuli is unclear. We hypothesized that arousal is a result of increasing ventilation during sleep. To determine if this is true we compared minute ventilation at the point of arousal from non-REM sleep produced by the respiratory stimulant adenosine to that resulting from progressive hypercapnic stimulation. If this hypothesis is correct, the quantity of breathing immediately preceding arousal from sleep should be similar for each stimulus. We monitored electroencephalogram (EEG), electromyogram (EMG), end-tidal CO2, and inspired minute ventilation (VI) in five healthy young men during full-night sleep studies. Sleep state was monitored during the baseline state, during an intravenous infusion of 80 micrograms/kg/min of adenosine, and during multiple trials of progressive hyperoxic hypercapnia. Arousal from sleep occurred in association with increased breathing 4.2 +/- 1.1 times during adenosine infusion, 2.0 +/- 0 times during hypercapnic stimulation, and 4.0 +/- 0.6 times in the absence of stimulated breathing (spontaneously) per subject. Minute ventilation for the breath preceding arousal associated with adenosine stimulation (13.0 +/- 1.4 L/min) was similar to that preceding arousal caused by hypercapnia (12.9 +/- 1.1 L/min). In each case this level of breathing was greater than that preceding spontaneously occurring arousals (8.2 +/- 1.1 L/min), p less than 0.05). Although variable between subjects, there was a high correlation for these two variables within subjects (R = 0.96, p = 0.01). These data support the hypothesis that increasing ventilation induces arousal from sleep when ventilation is increased regardless of the stimulus producing this rising drive to breathe.

Adenosine↗
PubMed1992

Effect of oxygen breathing following submaximal and maximal exercise on recovery and performance.

To determine whether supplemental oxygen following exercise hastens recovery or enhances subsequent performance we evaluated its effectiveness in 13 male athletes. The exercise periods consisted of two 5-min submaximal efforts on a treadmill ergometer followed by a single bout to exhaustion. Intervals of exercise were separated by a 4-min recovery period during which the subject breathed either 1) room air, 2) 100% oxygen, or 3) 2 min of 100% oxygen followed by 2 min of room air on three nonconsecutive days. We found that breathing 100% oxygen produced no significant difference on the recovery kinetics of minute ventilation or heart rate, or improvement in subsequent performance as measured by duration of exercise (3.33 +/- 0.04 min, air vs 3.46 +/- 0.03, oxygen) and peak VO2 (59.9 +/- 2.2 ml.kg-1.min-1, air vs 54.5 +/- 2.2, oxygen). In addition, the perceived magnitude of exertion estimated by the Borg scale was no different during oxygen breathing. These findings offer no support for the use of supplemental oxygen in athletic events requiring short intervals of submaximal or maximal exertion.

Adult↗
PubMed1991

Norepinephrine clearance is increased during acute hypoxemia in humans.

Acute hypoxemia leads to activation of the sympathetic nervous system (SNS), yet adrenergic vasoconstriction does not occur and venous plasma norepinephrine (NE) fails to rise as expected. To examine whether this dissociation between SNS tone and plasma NE is due to altered metabolism of NE, we measured arterial NE kinetics ([3H]NE infusion technique) and sympathetic nervous outflow to muscle (peroneal microneurography) during 25-30 min of hypoxemia (spontaneous breathing, mean O2 saturation 74%) in six healthy young men. During hypoxemia, muscle sympathetic nervous activity (MSNA) rose significantly from 12.2 +/- 3.3 to 18.6 +/- 3.5 bursts/min, and the total amplitude increased from 123 +/- 36 to 255 +/- 50 mm/min. NE spillover, an index of NE release at the sympathetic nerve terminals, rose from 1.66 +/- 0.30 to 2.33 +/- 0.40 nmol.min-1.m-2 (P = 0.014). However, NE clearance increased also from 0.99 +/- 0.05 to 1.19 +/- 0.11 l.min-1.m-2 (P = 0.014), and arterial NE rose from 281 +/- 50 to 339 +/- 64 pg/ml (P = 0.023). Hypoxemia resulted in a significant rise in forearm blood flow and a decrease in forearm vascular resistance. The fact that skin blood flow and vascular resistance did not change implies that forearm vasodilation was localized to skeletal muscle. Our results suggest that during acute hypoxemia in humans the SNS is activated but the rise in plasma NE is attenuated because NE clearance is increased.

Adult↗
PubMed1990

The influence of increasing ventilatory effort on arousal from sleep.

Arousal from sleep in response to asphyxia can be a lifesaving event. However, the mechanisms responsible for this important arousal response are uncertain. A unifying hypothesis is that arousal results from the increased respiratory effort that occurs as a result of ventilatory stimulation. If this is true, the magnitude of this effort during the breaths immediately preceding arousal from sleep should be similar regardless of the stimulus. Therefore, the negative inspiratory pleural pressure during the breaths preceding arousal would be similar, whether stimulated by added inspiratory resistive load, hypoxia, or hypercapnia. To test this hypothesis, we studied eight young, healthy men during full-night sleep studies. We measured their electroencephalography (EEG), electromyography (EMG), electrooculography (EOG), inspired ventilation (VI), end tidal PCO2 (PETCO2), O2 saturation, and esophageal pressure (esophageal balloon) while inducing arousal from non-REM sleep using (1) a 30-cm H2O/L/s added resistive load, (2) progressive hypoxia, and (3) progressive hyperoxic hypercapnia. All subjects were eventually aroused following the addition of the 30-cm H2O/L/s added load and during progressive hypercapnia. However, only six of the eight men were aroused when the O2 saturation was reduced to a minimum of 70%. For each stimulus, arousal occurred at very different levels of ventilation and arterial chemistry (SaO2 and CO2). However, ventilatory effort for each subject was similar at the point of arousal regardless of the stimulus. The peak-negative esophageal pressure for the single inspiration preceding arousal (for the six subjects arousing with all three stimuli) was 16.8 +/- 1.4 cm H2O for added resistive load, 15.0 +/- 2.4 cm H2O for hypoxia, and 14.7 +/- 2.1 cm H2O for hypercapnia. We conclude that increasing ventilatory effort may be the stimulus to arousal from sleep independent of the source of this rising drive to breathe.

Adult↗