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Biomedical subjects

E R Bleecker

Publications and source records attributed to E R Bleecker.

At least 127 records · Page 7Linked to original sources
PubMed1983

Computerized tomography in obstructive sleep apnea. Correlation of airway size with physiology during sleep and wakefulness.

Pathophysiologic changes during sleep in patients with obstructive apnea are often associated with alterations in upper airway function during awake periods. To determine whether these functional changes are related to abnormal airway structure, we performed computerized tomography (CT) in 20 awake patients with obstructive apnea and in 10 control subjects. The CT scan measurements of cross-sectional areas of the nasopharynx, oropharynx, and hypopharynx in apneic patients were significantly reduced (p less than 0.05) compared with those in the control subjects. Sites of obstruction varied, and apparent airway occlusion occurred in 6 patients. Reduced pharyngeal size correlated with increased sleep-disordered breathing rates (p less than 0.05), more severe nocturnal oxygen desaturation (p less than 0.05), and the presence of a saw-tooth pattern of flow-volume curves obtained during awake periods (p less than 0.05). Structural upper airway narrowing is detectable with CT in awake patients with obstructive sleep apnea.

Adult↗
PubMed1983

CT demonstration of pharyngeal narrowing in adult obstructive sleep apnea.

Sleep apnea is a major cause of daytime hypersomnolence. Among the proposed etiologies, focal obstruction of the airways at the level of the pharynx has been suggested but not proven. Using computed tomography, the cross-sectional area of the airway can be readily assessed. Thirty-three adults with clinically proven sleep apnea and 12 normal adults underwent systematic computed tomography of the neck. Significant airway narrowing was demonstrated in all the patients with obstructive sleep apnea, whereas no such narrowing was seen in the controls. In 11, the narrowing was at a single level, whereas in 22 patients two or more levels were affected. This study has shown that a structurally abnormal airway may serve as an anatomic substrate for the development of sleep apnea. On the basis of this evidence, uvulopalatopharyngoplasty has been performed in two patients with relief of symptoms in one.

Constriction, Pathologic↗
PubMed1983

The effect of alpha adrenergic blockade on non-specific airways reactivity and exercise induced asthma.

In asthmatics, alpha-adrenergic blockage with oral phentolamine partially or completely blocked bronchospasm after maximal exercise challenge. Bronchial reactivity to isocapnic hyperventilation with conditioned cold air was also reduced. However, non-specific airways reactivity to inhaled histamine did not change. Therefore, exercise and cold induced bronchospasm in asthma may be partially mediated by alpha adrenergic neural mechanisms perhaps through sensitization of alpha receptors during airway cooling.

Airway Resistance↗
PubMed1983

Hemodynamic mechanisms in anaphylaxis.

Intravenous administration of ascaris suum antigen (1 mg) as well as histamine (5 mg) was associated with rapid and marked reductions in cardiac output (QT) and systemic arterial pressure (Pa) in anesthetized mechanically ventilated dogs. When venous return was maintained constant by an external pump reservoir system, both antigen and histamine caused rapid reductions in the reservoir blood volume consistent with peripheral pooling. In addition, interruption of the splanchnic arterial inflow by occlusion of the descending thoracic aorta restored the cardiac output to control during histamine shock, whereas QT during antigen shock was unaffected by aortic occlusion, even though the circulatory failure was of similar magnitude. Therefore, we conclude that differences in responses of antigen and histamine shock to aortic occlusion indicate that mechanisms leading to peripheral pooling of blood are different with the two agents. In addition, stability of left atrial pressure following the administration of either agent, when the venous return is maintained constant, suggests that intrinsic myocardial dysfunction is not a major initiating mechanism in the two shock states studied.

Anaphylaxis↗
PubMed1982

Effects of antihistamines and indomethacin on hyperosmolar-induced vasodilation.

The circulatory effects of iv injections of hyperosmolar solutions were studied both in intact dogs with aortic flow probes and in dogs using a standard right heart-bypass preparation. Serial iv injections of 20 ml of 10% NaCl or 50 ml of 25% mannitol produced reproducible episodic vasodilation characterized by falls in mean aortic pressure from 99 +/- 10 (SE) to 61 +/- 6 Torr and increases in aortic flow from 2.20 +/- 0.06 1/min to 3.12 +/- 0.28 (P less than 0.01). Systemic vascular resistance decreased (P less than 0.01) with each injection and serum osmolarity increased (P less than 0.01); however, there was a poor correlation between these two variables (r = -0.24). Because the mechanism of these physiological changes is unclear, the following experiments were performed to determine whether they were due to the release of vasoactive chemical mediators. We measured arterial and venous plasma histamine, a mediator released systemically in IgE-mediated anaphylactic reactions, but found no changes in histamine levels. Furthermore, pretreatment with both H1 and H2 blockers (diphenhydramine and cimetidine), agents that blocked histamine-induced hypotension, did not prevent hyperosmolar vasodilation. Also, indomethacin (a cyclooxygenase pathway inhibitor of prostaglandin synthesis) did not affect hyperosmolar vasodilation or the fall in systemic vascular resistance. Therefore, hyperosmolar vasodilation is not caused by the systemic release of histamine or by the effects of prostaglandins. The mechanism of these reactions is unknown, but it may be due to direct local effects of hyperosmolar solutions on vascular smooth muscle, perhaps mediated by local fluid and electrolyte shifts.

Animals↗
PubMed1982

A screening test for airways reactivity. An abbreviated methacholine inhalation challenge.

A screening test to measure nonspecific airways reactivity was developed and compared to a standard methacholine inhalation challenge in 13 asthmatic patients and ten normal control subjects. The screening challenge consisted of one deep breath, then four breaths of a 5 mg/ml methacholine solution followed by one and four breaths of 25 mg/ml of methacholine. Subjects with a history of wheezing received the 5 mg/ml of methacholine first while those without a history of asthma began the challenge at the 25 mg/ml methacholine concentration. Spirometric test were employed and the challenge was terminated when FEV1 fell 20 percent from baseline. The standard methacholine challenge used a dosimeter and all subjects took five breaths of saline solution followed by seven increasing concentrations of methacholine. Dose response curves were constructed and the provocation dose of methacholine that caused a 20 percent fall in FEV1 was calculated for each protocol. Results of the screening methacholine challenge correlated with those obtained from the more lengthy standard protocol (r = 0.94), and correctly identified levels of airways reactivity in asthmatic patients and normal subjects. The abbreviated protocol was rapid (6-12 min), safe, and inexpensive. Since the equipment is readily available and easy to transport, it could be used at sites outside the hospital as a screening test for nonspecific airways reactivity.

Adult↗
PubMed1981

Abnormal inspiratory flow-volume curves in patients with sleep-disordered breathing.

Although flow-volume curves are valuable in detecting extrathoracic airway obstruction, their role in testing patients with sleep-disordered breathing is undefined. To determine whether patients with sleep-disordered breathing have abnormal flow-volume curves consistent with variable extrathoracic obstruction, 60 subjects referred with suspected sleep disorders prospectively underwent spirometry and assessment of flow-volume curves. These tests were interpreted independent of the outcome of polysomnography. Fourteen of 35 subjects (40%) with sleep-disordered breathing had abnormal flow-volume curves consistent with variable extrathoracic airway obstruction, and 2 of 25 (8%) with no breathing disorder had extrathoracic obstruction (p less than 0.02). The presence of extrathoracic airway obstruction in subjects with mixed or obstructive sleep apnea did not correlate with age, the presence of snoring, excessive daytime hypersomnolence, obesity, or the severity of sleep apnea. Abnormal flow-volume curves were found more frequently in women who had no obvious structural upper airway abnormality. Because of the high specificity (92%) of the flow-volume curve, the finding of extrathoracic obstruction in patients with a history consistent with sleep-disordered breathing substantially increases the likelihood that sleep apnea is present.

Adult↗
PubMed1980

Physiologic manifestations of human anaphylaxis.

In the course of a controlled study to evaluate different forms of immunotherapy for subjects with insect-sting hypersensitivity, we observed 11 subjects who had systemic cutaneous urticarial reactions and 3 subjects who experienced systemic anaphylaxis. With the exception of tachycardia, there were no cardiopulmonary changes in the subjects with urticaria, whereas the major manifestation of anaphylactic shock in the other three subjects was severe hypotension that was probably secondary to peripheral vasodilation. Significant abnormalities in gas exchange developed in two subjects. In one, bronchospasm precipitated a respiratory arrest followed by endotracheal intubation with mechanical ventilation. Although plasma histamine levels were not related to the development of cutaneous reactions, the plasma histamine levels correlated with the severity and duration of the cardiopulmonary changes observed during anaphylactic shock. The two subjects with the most severe shock showed evidence of intravascular coagulation characterized by a diminution of Factor V, Factor VIII, fibrinogen, and high molecular weight kininogen, as well as changes in components of the complement system. Standard therapy with epinephrine and fluids, usually recommended for the treatment of systemic anaphylaxis, did not immediately reverse either the hemodynamic or the respiratory abnormalities in the two subjects with the most severe anaphylactic shock. Hemodynamic recovery was gradual and did not seem directly related to any specific therapeutic intervention.

Anaphylaxis↗
PubMed1977

Rapid, shallow breathing after Ascaris suum antigen inhalation: role of vagus nerves.

In five treadmill-exercising, unsedated dogs, we studied the effect of inhaled Ascaris suum antigen aerosols on minute volume of ventilation (VE), respiratory frequency (f), tidal volume (VT), total pulmonary resistance (RL), and dynamic pulmonary compliance (CLdyn), before and during cooling of the vagus nerves. With the vagi warm, inhaled antigen increased VE (mean + 62%; P less than 0.01)by increasing f (mean + 180%; P less than 0.01), despite a decrease in VT (mean - 42%; P less than 0.01). RL increased (mean + 170%; P less than 0.001) and CLdyn decreased (mean - 43%; P less than 0.005). With the vagi cool, inhaled antigen no longer affected VE, f, or VT (P greater than 0.5), although RL still increased and CLdyn still decreased. Inhalation of a bronchodilator, terbutaline, prevented the broncho-constriction induced by antigen but did not prevent the ventilatory response. We conclude that vagal afferent pathways mediate the ventilatory response to inhaled antigen and suggest that the primary stimulus for this response is not airway narrowing.

Animals↗
PubMed1977

Effect of ozone on bronchomotor response to inhaled histamine aerosol in dogs.

To study the effect of ozone on bronchial reactivity to inhaled histamine diphosphate aerosol, we performed 14 experiments on 5 dogs anesthetized with pentobarbital sodium (25-30 mg/kg, iv) and ventilated with a Harvard respirator. Prior to ozone exposure, inhalation of histamine aerosol (2% solution; 5 breaths) increased total pulmonary resistance (RL) 5.1 +/- 0.5 cmH2O/1 per s (mean +/- SE). One day after ozone exposure (0.7-1.2 ppm; 2 h), the base-line RL was not significantly changed (P greater than 0.05), but the increase of RL caused by histamine (10.7 +/- 1.1 cmH2O/1 per s) was greater than in the control state (P less than 0.01). When the dogs were pretreated with atropine sulfate aerosol (1.5% solution; 10 breaths), the increase of RL after histamine was decreased to 3.8 +/- 0.3 cmH2O/1 per s before ozone, and this was not significantly different after ozone (4.5 +/- 1.1 cmH2O/1 per s; P greater than 0.5). Cooling blockade of conduction in the vagus nerves diminished the increase of RL after histamine to 3.9 +/- 0.5 cmH2O/1 per s before ozone, and this was not significantly different after ozone (4.4 +/- 0.6 cmH2O/1 per s; P less than 0.5). Since both atropine and vagal cooling abolished the ozone-induced bronchial hyperirritability, we conclude that it is mediated via vagal cholinergic pathways.

Aerosols↗
PubMed1976

The mechanism of rapid, shallow breathing after inhaling histamine aerosol in exercising dogs.

In 4 unsedated, exercising dogs, we studied the effects of inhaled histamine aerosol on minute volume of ventilation, respiratory frequency, tidal volume, total pulmonary resistance, and dynamic pulmonary compliance. Inhalation (5 breaths) of 1 to 2 per cent histamine aerosols increased minute ventilation (mean, 50 per cent; p less than 0.001) by increasing respiratory frequency (mean, 166 percent; P less than 0.001), despite decreasing tidal volume (mean, 42 percent; P less than 0.0001). Total pulmonary resistance increased (mean, 200 per cent; P less than 0.001.) Breathing supplemental O2 did not affect the ventilatory response to histamine. Adding external resistive loads to a dog's airway did not simulate the pattern of rapid, shallow breathing produced by histamine. Inhalation of terbutaline prevented the changes in total pulmonary resistance and dynamic pulmonary compliance but did not alter the ventilatory response to histamine. When conduction in the cervical vagus nerves (which were implanted chronically in skin loops) was blocked by cooling, the ventilatory response to histamine was abolished. We concluded that histamine stimulates breathing by stimulation of receptors whose afferent pathways are in the vagus nerves; the effective stimulus is not bronchoconstriction but is presumably due to direct stimulation of airway receptors.

Aerosols↗