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Dive into the research topics where Murray D. Altose is active.

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Featured researches published by Murray D. Altose.


The American Journal of Medicine | 1977

Airway function in sarcoidosis

Richard S. Levinson; Louis F. Metzger; Nigel N. Stanley; Steven G. Kelsen; Murray D. Altose; Neil S. Cherniack; Jerome S. Brody

Airway function was studied in 18 patients with sarcoidosis, aged 18 to 49 years. Eleven of the patients were smokers. All patients had the characteristic functional changes of restrictive lung disease: decreased lung volumes and single breath diffusing capacity, and increased static transpulmonary pressures. Abnormal airway function was demonstrated in every patient by at least one test, and nearly always by multiple tests. Specific airway conductance was abnormally low in two patients. The ratio of the 1 second forced expiratory volume to the forced vital capacity was decreased in six patients. Frequency dependence of dynamic compliance was demonstrated in eight patients. The ratio of closing volume to vital capacity was increased above age-corrected predictions in all but two patients. Upstream airway resistance was abnormally increased in 16 of the patients. These results suggest that airway dysfunction is not uncommon in sarcoidosis.


Respiration Physiology | 1986

Effects of volume and frequency of mechanical ventilation on respiratory activity in humans

Murray D. Altose; Robert J. Castele; Alfred F. Connors; Anthony F. DiMarco

This study evaluated the interaction between respiratory chemical drive and non-chemical factors related to the frequency and level of thoracic displacement during mechanical ventilation in shaping respiratory activity. Ten normal subjects were artificially hyperventilated with a positive-pressure mechanical respirator to a baseline end-tidal PCO2 of approximately 30 Torr. Thereafter, in separate trials, the end-tidal PCO2 was increased by (a) progressively raising the concentration of CO2 in the inspired gas (FICO2) while holding tidal volume (VT) and breathing frequency (f) constant, (b) lowering f while holding VT and FICO2 constant, and (c) lowering VT while maintaining a constant f and FICO2. Initially, as the PCO2 rose above baseline levels with increases in FICO2, there was no change in inspiratory muscle activity, as measured by the peak inspiratory airway pressure, until the PCO2 reached 40 Torr. This PCO2 threshold for a change in respiratory activity was significantly reduced when the tidal volume or frequency of mechanical ventilation was lowered. These results suggest that non-chemical drives related to the frequency and level of thoracic displacement interact with chemical stimuli in shaping respiratory activity.


Shock | 1999

Rehabilitation of the patient with respiratory disease

Neil S. Cherniak; Murray D. Altose; Ikuo Homma; Christopher Winslow

The first comprehensive and authoritative reference on pulmonary rehabilitation written specifically for physicians. An introductory section covers basic science aspects and provides the foundation for the understanding of the basis of respiratory impairment and disability. Specific pathophysiological mechanisms of respiratory impairments are covered in chapters dealing with the full spectrum of respiratory diseases or disease categories. Subsequent chapters cover approaches to assessment of respiratory function and performance, measurement of impairment and disability determination, and evaluation of dyspnea. A comprehensive review of rehabilitation management and treatment regimens follows, covering pharmacological approaches, improvement of muscle function, exercise training, and nutritional supplementation. Final chapters focus on psychosocial factors as well as relevant medical economic and bioethical issues.


Respiration Physiology | 1983

Effects of an increase in end-expiratory volume on the pattern of thoracoabdominal movement

Donn A. Wolfson; Kingman P. Strohl; Anthony F. DiMarco; Murray D. Altose

Changes in end-expiratory lung volume can alter the mechanical function of the muscles of inspiration and may affect the pattern of thoracoabdominal movements. The present study examined the effect of increasing end-expiratory lung volume on the motion of the rib cage and abdomen during inspiration. In six seated subjects, end-expiratory volume was increased by expiratory threshold loading. The end-expiratory thoracoabdominal configuration shifted to the left of the relaxation curve presumably as a result of the activation of the abdominal expiratory muscles. There was outward displacement of both the rib cage and the abdomen with inspiration at the elevated volume but the relative volumetric contribution of abdominal displacement to the inspired volume was significantly less than during breathing from FRC. When at an enlarged lung volume subjects were constrained to initiate inspiration from a point on the thoracoabdominal relaxation configuration, there was inward movement of the abdomen and a decrease in abdominal dimensions during inspiration. Inward abdominal movement occurred despite large increases in diaphragm electrical activity and was associated with an inspiratory fall in gastric pressure. These results suggest that at large lung volumes, the function of the diaphragm as an agonist is lost and its function as a fixator may be impaired unless there is an activation of the abdominal muscles and the diaphragm is appropriately lengthened.


Thorax | 1985

Cavitating lung infarction after bland pulmonary thromboembolism in patients with the adult respiratory distress syndrome.

Susan Redline; Joseph F. Tomashefski; Murray D. Altose

During one year five patients were observed with the adult respiratory distress syndrome who were found at necropsy to have cavitated lung infarcts following bland (non-infected) pulmonary thromboembolism. There were three instances of bronchopleural fistula and in one person a tension pneumothorax was the immediate cause of death. Four of the five patients had severe lung infections. In all patients airway pressure was raised as a result of positive pressure mechanical ventilation. It is postulated that diffuse microvascular injury, bacterial pneumonia, and high airway pressures may be important factors predisposing patients with adult respiratory distress syndrome to develop lung necrosis, cavitation, and bronchopleural fistula after bland pulmonary thromboembolism. This complication may occur more frequently than has been previously recognised.


Annals of Internal Medicine | 1984

Lymphocyte subpopulations in sarcoid pleural effusion

George S. Groman; Robert J. Castele; Murray D. Altose; James Scillian; Mary E. Kleinhenz; Rolf Ehlers

Excerpt Sarcoidosis is a disease characterized by the formation on noncaseating granulomas in several organs of the body (1). Recent attention has been directed to the study of pulmonary lymphocyte...


Annals of Biomedical Engineering | 1993

Perceptual contributions to optimization of breathing.

Yoshitaka Oku; Gerald M. Saidel; Murray D. Altose; Neil S. Cherniack

AbstractBesides regulating the energetic cost of breathing, optimization of breathing may involve the alleviation of an uncomfortable breathing sensation. In this article, we consider perceptual contributions to the optimization of breathing. Just as the cost function proposed by Poon depends on ventilation and arterial


Annals of Biomedical Engineering | 1991

Sensation and control of breathing: A dynamic model

Yoshitaka Oku; Gerald M. Saidel; T. Chonan; Murray D. Altose; Neil S. Cherniack


Respiration Physiology | 1984

Effects of expiratory threshold loading on thoracoabdominal motion in cats

Anthony F. DiMarco; Marianne S. Dimarco; Kingman P. Strohl; Murray D. Altose

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Respiration | 1996

Effects of Willful Ventilatory Control on Respiratory Sensation during Hypercapnia

Yoshitaka Oku; Gerald M. Saidel; Neil S. Cherniack; Murray D. Altose

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Neil S. Cherniack

Case Western Reserve University

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Anthony F. DiMarco

Case Western Reserve University

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T. Chonan

Case Western Reserve University

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Kingman P. Strohl

Case Western Reserve University

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Susan Redline

Brigham and Women's Hospital

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Gerald M. Saidel

Case Western Reserve University

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Robert A. Wise

Johns Hopkins University

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