The autonomic nervous system and breathing
TL;DR: This work has shown that stimulation of pulmonary stretch receptors inhibits breathing and causes bronchodilation; hypoxia has a direct constrictor action on the pulmonary vascular bed; and stimulation of tracheal irritant receptors causes coughing, bronchoconstriction, and hypertension.
Abstract: The role of the autonomic nervous system in the control of lung ventilation and gas exchange can be considered in two ways. The first is the analysis of primary control mechanisms involving, for example, specific groups of receptors and their afferent nerves in the autonomic nervous system and their reflex action on breathing or on lung effector tissues. This analytical approach has been used extensively in studies with experimental animals, in which it is possible to isolate single components of the control mechanisms and to determine their properties. These studies lead to clear, forthright, and usually reliable statements such as the following: stimulation of pulmonary stretch receptors inhibits breathing and causes bronchodilation; hypoxia has a direct constrictor action on the pulmonary vascular bed; and stimulation of tracheal irritant receptors causes coughing, bronchoconstriction, and hypertension. However, such statements may have little applicability to conditions in intact animals, in particular man, and
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01 Nov 1973
TL;DR: In this paper, Sensory Irritation by Airborne Chemicals: Critical Reviews in Toxicology: Vol. 2, No. 3, pp. 299-363, was discussed.
Abstract: (1973). Sensory Irritation by Airborne Chemicals. CRC Critical Reviews in Toxicology: Vol. 2, No. 3, pp. 299-363.
389 citations
TL;DR: The present results demonstrate that very low levels of NO2 can adversely affect some asthmatics and could be related to any physical or clinical characteristics of the subjects tested.
Abstract: Our purpose was to determine whether exposure to a realistic concentration of nitrogen dioxide (NO2) could increase the bronchial sensitivity of asthmatic patients to bronchoconstrictor agents. We established dose-response curves for changes in specific airway resistance (SRaw) in response to aerosolized carbachol in 20 asthmatics after each had spent 1 h in an exposure chamber breathing on one occasion unpolluted air and on a separate occasion 0.1 ppm NO2: sequence of exposures to unpolluted air and to low levels of NO2 were randomized in a single-blind fashion. NO2 induced a slight but significant increase in initial SRaw and enhanced the bronchoconstrictor effect of carbachol in 13 subjects: curves were shifted to the left and the mean dose of carbachol producing a twofold increase in initial SRaw was decreased from 0.66 mg to 0.36 mg (P less than 0.001). In contrast, NO2 neither modified the initial SRaw nor the bronchoconstrictor effect of carbachol in seven subjects. In 4 out of the 20 subjects, exposure to a higher concentration of NO2 (0.2 ppm) yielded variable results. Potentiation of the carbachol bronchoconstrictor response by NO2 could not be related to any physical or clinical characteristics of the subjects tested. Although the mechanisms underlying the NO2 effect remain controversial, the present results demonstrate that very low levels of NO2 can adversely affect some asthmatics.
277 citations
TL;DR: The results indicate that preservation of an upper motor neurone supply to the phrenic nucleus is of critical importance for fetal lung growth, and confirm the growth-promoting effects of liquid distension of the fetal lungs.
167 citations
TL;DR: It is concluded regarding the neural actions to the dog trachea that a constriction is induced by cholinergic and adrenergic alpha-action and a dilation is inducedby adrenergic beta-action.
Abstract: The membrane potential of dog tracheal muscle was stable at -59.2mV. The length constant of the muscle tissue was 3.2mm and the time constant of the membrane was 449msec. Outward current pulses could not evoke a spike and showed marked rectification of the membrane.Tetraethylammonium, TEA, depolarized the membrane, suppressed the rectification of the membrane, and increased the membrane resistance, and in the presence of TEA outward current pulses could evoke a spike. Acetylcholine and histamine depolarized the membrane but could not evoke a spike. Mechanical response could be evoked by field stimulation via either nerve stimulation or direct muscle stimulation. The mechanical response induced by nerve stimulation was markedly suppressed by atropine. Phentolamine suppressed the contraction which was produced in the presence of atropine, and propranolol suppressed the relaxation. It is unlikely that nonadrenergic-non-cholinergic inhibitory nerves played an important role in the mechanical response. It is concluded regarding the neural actions to the dog trachea that a constriction is induced by cholinergic and adrenergic α-action and a dilation is induced by adrenergic β-action.The relationship between the membrane potential and tension was measured in various [K]O. The mechanical response was triggered by only 5mV depolarization. The physiological evidence and histological finding were compared in relation to nerve activity on the tracheal muscle activity.
113 citations
TL;DR: Use of racemic epinephrine hydrochloride (Vaponefrin) in the treatment of laryngotracheobronchitis (croup) produced acute beneficial results in a controlled study, suggesting that the natural history of the disease was not drastically altered by this form of treatment.
Abstract: Use of racemic epinephrine hydrochloride (Vaponefrin), delivered by intermittent positive-pressure breathing, in the treatment of laryngotracheobronchitis (croup) produced acute beneficial results in a controlled study However, symptoms often recurred within two hours, suggesting that this form of treatment should not be used in the emergency room and the patient then sent home This treatment had no effect on arterial oxygen gas pressure The changes in clinical status 24 to 36 hours after admission into the study were similar for the patients in the treatment and control groups, suggesting that the natural history of the disease was not drastically altered by this form of treatment
112 citations
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TL;DR: This report presents a new method for accomplishing this measurement, and gives data for airway resistance obtained in normal subjects and in patients with respiratory disease.
Abstract: Satisfactory methods, utilizing measurements of transthoracic or transpulmonary pressure and airflow, are now available for determining \"nonelastic\" pulmonary resistance. However, the nonelastic pulmonary resistance has two components, tissue resistance and airway resistance, and no valid direct method is available for measuring either of these components separately in man. Since airway resistance is the ratio of alveolar pressure during flow to airflow, airway resistance alone could be measured if there were a method for determining alveolar pressure during flow. This report presents a new method for accomplishing this measurement, and gives data for airway resistance obtained in normal subjects and in patients with respiratory disease. Of previous attempts to measure airway resistance, one of the earliest was the painstaking study by Rohrer (1) who made anatomical measurements on the tracheobronchial tree of a human lung post mortem and calculated the cumulative resistance to airflow of the entire system using Poiseuille's law and turbulence theory. The first important experimental study of pulmonary resistance in the living animal was made by von Neergaard and Wirz who, in 1927 (2), analyzed intrapleural pressure into two major components, \"dynamic\" (which is essentially resistive) and \"static\" (which is predominantly elastic in nature). This approach made it possible to obtain values for total pulmonary resistance, though not for airway resistance alone. Bayliss and Robertson (3), reasoning that airway resistance, but not tissue resistance, would vary with the viscosity of the gases breathed, ventilated isolated animal lungs with gases of different density and viscosity;
1,251 citations
TL;DR: Experiments done between 1877 and 1926 showed that a rise of blood pressure in the carotid-cephalic circulation induces bradycardia and a fall of the systemic arterial pressure, while a drop in the vehicle pressure provokes acceleration of the heart rate and a rise in the systemicarterial pressure.
Abstract: After the discovery ofthe pulmonary circulation by Ibn-an-Nafis in the thirteenth century and by Servetus in the sixteenth century and the discovery of the systemic circulation of the blood by Harvey in 1628, arterial pressure was first measured by Stephen Hales in 1733 and then by Poiseuille in 1828 and Ludwig in 1847, wno recorded arterial blood pressure by means ofa glass tube or a mercury manometer connected with an artery. As a result of numerous observations, the physiologists concluded that the arterial pressure was subject to regulation and tried to clarify the mechanisms. In 1836 Astley Cooper observed that compression of both common carotid arteries, which induced a fall of arterial pressure in the head and brain, provoked acceleration of the heart rate and a rise in the systemic arterial pressure (1). This observation was confirmed by Magendie in 1838 (2). Experiments done between 1877 and 1926 by several workers (3-10) showed that a rise of blood pressure in the carotid-cephalic circulation induces bradycardia and a fall of the systemic arterial pressure, while a drop in the carotid-cephalic pressure provokes acceleration ofthe heart rate and a rise ofsystemic arterial pressure. All these experimental observations were considered to be a demonstration ofa direct sensitivity of the cardiovascular centers to blood pressure variations. The direct central regulation and homeostasis of arterial pressure by means of the action of blood pressure variations on the cardiovascular centers was thus generally accepted. But as early as 1900 Pagano (11) and Siciliano (12), of the laboratory of Spallitta in Palermo, published an interesting series of experiments. Siciliano showed that while clamping of both common carotid arteries induced tachycardia and a rise in the systemic arterial pressure, clamping of
902 citations
761 citations
TL;DR: The body plethysmograph affords a good technique for comparing changes in airway resistance with changes in lung volume in an individual, since each measurement ofAirway resistance includes as an essential stage in its derivation, a measurement of intrathoracic gas volume.
Abstract: The resistance of the airways to the airflow through them depends on the radius, length and number of the airways. It has long been apparent (1, 2) that the bronchi are distended as well as lengthened in the inspiratory position of the lung. These two changes in the dimensions of these airways would have opposite effects on their resistance to airflow, lengthening increasing resistance and widening reducing it. More recent measurements of airway resistance have shown that it is reduced in the inspiratory position of the lung (3, 4, 5) and is more in individuals with small lungs (6). The body plethysmograph affords a good technique for comparing changes in airway resistance with changes in lung volume in an individual, since each measurement of airway resistance includes as an essential stage in its derivation, a measurement of intrathoracic gas volume. It therefore seemed desirable to explore further the relationship between airway resistance and lung volume at different degrees of inflation of the lung in normal subjects.
608 citations