A B S T R A C T The effects of resistive loads applied at the mouth were compared to the effects of bronchospasm on ventilation, respiratory muscle force (occlusion pressure), and respiratory sensations in 6 normal and 11 asthmatic subjects breathing 100% 02. External resistive loads ranging from 0.65 to 13.33 cm H20/liter per s were applied during both inspiration and expiration. Bronchospasm was induced by inhalation of aerosolized methacholine. Bronchospasm increased ventilation, inspiratory airflow, respiratory rate, and lowered PACO.. External resistive loading, on the other hand, reduced respiratory rate and inspiratory flow, but left ventilation and PACO, unaltered. FRC increased to a greater extent with bronchospasm than external flow resistive loads. With both bronchospasm and external loading, occlusion pressure increased in proportion to the rise in resistance to airflow. However, the change in occlusion pressure produced by a given change in resistance and the absolute level of occlusion pressure at comparable levels of airway resistance were greater during bronchospasm than during external loading. These differences in occlusion pressure responses to the two forms of obstruction were not explained by differences in chemical drive or respiratory muscle mechanical advantage. Although the subjects' perception of the effort involved in breathing was heightened during both forms of obstruction to airflow, at any given level of resistance the sense of effort was greater with bronchospasm than external loading. Inputs from mechanoreceptors in the lungs (e.g., irritant receptors) and/or greater stimulation of chest wall mechanoreceptors as a result of increases in lung elastance may explain the differing responses elicited by the two forms of resistive loading.
The mechanism of cardiovascular changes produced by activation of the central nervous system with picrotoxin (2 mg/kg, iv) was studied in chloralose-anesthetized cats. Effects occurred in two phases. During the early phase, there were decreases in arterial blood pressure and heart rate, and in a few cats, bradyarrhythmias. These changes were transient and superceded by an increase in arterial blood pressure and, in most cases, ventricular tachyarrhythmias. The early phase changes were mediated primarily by the cardiac vagus nerve whereas the later phase changes were mediated primarily by sympathetic nerves and the adrenal medulla. The ventricular tachyarrbythmias were unaffected by pretreatment with atropine, bilateral vagotomy, or beta adrenergic blocking agents. On the other hand, bilateral extirpation of the stellate ganglia and adrenal glands prevented the ventricular arrhythmias from occurring. In addition, administration of drugs that blocked alpha adrenergic receptors effectively counteracted picrotoxin-induced ventricular arrhythmias. These results indicate that the centrally induced ventricular arrhythmias were mediated by cardiac sympathetic nerves and/or release of catecholamines from the adrenal medulla. More importantly, these results indicate that one cannot equate beta adrenergic blockade with elimination of sympathetic influence on the heart. Finally, sympathetically induced arrhythmias resistant to beta adrenergic blockade appear to respond to drugs that block cardiac adrenergic alpha receptors.A GROWING BODY of clinical and experimental data indicates that the central nervous system exerts a major role in causing cardiac arrhythmias. Subjects suffering from cerebrovascular accidents, head injury, brain tumors, or undergoing brain operations exhibit a high incidence of electrocardiographic abnormalities and arrhythmias. 1 ' 2 Most of these data implicate cardiac sympathetic outflow with consequent activation of beta adrenergic receptors as the neural pathway involved in producing these arrhythmias. For this reason, propranolol commonly is employed to treat these cardiac rhythm disturbances. 3 -4 However, the arrhythmias, in some instances, do not respond to propranolol therapy but do respond to surgical removal of sympathetic cardiac ganglia. 3 The reason for the disparity in the antiarrhythmic effects of propranolol and surgical sympathectomy is unclear.The purpose of the present study was to examine central nervous system arrhythmias further to: (1) investigate the mechanism of central nervous system-induced arrhythmias, and (2) determine what drugs are effective in counteracting these arrhythmias. As a model, we chose to activate the central nervous system by administering the central nervous system stimulant, picrotoxin. This agent demonstratedly produces cardiac arrhythmias in experimental animals through activation of the central nervous system, with consequent augmentation of sympathetic outflow to the heart. 5 -6 Methods Cats unselected as to age and sex were anesthetized with alpha chlor...
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