Biomedical subjects
Publications and source records attributed to K H Ginzel.
Tobacco smoke is the single most important source of exposure for the nonsmoking population to harmful air pollution. Uptake, biological reaction, and associated pathology document the potential for serious health consequences, raise ethical and legal questions, and demand comprehensive legislative action.
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To avoid the modifying influence of general anesthesia on vagal control of respiration, we investigated the effect of phenyldiguanide (PDG), a drug known to stimulate juxta-pulmonary capillary ("J") receptors, in the non-anesthetized, unrestrained cat and recorded EEG, eye movements, neck muscle EMG, EKG and respiratory movements. The response to bolus injection of PDG into the right atrium was qualitatively similar to the one seen in cats under anesthesia, consisting of bradycardia and apnea followed by rapid shallow breathing (RSB). The injection-response latencies ranged from 1.5 to 3 s, indicating that the effect originated on the venous side of the cardiopulmonary region. Vagal block with lidocaine, which was applied via external tubings feeding into implanted vagal "sleeves", abolished the responses to PDG, demonstrating their dependence on vagal mediation. Atropine blocked the bradycardia but did not affect the apnea. All doses of PDG which affected respiration uniformly produced initial apnea, whose duration, in any given animal and trial session, exhibited a consistent dose-response relationship. Slow injections also produced apnea. RSB following the apnea was variable in frequency and amplitude of excursions and in its overall duration, and failed to reveal a dose-response relationship. Apnea lasted significantly longer when injections were made during slow wave sleep or REM sleep as compared to injections given during wakefulness or drowsiness. Arousal from all states of sleep occurred simultaneously with the onset of apnea and bradycardia and was also dependent on the vagi. Spontaneous awakening from sleep, by contrast, was always associated with an increase in breathing.(ABSTRACT TRUNCATED AT 250 WORDS)
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The effects of nicotine on the stretch reflex and on electrically induced monosynaptic and cutaneous polysynaptic reflex responses at a lumbosacral level were studied in lightly anesthetized (chloralose-urethane) cats in which the regional fusimotor-spindle loops had been interrupted by ventral rhizotomy. Doses of 15-40 mug/kg injected into the superior vena cava or the right atrium produced depression of the reflex responses in extensor and flexor alpha motoneurons after latent periods of 1-3 sec, while gamma activity was initially accelerated. The early phase of this alpha depression was abolished by bilateral vagotomy. Sebacylcholine (a nicotinic agent) and acetylcholine also caused depression of evoked alpha activity in the absence of spindle feedback. It is concluded that nicotine activates a viscerosomatic reflex by exciting sensory receptors in the cardiopulmonary region and that alpha motor depression results independent of the changes in gamma activity. However, alpha depression with delayed onset can still be elicited by nicotine after vagotomy and Renshaw blockade, and this effect is also duplicated by sebacylcholine and abolished by hexamethonium. In the doses used, spindle or skin afferents were not excited by nicotine. Thus, two more mechanisms are described by which nicotine can depress alpha activity. Both are reflex in nature, one implicating vagal, the other nonvagal peripheral receptors.
The role that sensory nerve endings can play in drug action and the strategy used for its experimental analysis and proof is first exemplified by three effects of nicotine which are seen when the lowest effective doses of the drug are given intravenously in the cat: (1) a vasopressor effect due to arterial chemoreceptor stimulation; (2) a triad of bradycardia, hypotension and apnea, and (3) a depressant effect upon somatic motor activity, both of which are traced to vagal afferent endings in the pulmonary circulation. While receptors in the lung are responsible at least for the initial phase of the reflex responses listed in (2) and (3), sensory endings in heart, aorta, and carotid sinus region may be recruited into action as the drug reaches them. Several of these reflex effects can also be elicited by other sensory stimulant agents such as phenyldiguanide, 5-hydroxytryptamine, and veratrum alkaloids. In the second part, a general outline is given of what may be classified as 'Afferent Pharmacology', dealing with drug action upon sensory receptors and with the resulting remote drug effects. The action upon sensory receptors can either be a direct one ('primary' drug effect) consisting of stimulation, sensitization, desensitization, depression or combinations thereof, or an indirect ('secondary') effect brought about by a variety of drug-induced changes in the tissues surrounding the receptors. Depending on the nature of the primary or secondary action, the remote drug effect can be either an initiation, modification or impairment of those reflexes which have their origin in the sensory endings acted upon. Indeed, the grossly observable pharmacological actions of 'afferent drugs' are generally those relating to the reflex response. To avoid blurring of the boundaries of afferent pharmacology, drugs acting on central synapses of reflex pathways, or on the elaborate efferent control system of afferent input, are not included. A discussion follows of the topics of investigation, the influence of experimental conditions and anesthesia, various approaches and methods, the physiological and pharmacological importance of inquiry in this area, and some of the therapeutic aspects. Finally, brief mention is made of certain features and problems which appear to be characteristic of afferent pharmacology.
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