Browsing by Author "ZUAZO, A"

Now showing 1 - 9 of 9
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    ACUTE CHANGES IN VENTILATION AND BLOOD-PRESSURE INDUCED BY INHALATION OF TOBACCO-SMOKE
    (1976) ZAPATA, P; ZUAZO, A; LLADOS, F
    Inhalation of cigarette smoke through a tracheal cannula was induced in cats anesthetized with pentobarbital. Smoking of tobacco cigarettes produced increased ventilation and systemic hypertension, which were found to be due to their nicotine content. Respiratory stimulation and the increase in diastolic pressure were abolished by acute section of buffer nerves, but the mediation of carotid nerves was more important than that of the vagi for evoking reflex hyperventilation. Tobacco smoking induced a marked increase in the frequency of chemosensory impulses recorded from the carotid nerves, an effect due to its nicotine content.
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    ANDROGENS AND EFFECTS OF OPIOIDS AND CATECHOLAMINES ON THE SMOOTH-MUSCLE OF THE RAT VAS-DEFERENS
    (1985) MIRANDA, H; PEREZ, E; FERNANDEZ, E; ROSSELOT, F; VERGARA, JF; WOLSTENHOLME, WW; ZUAZO, A
    In the neuronal electrically stimulated vas deferens of the rat, the responses evoked by morphine, .beta.-endorphin and catecholamines were studied. The tissue was obtained from rats at various times (7-60 days) following castration, adrenalectomy and castration with adrenalectomy. Pharmacological data are presented which verify an increased responsiveness to morphine after castration with or without adrenalectomy. Decreased responsiveness was observed after adrenalectomy alone. Decreased responsiveness of the vas deferens to catecholamines was observed after castration, adrenalectomy and castration with adrenalectomy. Since the responsiveness of the electrically stimulated vas deferens to .beta.-endorphin was unchanged by this treatment (castration, adrenalectomy), the .epsilon.-opioid receptor may be unaffected by androgens.
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    EFFECTS OF 6-HYDROXY-DOPAMINE ON CAROTID-BODY CHEMO-SENSORY ACTIVITY
    (1978) ZUAZO, A; ZAPATA, P
    6-OH-DA [6-hydroxy-dopamine] HBr (5-25 mg) injected into 1 common carotid artery of pentobarbitone-anesthetized cats, induced a transient inhibition of chemosensory discharges recorded from the ipsilateral carotid nerve, but did not change chemosensory frequency during spontaneous ventilation, periodic deep breaths and asphyxia. Chemosensory activities recorded simultaneously from both carotid nerves showed no differences in their inhibitory responses to dopamine and their excitatory responses to NaCN, up to 48 h after the injections of 6-OH-DA. Apparently 6-OH-DA acts initially as a dopamine analog, and does not impair subsequent carotid body chemoreception or dopamine-induced inhibition, as doses producing abolition of noradrenergic transmission.
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    REGIONAL SYMPATHECTOMY INDUCED BY INTRA-ARTERIAL 6-HYDROXY-DOPAMINE
    (1978) ZUAZO, A; ZAPATA, P
    Single intra-carotid injections of 5-15 mg of 6-OHDA [6-hydroxydopamine] HBr in adult cats reduced or abolished the responses of the ipsilateral nictitating membrane to electrical stimulation of post-ganglionic sympathetic nerves and intra-carotid injections of tyramine; the responses of the contralateral nictitating membrane to the same stimuli remained normal. One to five days after 6-OHDA, the ipsilateral nictitating membranes, unresponsive to sympathetic stimulation, were hypersensitive to i.v. injections of adrenaline [epinephrine] or noradrenaline [norepinephrine]. The advantages of regional over systemic chemical sympathectomy are discussed.
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    RESPIRATORY AND CIRCULATORY REFLEXES INDUCED BY NICOTINE INJECTIONS - ROLE OF CAROTID-BODY CHEMORECEPTORS
    (1976) ZAPATA, P; ZUAZO, A; LLADOS, F
    I.v. and intracarotid injections of nicotine were delivered to cats anesthetized with pentobarbital. Low doses of nicotine induced reflex hyperventilation and hypertension, mainly due to excitation of carotid body chemoreceptors. The frequency of discharge of carotid nerve chemosensory fibers was increased by nicotine in doses as low as 1 .mu.g/kg when injected i.v. and 50 ng when injected into the carotid artery. Nicotine also activates vagal afferent fibers; some of them produce reflex excitation of the respiratory and vasomotor centers, but others provoke reflex inhibition. High doses of nicotine can act directly upon the medulla provoking acceleration or arrest of ventilation. Nicotine can also induce late changes of b.p. [blood pressure] (delay 5 s or more) which are not mediated by the carotid or vagus nerves.
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    RESPIRATORY EFFECTS OF DOPAMINE-INDUCED INHIBITION OF CHEMOSENSORY INFLOW
    (1980) ZAPATA, P; ZUAZO, A
    In pentobarbitone anesthetized cats, intracarotid injections of dopamine (DA) 0.05-20 .mu.g produced transient ventilatory depression, enhanced by section of the contralateral carotid nerve and abolished by section of the ipsilateral one. I.v. injections of DA 0.02-2 .mu.g .cntdot. kg-1 also induced transient hypoventilation; this effect was abolished by bilateral section of the carotid nerves. Slow i.v. infusion of DA 10 .mu.g .cntdot. kg-1 .cntdot. min-1 elicited initially a pronounced hypoventilation followed by a steady-state of mild ventilatory depression; these changes were absent after bilateral carotid neurotomy. Recordings from carotid nerves showed that DA-induced decreases of chemosensory activity to 50% of its control did not modify ventilation; chemosensory arrests transiently depressed ventilation to 40-75% of its control level. Interactions between the ventilatory and chemosensory depressant effects of hyperoxia and DA administration were studied. Reflex decrease in ventilation caused by DA injections apparently provides a measure of the tonic chemosensory drive exerted upon the respiratory center.
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    REVERSAL OF RESPIRATORY RESPONSES TO DOPAMINE AFTER DOPAMINE ANTAGONISTS
    (1982) ZAPATA, P; ZUAZO, A
    The effects of dopamine (DA) antagonists on resting ventilation and ventilatory reactions to DA, apomorphine, hyperoxia and hypoxia were studied in pentobarbitone-anesthetized cats. Administration (i.v.) of spiroperidol, haloperidol, perphenazine and chlorpromazine increased resting ventilation, the intensity and duration of the effect being dependent on the dose of the blocker. The enhanced ventilation was associated to increased frequency of chemosensory discharges recorded from 1 carotid nerve and it was absent after section of the 4 buffer nerves. The drugs provoked a dose-dependent block of the transient chemosensory inhibitions and ventilatory depressions induced by DA or apomorphine. Spiroperidol and perphenazine reversed the inhibitory reactions to DA into excitatory ones, the ventilatory responses being abolished by section of carotid and aortic nerves. The ventilatory depressions caused by a few breaths of 100% O2 and the ventilatory excitations onset by a few breaths of 100% N2 persisted after applying DA blockers. DA antagonists apparently enhance ventilation by increasing peripheral chemosensory drive and may invert DA-induced reflex withdrawal into transient ventilatory excitation, without reversing the reflex ventilatory depression provoked by hyperoxia.