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Biomedical subjects

P Zapata

Publications and source records attributed to P Zapata.

At least 55 records · Page 3Linked to original sources
PubMed1988

Contribution of carotid body chemoreceptors and carotid sinus baroreceptors to the ventilatory and circulatory reflexes produced by common carotid occlusion.

The effects evoked by 1 min occlusions of the common carotids were studied in 16 spontaneously breathing pentobarbitone anesthetized cats. Unilateral occlusions induced increases in systemic arterial pressure (to 111.5% of basal), but no changes in ventilation. Bilateral occlusions provoked larger increases in systemic arterial pressure (to 137.5% of basal) and mild tachycardia, associated with pulmonary and alveolar hyperventilation. Breath-by-breath minute volume augmented (to an averaged maximum of 144.7% of basal), the increase in tidal volume being more important than that of respiratory frequency. The maximal changes occurred shortly after occlusion and they were inversely but not linearly related to the minimal levels of intrasinusal pressure attained. Changes were subsequently attenuated during each occlusion, depending on the partial restoration of intrasinusal pressure. After barosensory denervation of the carotid sinuses, the cardiovascular responses to bilateral occlusions were reduced, but the respiratory ones were not affected. During 100% O2 breathing in cats with intact innervation or carotid barodenervation, the respiratory responses to bilateral occlusions were much reduced and delayed, or even absent. That the above circulatory and respiratory effects of carotid occlusions were of reflex nature was demonstrated by their elimination after bilateral section of the carotid (sinus) nerves. Results indicate that while barosensory withdrawal during carotid occlusion is mostly responsible for reflex hypertension and bradycardia, chemosensory excitation induced by this maneuver is the major cause of reflex hyperventilation.

Animals↗
PubMed1986

Carotid body chemoreceptor excitation produced by carotid occlusion.

The effects of common carotid artery occlusions on the afferent activity recorded from the carotid (sinus) nerve were studied in 20 pentobarbitone anesthetized cats. Ipsilateral occlusions lowered intrasinusal pressure down to 15-100 torr, depending on previous pressures, and resulted in silencing of carotid barosensory impulses. For cats breathing room air and with mean systemic arterial pressure below 125 torr, chemosensory excitation was induced whenever these occlusions lasted 5 sec or longer and it persisted during 10 min occlusions. The chemosensory excitation had a delay of about 4 sec and the maximal frequency of discharges was attained at nearly 30 sec, followed by a maintained submaximal level of about 80-90% of the peak frequency. For ipsilateral occlusions performed under 100% O2 inhalation, the delay of the excitation was increased to ca. 20 sec and the maximal frequency attained only 30-40% of that obtained for the same animal when breathing room air. Bilateral occlusions caused deeper falls in intrasinusal pressure and stronger chemoreceptor excitation. When arterial pressure was above 130 torr, ipsilateral occlusions only produced transient increases in chemosensory discharges or suppression of their ventilatory fluctuations. Chemical stimuli further increased chemosensory frequency during occlusions, indicating that blood flow through carotid body was not arrested. It is concluded that occlusions of the common carotid may induce an increased frequency of carotid chemosensory discharges. This increment is dependent on systemic arterial pressure, ventilatory conditions and duration of the occlusion. It is suggested that the increased carotid chemosensory activity may interact with the withdrawal of barosensory discharges to elicit the reflex changes observed during carotid occlusions.

Animals↗
PubMed1985

Bioelectric potentials in the carotid body.

Simultaneous recordings of focal slow potentials (sVs) and chemosensory discharges were made from cat carotid body-nerve preparations in situ. Chemoreceptor stimulants (100% N2, asphyxia, NaCN, ACh and nicotine), and depressants (100% O2, spontaneous gasps and dopamine) changed receptor polarization. sVs evoked by stimulants had a negative polarity whereas depressants elicited positive deflections. There was a direct correlation between maximal frequency of chemosensory discharges and peak sV amplitude when NaCN injections or N2 inhalation were used. However, cholinergic agents, dopamine and substance P evoked sVs which lacked correlation in time-course, amplitude or polarity with changes in sensory frequency. After a 6-day carotid nerve crush, different stimuli still evoked sVs even in the absence of sensory discharges. Both sVs and chemosensory discharges were abolished after 1 h ischemia produced by ligature of carotid body blood vessels. Thus, sVs from carotid body chemoreceptors probably include a neuronal component (the generator potential) directly responsible for the origin of chemosensory discharges, and a non-neuronal component (receptor or secretory potentials) probably originating in glomus and/or sustentacular cells.

Acetylcholine↗
PubMed1984

Blockade of dopamine-induced chemosensory inhibition by domperidone.

The sensory discharges from the carotid body chemoreceptors of the cat are transiently inhibited by dopamine (DA) injections. This chemosensory inhibition was effectively blocked by domperidone, a selective antagonist of D2 dopaminoceptors. The basal frequency of spontaneous chemosensory impulses was immediately and sustainly increased after domperidone, suggesting the withdrawal of a tonic inhibition of chemosensory discharges by endogenous DA released from glomus cells. The peripheral dopaminergic modulation of chemoreflexes may be separately blocked by domperidone, a drug unable to cross the blood-brain barrier.

Animals↗
PubMed1984

Perspectives in carotid body research.

This review deals with some basic mechanisms that are operative in carotid body chemoreception. It describes the evolution of concepts and different hypotheses or theories developed to explain possible mechanisms responsible for the onset of sensory discharges in the carotid nerve. Unfortunately, no single hypothesis has been proved beyond doubt, and this may explain their variety. At present, we do not know why this task has been so difficult, although one may think of several possibilities. 1) Carotid body chemoreceptors are anatomically complex being formed by glomus (type I) and sustentacular (type II) cells. Branches of the carotid (sinus) nerve innervate the glomus cells forming sensory synapses oriented in either or both directions and the junction is enveloped by processes of the sustentacular cells. 2) Chemoreceptors are polymodal, since they respond to a variety of natural and chemical stimuli. 3) It is possible that various stimuli may act on different elements of the receptor complex. 4) It is also possible that stimuli may act using different mechanisms. In addition, the multitude of biochemical and biophysical processes (some of them still unknown) operating at different receptor levels has made it very difficult to propose a unified mechanism of action.

Acid-Base Equilibrium↗
PubMed1983

Inhibition in carotid body chemoreceptors mediated by D-2 dopaminoceptors: antagonism by benzamides.

Inhibition of chemosensory nerve impulses in the cat is evoked by dopamine (DA) applied to carotid body chemoreceptors. Pharmacological characterization of the dopaminoceptors involved in this action was determined through their blockade with benzamides, selective antagonists of D-2 receptors. Both metoclopramide and sulpiride were effective blockers of DA-induced chemosensory inhibition. Furthermore, both drugs induced an immediate increase in the frequency of carotid nerve chemosensory impulses, suggesting the presence of previous tonic inhibition of chemoreceptor discharges by endogenous DA released from glomus cells.

Animals↗
PubMed1983

Ventilatory reflexes originated from carotid and extracarotid chemoreceptors in rats.

Ventilatory responses to transient stimulation and inhibition of arterial chemoreceptors--by hypoxia and hyperoxia, respectively--were studied in 10 pentobarbitone-anesthetized rats. N2 tests and intravenous injections of NaCN provoked transient increases in tidal volume and respiratory frequency, while O2 tests elicited decreases of these parameters. After bilateral carotid neurotomy, ventilatory responses to N2 and NaCN were still present although reduced in all rats, while ventilatory depression in response to O2 tests was observed in 60% of these rats. Further bilateral sectioning of main vagus, aortic, and superior laryngeal nerves immediately below the nodose ganglia abolished the ventilatory responses to NaCN in only one of the five rats subjected to this procedure, the remaining animals showing moderate hyperventilation in response to large doses of this drug. Mild ventilatory depression in response to hyperoxia, indicative of a persistent peripheral chemosensory drive, was still present in two of these rats. It is concluded that, although the carotid bodies constitute the main source of ventilatory chemoreflexes in rats, other vagally and nonvagally innervated chemoreceptors (presumably thoracic and abdominal) may elicit ventilatory reflexes in this species.

Animals↗
PubMed1983

Cardiovascular responses to hypoxia in the spontaneously breathing cat: reflexes originating from carotid and aortic bodies.

The heart rate (fH) and systemic arterial pressure (Pa) responses to transient anoxemic and cytotoxic hypoxia were studied in 18 pentobarbitone-anesthetized, spontaneously breathing cats, by applying N2 tests and i.v. injections of NaCN. Hyperventilation was accompanied by short-latency increases in Pa and fH; they persisted after bilateral vagotomy, sparing the aortic nerves. Acute section of carotid or aortic nerves in different sequences reduced both fH and Pa responses, the contribution of both pairs of nerves being similar. The recording of carotid chemosensory discharges showed transient stimulus-dependent increases in their frequency, to which the ensuing fH and Pa rises were correlated. After sectioning the four buffer nerves, hypoxia provoked long-lasting hypotension and bradycardia. Tachycardia was also observed in response to hypoxia in 4 out of 6 chloralose-anesthetized spontaneously breathing cats, the other two presenting bradycardia. The direction of these cyanide-induced changes in fH was not modified by bilateral vagotomy. It is concluded that tachycardia and hypertension in response to hypoxia are not vagally-mediated consequences of hyperventilation.

Animals↗
PubMed1982

Reversal of respiratory responses to dopamine after dopamine antagonists.

The effects of dopamine (DA) antagonists upon resting ventilation and ventilatory reactions to DA, apomorphine, hyperoxia and hypoxia were studied in pentobarbitone-anesthetized cats. Intravenous administration 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 one carotid nerve, and it was absent from section of the four buffer nerves. The drugs also provoked a dose-dependent block of the transient chemosensory inhibitions and ventilatory depressions induced by DA or apomorphine. In addition, 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. Results indicate that DA antagonists 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.

Animals↗
PubMed1981

Dopamine-induced ventilatory depression in the rat, mediated by carotid nerve afferents.

In pentobarbitone-anesthetized rats, i.v. injections of dopamine (DA) at (10-8)-(10-5 g/kg led to transient ventilatory depression, usually not associated with changes in systemic arterial pressure. DA-induced ventilatory depression consisted of decreases in tidal volume and respiratory frequency in 12 rats, and in bradypnea without changes in tidal volume in 5 rats. After bilateral section of the carotid nerves, ventilatory responses to DA were abolished or greatly diminished. It is concluded that DA inhibits carotid body chemosensory discharges in the rat. The possibility that chemosensory activity directly affects respiratory frequency is discussed.

Afferent Pathways↗
PubMed1981

Relative contribution of carotid and aortic bodies to cyanide-induced ventilatory responses in the cat.

The participation of afferences from carotid and aortic bodies to the hyperventilation caused by cytotoxic hypoxia was assessed in pentobarbitone-anesthetized cats. Dose-response curves for the ventilatory effects induced by i.v. injections of NaCN were obtained before and after successive denervations of peripheral chemoreceptors, in different sequences. Bilateral aortic neurotomy (BAN) or unilateral carotid neurotomy (UCN) did not affect significantly the minimal sensitivity to the drug, although maximal reactivity was reduced in some cats. After bilateral carotid neurotomy (BCN), with preservation of aortic nerves, sensitivity was reduced, but hyperventilation was still provoked by large doses of cyanide. BAN + BCN abolished the ventilatory responses to the drug. In cats with BAN + UCN, ventilatory responses had a high degree of correlation with increases of carotid chemosensory discharges in the range between ca 200% of control and the gasping threshold. It is concluded that the aortic bodies of the cat play a significant role in the hyperventilation produced by cytotoxic hypoxia, although it is less marked than that induced through the carotid bodies.

Animals↗
PubMed1980

Respiratory effects of dopamine-induced inhibition of chemosensory inflow.

In pentobarbitone-anesthetized cats, intracarotid injections of dopamin (DA) 0.05--20 micrograms 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 micrograms-kg-1 also induced transient hypoventilation; this effect was abolished by bilateral section of the carotid nerves. Slow i.v. infusion of DA 10 micrograms-kg-1-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, while chemosensory arrests transiently depressed ventilation to 40--75% of its control level. Interactions between the ventilatory and chemosensory depressant effects of hypertoxia and DA administration were also studied. It is proposed that the reflex decrease in ventilation caused by DA injections provides a measure of the tonic chemosensory drive exerted upon the respiratory center.

Animals↗
PubMed1980

Regulatory role of carotid nerve afferences upon the frequency and pattern of spontaneous gasp complexes.

Spontaneous gasps were recorded in pentobarbitone-anesthetized adult cats. Mean interval between gasps in 11 cats with their buffer nerves intact was of 65 sec; it was significantly prolonged to 174 sec after unilateral carotid neurotomy and to 403 sec after bilateral carotid neurotomy. Additional sectioning of both aortic nerves in two cats led to a further increase of intervals between gasps. Inhibition of chemosensory activity during dopamine infusions also reduced the frequency of gasps. Recording of chemosensory impulses from one carotid nerve after unilateral carotid neurotomy, showed reduced discharge frequency or silencing immediately after the augmented inspiration. This effect probably mediated the reduced amplitude of the following series of ventilatory cycles. It is suggested that the peripheral chemosensory in flow adjusts the gain of the vagal inspiration-augmenting reflex.

Afferent Pathways↗
PubMed1980

Dual effects of dopamine upon chemosensory responses to cyanide.

Changes in chemosensory responses to i.v. NaCN during i.v. infusions of dopamine (DA) were studied in pentobarbitone-anesthetized cats. After sectioning both carotid nerves, one of them was prepared for electrophysiological recordings of its chemosensory impulses. Basal chemosensory activity was maintained at a reduced level during DA infusions at a rate of 10 micrograms/kg/min. While sensitivity to NaCN was not modified, reactivity to this agent was reduced for low doses, but enhanced for high doses. It is concluded that chemoreceptor responses to histotoxic hypoxia are rectified by DA. This is discussed in terms of a modulatory role of endogenous DA in the generation of carotid body sensory impulses.

Animals↗
PubMed1979

[Design of a course in physiology for medical training].

This article describes a course in general physiology and neurophysiology being offered at the School of Medicine of the Catholic University in Chile since 1971. The course was designed to provide the student skills in the planning, performance, and analysis of experimental problems. An account is given of the changes made in the course in response to annual evaluations over seven years. The procedures for grading student progress in developing critical judgment, handling information, and solving problems are analyzed. The authors are of the view that a course of this kind helps improve the ability to judge problems beyond the course curriculum. The describe the advantage of such courses for the training of physicians and recommend that activities that could be continued throughout medical training be designed and evaluated to stimulate the development of the students' critical faculties.

Chile↗
PubMed1978

Effects of dopamine analogues and antagonists on carotid body chemosensors in situ.

1. The effects of dopamine, its analogues and antagonists on the chemosensory discharges originating from carotid bodies in situ were studied in anaesthetized cats. 2. Intracarotid (I.C.) injections of 100 ng or more of dopamine produced transient depression of the frequency of carotid nerve chemosensory discharges. Short term (1-5 sec) complete inhibition was usually elicited by 2 microgram dopamine. 3. I.V. injections of dopamine also produced inhibition of chemosensory discharges, an effect observed with doses which were still too low to produce changes in systemic arterial pressure. Half-maximal inhibition (ID50) of chemoreceptors was elicited with a mean dose of 84 ng.kg-1. 4. I.C. and I.V. injections of apomorphine and amantadine also produced transient inhibition of chemosensory activity. Higher doses of these analogues of dopamine were needed to produce this effect, and the resulting inhibition usually did not silence the nerve discharges. Apomorphine inhibition was slightly more prolonged than that with dopamine. 5. Large doses of amphetamine and tyramine, inducers of dopamine release, did not produce inhibition of chemosensory discharges. 6. The effects of two classes of dopamine antagonists were tested. Dose-response curves for dopamine and apomorphine inhibition were displaced to the right by administration of phenothiazines (chlorpromazine and perphenazine) and butyrophenones (haloperidol and spiroperidol). In animals treated with perphenazine or spiroperidol, dopamine became a stimulator of chemoreceptor activity. 7. It is suggested that dopamine present in carotid body may operate as a modulator of chemosensory activity.

Action Potentials↗
PubMed1978

Effects of adrenoceptor stimulating and blocking agents on carotid body chemosensory inhibition.

1. The effects of alpha- and beta-adrenoceptor agonists and antagonists on chemosensory discharges originating from carotid bodies in situ were studied in anaesthetized cats.2. Noradrenaline (NA) injections commonly resulted in increased frequency of carotid nerve chemosensory discharge, an effect ascribed to reduced blood flow through the glomus, and reduced or eliminated by alpha-adrenergic block.3. NA injections occasionally produced an initial reduction of chemosensory discharge frequency, which was however less intense and of shorter duration than that caused by dopamine. This effect of NA is not mediated by alpha-adrenoceptors, since it is not blocked by dibenamine, but probably by low affinity for dopamine receptors.4. Dopamine and apomorphine-elicited chemosensory inhibition were not affected by low doses of phenoxybenzamine, which blocked NA-evoked hypertensive reactions.5. Higher doses of phenoxybenzamine and dibenamine produced a displacement to the right of dose-response curves for dopamine- and apormorphine-elicited chemosensory inhibition. However, this interference by alpha-adrenergic blockers was attributed to the resultant hypotension, since it was reversed upon restoration of blood pressure.6. Isoprenaline, a beta-adrenergic agonist, did not induce chemosensory inhibition, whilst beta-adrenergic blockers (propranolol and dichloroisoproterenol) did not modify dopamine- and apomorphine-elicited chemosensory inhibition.7. These results provide further support for the hypothesis that chemosensory inhibition could be mediated by specific dopamine receptors, distinct from alpha- and beta-adrenoceptors.

Action Potentials↗