Browsing by Author "LARRAIN, C"

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    ANTAGONISM OF DOPAMINE-INDUCED CHEMOSENSORY INHIBITION BY ERGOT ALKALOIDS
    (1978) ZAPATA, P; LARRAIN, C
    Intracarotid and i.v. injections of ergometrine, methylergometrine, ergotamine, dihydroergotamine, dihydroergotoxine and 2-Br-.alpha.-ergocryptine depressed the frequency of chemosensory impulses, recorded from the carotid nerve of anesthetized cats. After administration of ergot alkaloids, dopamine-induced inhibition of chemosensory activity was blocked; this effect was not associated with blocking of .alpha.-adrenoceptors for ergometrine, methylergometrine, ergotamine and 2-Br-.alpha.-ergocryptine, but it coincided with .alpha.-adrenergic antagonism for dihydroergotamine and dihydroergotoxine. Ergot alkaloids can act on carotid body chemoreceptors as dopamine analogs and antagonists.
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    COMPARISON OF THE SUBCELLULAR-DISTRIBUTION OF ALVEOLAR SURFACTANT IN 2 MAMMALIAN-SPECIES OF SIMILAR BODY-WEIGHT - CAT AND RABBIT
    (1992) OYARZUN, MJ; MORGADO, E; DUSSAUBAT, N; LATHROP, ME; ITURRIAGA, R; LARRAIN, C; ZAPATA, P
    1. We studied the total amount and subcellular distribution of alveolar surfactant, extracted through bronchoalveolar lavage of anesthetized cats and rabbits. This was correlated to several morphometric and ventilatory variables of these animals.
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    CORRELATIVE CONTRIBUTION OF CAROTID AND AORTIC AFFERENCES TO THE VENTILATORY CHEMOSENSORY DRIVE IN STEADY-STATE NORMOXIA AND TO THE VENTILATORY CHEMOREFLEXES INDUCED BY TRANSIENT HYPOXIA
    (1989) EUGENIN, J; LARRAIN, C; ZAPATA, P
    The contributions of the peripheral arterial chemoreceptors to the tonic and phasic reflex ventilatory regulation were studied in spontaneously breathing pentobarbitone anesthetized adult cats. The chemosensory drive during eucapnic normoxia was inferred from the transient ventilatory effects induced by anesthetic blockade of the buffer nerves. Aortic nerves block did not modify ventilation. Carotid nerves block provoked transient ventilatory depression, decreasing VT by 46% and fR by 26%, followed by recovery to steady-state values in VT, fR and PETCO2. Changes in PETCO2 were correlated with those in VT, but not with those in fR. The ventilatory effects of blocking a given carotid nerve were more intense when the contralateral carotid nerve was already blocked. This effect may be an expression of hypoadditive interactions between carotid nerves inputs with respect to chemosensory drive of ventilation. Analysis of the dose-response curves for the ventilatory reflexes evoked by NaCN i.v., before and after blockade of the buffer nerves, revealed major contributions of the carotid nerves, with small contributions of the aortic nerves to the responses to high doses of NaCN. The contributions of each carotid nerve to the tonic chemosensory drive and to the phasic ventilatory chemoreflexes were highly correlated (rs = 0.90; p < 0.01). We propose that a family of modulatory functions may describe the effects exerted by the peripheral arterial chemoreceptors upon the tonic ventilatory drive in normoxia and the phasic reflex responses evoked by hypoxia. While the carotid nerves mediated modulation is evident in normoxia, that provided by both aortic nerves is only expressed during pronounced hypoxia.
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    EFFECTS OF BODY-TEMPERATURE ON CHEMOSENSORY ACTIVITY OF THE CAT CAROTID-BODY INSITU
    (1991) LOYOLA, H; FADIC, R; CARDENAS, H; LARRAIN, C; ZAPATA, P
    The effects of changes in body core temperature (T(B)) upon the frequency of chemosensory discharges (f(x)) from one carotid nerve were studied in pentobarbitone anesthetized cats. Raising T(B) from 35 to 40-degrees-C increased f(x) in some cats, an effect more commonly seen after contralateral carotid neurotomy. In other animals, the simultaneously increased alveolar ventilation counteracted the above effect. A multiple correlation analysis of global data showed predicted increases in f(x) in response to raising T(B) at different CO2 levels.
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    THERMAL EFFECTS ON VENTILATION IN CATS - PARTICIPATION OF CAROTID-BODY CHEMORECEPTORS
    (1991) FADIC, R; LARRAIN, C; ZAPATA, P
    In pentobarbitone anesthetized cats, raising body temperature from 37 to 40-degrees-C by external heat increased respiratory frequency, tidal volume, frequency of spontaneous gasps and mean inspiratory flow. It reduced end-tidal CO2 pressure, together with inspiratory and expiratory durations. After bilateral section of the carotid nerves, raising body temperature still induced hyperventilation, but the increase in gasp frequency was less pronounced and no significant change in tidal volume was observed. In comparison to steady ventilatory values in the intact condition, significant reductions in tidal volume at 38-degrees-C and in gasp frequency at 37, 39 and 40-degrees-C were observed after bilateral carotid neurotomy. Brief hyperoxic tests induced transient decreases in tidal volume and increases in end-tidal CO2 pressure which were significantly larger at 40-degrees-C than at 37-degrees-C. These changes disappeared after bilateral carotid neurotomy. Anesthetic block of both carotid nerves produced transient reductions in tidal volume at any given temperature. We conclude that carotid body afferents contribute to the hyperventilation evoked by hyperthermia. After their interruption, such contribution is replaceable from other thermal afferents.