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Biomedical subjects

E H Vidruk

Publications and source records attributed to E H Vidruk.

At least 19 recordsLinked to original sources
PubMed1988

Response of the goat carotid body to acute and prolonged hypercapnia.

The effect of prolonged hypercapnia on carotid chemoreceptor discharge frequency has not been elucidated. In addition, the effect of acute hypercapnia on chemoreceptor discharge has not been determined in the goat, a species commonly used for ventilatory control studies. Therefore, we determined the effects of acute and prolonged normoxic-hypercapnia on single fiber output of the carotid body of chloralose anesthetized goats. The animals were paralyzed and artificially ventilated. The average acute response curve for 12 single fibers was linear over the range of 30-80 Torr PaCO2 with a mean slope of 0.115 +/- 0.057 (SD) imp.sec-1.Torr-1 PaCO2. Elevated discharge frequency was maintained during prolonged (up to 240 min, n = 11) steady-state hypercapnia (X PaCO2 = 85 Torr). No systematic time-dependent changes in afferent discharge frequency occurred during the period. The findings obtained during sustained hypercapnia are in contrast to the time-dependent increase in carotid body activity seen previously in our laboratory with prolonged normocapnic-hypoxia of up to 240 min duration.

Animals↗
PubMed1988

Carotid body excision significantly changes ventilatory control in awake rats.

We determined the effects of carotid body excision (CBX) on eupneic ventilation and the ventilatory responses to acute hypoxia, hyperoxia, and chronic hypoxia in unanesthetized rats. Arterial PCO2 (PaCO2) and calculated minute alveolar ventilation to minute metabolic CO2 production (VA/VCO2) ratio were used to determine the ventilatory responses. The effects of CBX and sham operation were compared with intact controls (PaCO2 = 40.0 +/- 0.1 Torr, mean +/- 95% confidence limits, and VA/VCO2 = 21.6 +/- 0.1). CBX rats showed 1) chronic hypoventilation with respiratory acidosis, which was maintained for at least 75 days after surgery (PaCO2 = 48.4 +/- 1.1 Torr and VA/VCO2 = 17.9 +/- 0.4), 2) hyperventilation in response to acute hyperoxia vs. hypoventilation in intact rats, 3) an attenuated increase in VA/VCO2 in acute hypoxemia (arterial PO2 approximately equal to 49 Torr), which was 31% of the 8.7 +/- 0.3 increase in VA/VCO2 observed in control rats, 4) no ventilatory acclimatization between 1 and 24 h hypoxia, whereas intact rats had a further 7.5 +/- 1.5 increase in VA/VCO2, 5) a decreased PaCO2 upon acute restoration of normoxia after 24 h hypoxia in contrast to an increased PaCO2 in controls. We conclude that in rats carotid body chemoreceptors are essential to maintain normal eupneic ventilation and to the process of ventilatory acclimatization to chronic hypoxia.

Acute Disease↗
PubMed1988

Carotid chemoreceptor activity during acute and sustained hypoxia in goats.

The role of carotid body chemoreceptors in ventilatory acclimatization to hypoxia, i.e., the progressive, time-dependent increase in ventilation during the first several hours or days of hypoxic exposure, is not well understood. The purpose of this investigation was to characterize the effects of acute and prolonged (up to 4 h) hypoxia on carotid body chemoreceptor discharge frequency in anesthetized goats. The goat was chosen for study because of its well-documented and rapid acclimatization to hypoxia. The response of the goat carotid body to acute progressive isocapnic hypoxia was similar to other species, i.e., a hyperbolic increase in discharge as arterial PO2 (PaO2) decreased. The response of 35 single chemoreceptor fibers to an isocapnic [arterial PCO2 (PaCO2) 38-40 Torr)] decrease in PaO2 of from 100 +/- 1.7 to 40.7 +/- 0.5 (SE) Torr was an increase in mean discharge frequency from 1.7 +/- 0.2 to 5.8 +/- 0.4 impulses. During sustained isocapnic steady-state hypoxia (PaO2 39.8 +/- 0.5 Torr, PaCO2, 38.4 +/- 0.4 Torr) chemoreceptor afferent discharge frequency remained constant for the first hour of hypoxic exposure. Thereafter, single-fiber chemoreceptor afferents exhibited a progressive, time-related increase in discharge (1.3 +/- 0.2 impulses.s-1.h-1, P less than 0.01) during sustained hypoxia of up to 4-h duration. These data suggest that increased carotid chemoreceptor activity contributes to ventilatory acclimatization to hypoxia.

Adaptation, Physiological↗
PubMed1987

Effects of hypercapnia on phrenic and stretch receptor responses to lung inflation.

To determine if hypercapnia and reflex bronchoconstriction attenuate lung inflation effects on ventilatory activity by indirect effects on intrapulmonary stretch receptors (PSR), phrenic nerve activity and single unit PSR were monitored at controlled levels of static airway pressure (Paw) and arterial PCO2 in 15 anesthetized dogs. Paw in a vascularly isolated lung was varied between 2 and 14 cm H2O at levels of PaCO2 between 35 and 85 mm Hg. PSR activity (n = 38) in fine strands dissected from an otherwise intact vagus nerve and the integrated phrenic neurogram were recorded. The response to Paw varied from one PSR to another, but was consistent in a given unit; PaCO2 had no consistent effect on individual responses. Selected PSR (n = 15) were averaged to yield a population response to Paw; the selection criteria were: phrenic activity responded briskly to Paw and measurements were made at three levels of PaCO2. Average PSR discharge increased linearly with Paw but was unaffected by PaCO2. On the other hand, phrenic burst frequency decreased as Paw increased and hypercapnia attenuated the slope of this relationship. These results suggest that effects on the relationship between PSR activity and Paw cannot account for attenuation of the relationship between phrenic frequency and Paw in hypercapnia. The effect of PaCO2 on the phrenic frequency vs Paw relationship probably arises from integrative mechanisms in the central nervous system.

Animals↗
PubMed1986

Ventilatory responses to hypoxia nullify hypoxic tracheal constriction in awake dogs.

Three awake dogs with chronic tracheostomies were used to study the effects of hypoxia (12% O2) on tracheal smooth muscle tone. Pressure changes within a water-filled cuff in an isolated portion of the cervical trachea reflected changes in tracheal tone. During spontaneous ventilation, hypoxia produced hyperventilation, but no significant change in tracheal tone. If hypocapnia was prevented with inspired CO2 during hypoxia, one of three dogs increased tracheal tone, and all dogs increased ventilation beyond that measured with hypoxia alone. When the awake dogs were ventilated mechanically to prevent changes in ventilation, hypoxia always increased tracheal tone. We made independent changes in ventilation and CO2 similar to the spontaneous responses to hypoxia to test these effects on tracheal tone. When the dogs were ventilated mechanically first with 2% CO2, and then with no CO2, the resulting drop in end-tidal CO2 always decreased tone. When the tidal volume on the ventilator was increased under hyperoxic, isocapnic conditions, tracheal tone always decreased. We conclude that the normal ventilatory response to hypoxia opposes the bronchoconstrictor effect of hypoxia, resulting in no net change in tracheal smooth muscle tone.

Airway Resistance↗
PubMed1985

Neural and humoral factors in control of tracheal caliber.

To assess the contributions of neural (vagal) and humoral (blood borne) mechanisms in the tracheal constriction that occurs when pump ventilation is transiently withheld, experiments were conducted on decerebrate dogs. The dogs were paralyzed and thoracotomized, and each lung was independently ventilated. Pressure changes within an isolated tracheal segment (Ps) were monitored as an index of tracheal caliber. In series I, pump ventilation was withheld 20 s at the prevailing end-expiratory pressure (3-5 cmH2O) from both lungs or either lung alone when 1) both lungs were intact; or 2) the left lung was vascularly isolated (VIL) by occluding the pulmonary artery and the right gas exchange lung (GEL) was vagally denervated. In series II, steady-state pressure changes in the VIL were made with constant GEL ventilation. With both lungs intact, 20-s apnea elicited a 17.3 +/- 2.6 cmH2O increase in Ps; the left and right lungs contributed equally to this response. Following vagotomy and pulmonary arterial occlusion, a 7.8 +/- 2.6 cmH2O increase in Ps was elicited from two lungs; the VIL response was 60 +/- 11% and the GEL 41 +/- 15%. Onset and one-half response times were faster from the VIL than GEL. Prolonged maneuvers elicited progressively larger responses from the GEL, but the VIL response plateaued within 30 s and then adapted towards the control level. In series II, steady-state increases or decreases in VIL pressure elicited small decreases or increases in Ps, respectively, which showed nearly complete adaptation within several minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Hypoxia potentiates, oxygen attenuates deflation-induced reflex tracheal constriction.

The reflex tracheomotor responses of in situ isolated segments of the extrathoracic trachea of anesthetized, paralyzed, and ventilated dogs were monitored. Reflex tracheal constriction was evoked by passive lung deflation. The purpose of this study was to determine whether the prevailing state of oxygenation altered the magnitude of this reflex. Compared with the magnitude of the response during normoxia [arterial O2 tension (PaO2) = 78 Torr], that during hypoxia (PaO2 = 44 Torr) was nearly threefold larger while that during hyperoxia (PaO2 greater than 250 Torr) was about 50% smaller. The isocapnic changes in oxygenation by themselves usually had no effect on tracheomotor tone. The deflation-induced reflex tracheal constriction was eliminated by complete denervation of the tracheal segment but usually only diminished by partial denervation. Bilateral vagotomies or bilateral carotid body denervation also usually decreased the magnitude of the reflex. It appears that the magnitude of this reflex is dependent on the prevailing state of oxygenation and that a pulmonary stretch receptor-carotid body chemoreceptor interaction accounts for the exaggerated reflex tracheal constriction during hypoxia and the attenuated response during hyperoxia.

Airway Resistance↗
PubMed1985

Histamine-induced reflex tracheal constriction is attenuated by hyperoxia and exaggerated by hypoxia.

The effect of vagal reflexes on bronchomotor tone can be altered by their interaction with other bronchomotor factors, such as the prevailing state of oxygenation. In anesthetized, paralyzed, and artificially ventilated dogs, a reflex constriction was induced in an isolated tracheal segment by administration of aerosolized histamine to the lungs. When the challenge was repeated during hypoxic conditions (PaO2, 45 mmHg), the magnitude of the reflex response was significantly larger than during normoxia. In contrast, during hyperoxia (PaO2, 344 mmHg), the response was significantly smaller than the normoxic response. The changes in the prevailing state of oxygenation were done under isocapnic and isohydric conditions. Hyperoxia alone had no effect upon baseline bronchomotor tone, whereas hypoxia caused an increase in baseline tone in approximately half the animals. The effect of hypoxia upon the reflex response to histamine was not affected by the baseline changes. We think that the potentiating effects of hypoxia and the attenuating effects of hyperoxia are mediated by an interaction between lung sensory receptors and carotid body chemoreceptors.

Aerosols↗
PubMed1985

Pulmonary control systems in exercise: update.

We examined recent ideas and findings concerned with the regulation of ventilation and gas transport in moderate and heavy exercise. The primary mediation of exercise hyperpnea remains unknown and highly controversial, but two unique approaches to the problem have advanced our understanding of this neurohumoral regulatory scheme. On the one hand, experimental separation of the pulmonary and systemic circulations was used to reveal a vagally mediated ventilatory response that is clearly attributable to CO2 flow to the lung. This mechanism seems to be most effective as a homeostatic regulator of ventilatory control near resting levels of metabolic rate. On the other hand, a descending neurogenic drive to hyperpnea from the locomotor regions of the central nervous system was also demonstrated experimentally. The importance of regulatory feedback by conventional chemoreceptors in determining the precision of the hyperpneic response was emphasized in explaining the wide spectrum of arterial acid-base regulation during exercise in humans and non-human species. Two commonly accepted homeostatic regulators believed to be operative during heavy exercise were questioned, i.e., the compensatory hyperventilatory response and the maintenance of arterial oxygenation. For example, the hyperventilatory response was shown not to require metabolic acidosis; hyperventilation was not always observed at high work rates despite an abundance of chemical stimuli; and arterial hypoxemia occurred at very high metabolic rates in a significant number of highly fit athletes. These data implied that the capabilities of some aspects of even the healthy pulmonary system may be approached-or even exceeded-during heavy exercise.

Animals↗
PubMed1983

Monoamine neurotransmitter metabolism during acclimatization to hypoxia in rats.

The levels and turnovers of NE, DA and 5HT were determined in whole brain, brain stem, cervical and thoracic spinal cord and carotid bodies (CB) of rats exposed to from 1 h to 7 days of hypobaric hypoxia (PB = 450 torr). Monoamine levels decreased only transiently upon acute exposure to hypoxia. Monoamine turnover in the CNS was estimated from the average of (a) monoamine buildup following inhibition of catabolism, and (b) monoamine breakdown following inhibition of synthesis. Hypoxic effects on CNS monoamine turnover showed that: (a) NE was not affected; (b) DA was not affected in acute hypoxia, but was reduced to about 40% of normoxia control after 1-7 days hypoxia; (c) 5HT fell 50-60% during acute hypoxia but returned to and was maintained at control over 1-7 days of hypoxia; (d) acute restoration of normoxia following acute hypoxia restored 5HT and DA to control or above and in the acclimatized animal acute normoxia increased DA and 5HT turnover to about 1.4 and 1.8 X control. In the CB, DA levels gradually increased to 4 X control after 7 days of hypoxia and further increased to 6 X control upon acute restoration of normoxia. Changes in the metabolism of both central 5HT and CB DA may be related to the mechanisms mediating ventilatory acclimatization to chronic hypoxia.

Adaptation, Physiological↗
PubMed1983

Extravagal innervation of canine tracheal stretch receptors.

In dogs an extravagal pathway consisting of the pararecurrent nerve, the ramus anastomoticus, the internal branch of the superior laryngeal nerve, and the superior laryngeal nerve carries nerve fibres from the upper trachea. A segment of the upper trachea innervated by fibres in this pathway was isolated in situ and ventilated separately from the rest of the respiratory tract. Single unit and whole nerve neurograms recorded from the pararecurrent nerve, the ramus anastomoticus, and the interior branch of the superior laryngeal nerve demonstrated discharge patterns characteristic of airway stretch receptors. The discharge was strongly modulated by ventilatory manoeuvres of the isolated tracheal segment but not the rest of the respiratory tract. The number of tracheal stretch receptors with fibres in this non-vagal pathway was found to be similar to the number innervated by vagal pathways. A search for the presence of extravagal fibres innervating rapidly adapting receptors, however, was unsuccessful. A non-vagal pathway exists between tracheal stretch receptors and the nodose ganglion. The functional significance of this pathway was not determined.

Action Potentials↗
PubMed1983

Effects of p-chlorophenylalanine on ventilatory control in goats.

The effects of tryptophan hydroxylase inhibition with p-chlorophenylalanine (PCPA; 100 mg/kg iv) on ventilatory control were studied in awake goats. Ventilation, CO2 production, and blood gases were measured 16-24 h after PCPA at rest and during mild exercise in normoxia and at rest in hypoxia and hypercapnia. PCPA increased ventilation 36% at rest, predominantly through an effect on respiratory frequency, and decreased arterial PCO2 (PaCO2) 6.5 Torr. Ventilatory gain in exercise (delta VI/deltaVCO2) was increased 20% by PCPA thereby maintaining PaCO2 at its new resting value. Hypoxia (fractional inspired O2 concentration = 0.12) had little effect on ventilation or PaCO2 at rest, either on control or on PCPA test days. Ventilatory sensitivity to CO2 at rest (delta VI/delta PaCO2) was unaffected by PCPA. Bilateral carotid body denervation (CBX) was performed in the animals, and experiments were repeated 3 mo after the first administration of PCPA. CBX alone decreased ventilation 29% and increased PaCO2 9.4 Torr. Administration of PCPA increased ventilation 35%, decreased PaCO2 by 10.2 Torr at rest, and increased ventilatory gain in exercise 26%. Thus carotid bodies are not necessary for the ventilatory response to PCPA. Furthermore, the primary neural pathways associated with exercise or hypercapnia are not specifically affected by inhibition of serotonin metabolism via PCPA.

Animals↗
PubMed1980

Pulmonary control systems in exercise.

We reviewed the response and regulation of alveolar ventilation, chest wall mechanics, and alveolar-to-arterial gas exchange to the demands imposed by increases in tissue metabolic rate. The primary mediator of iso-capnic exercise hyperpnea remains a dilemma--with conflicting evidence presented on both sides of a "CO2 flow" humoral hypothesis versus a "neurogenic" non-humoral hypothesis. The increased expiratory flows and tidal volumes at any given level of hyperpnea are achieved at a "minimum" of increased mechanical work exerted on the lung and chest wall, owing to a control system that has multiple levels of nervous integration (from cortex to spinal motor neuron) readily accessible to a wide variety of sensory information concerning the mechanical status of the lung and respiratory muscles. The maintenance of arterial PO2 in the face of a falling CVO2 during exercise was attributed to a precise regulation over factors that limit diffusion equilibrium and intra- and interregional ventilation: perfusion distributions in the lung. Finally, we noted that the near-optimal nature of these responses and their control during exercise had many exceptions in the real world of physical exercise outside of the laboratory.

Carbon Dioxide↗
PubMed1979

Effects of prostaglandins E1 and E2 on activity in laryngeal and pharyngeal afferent fibers.

Prostaglandins (PG) E1 and E2 were applied topically to the receptive fields of feline laryngeal and pharyngeal sensory receptors, while action potentials were recorded from single - or few-fiber preparations of the superior laryngeal nerve. When initially dissolved in ethanol, PGs stimulated these sensory receptors. If ethanol was not used as a solvent for the PGs they did not stimulate the sensory receptors. Similarly, local application of dilute (0.025%, v/v) solutions of ethanol alone excited the receptors, whereas phosphate buffer alone did not. Thus PGE1 and PGE2 do not themselves stimulate sensory receptors in the larynx and pharynx. These findings suggest that irritant properties of PGEs on upper airways are attributable to the ethanol used as a solvent.

Action Potentials↗
PubMed1979

The nature of the receptor mediating stimulant effects of histamine on rapidly adapting vagal afferents in the lungs.

1. The effects of histamine H1- and H2-agonists on these airway sensory receptors were also examined. 2. Neither I.V. infusion of metiamide (5 mg/kg, min for 35 min) in seven experiments, nor I.V. bolus injection of burimamide (15 mg/kg) in six other experiments, both substances being H2-antagonists, altered the response of rapidly adapting receptors to aerosols of histamine (from 0.1 or 1.0% solutions). 3. Chlorpheniramine (H1-antagonist), 2--5 mg/kg, I.V., completely abolished responses of rapidly adapting receptors to histamine in seven experiments in which metiamide had been given previously and in seven other preparations in which it had not, but had no effect on responses to prostaglandin F2 alpha. Chlorpheniramine itself caused a brief stimulation of rapidly adapting receptors. 4. The H2-agonist S-[3-(N,N-dimethylamino) propyl] isothiourea (Dimaprit), given as aerosol (1% solution for 2 min) or I.V. (2 mg/kg), was without effect on activity of four airway rapidly adapting receptors. These receptors were stimulated, however, by the H1-agonist 2,(2 pyridylethylamine) dihydrochloride (PEA), administered both as aerosol (from a 10% solution) and I.V. (0.4--2 mg/kg). These stimulant effects were abolished by chlorpheniramine. 5. The results indicate that stimulation of airway rapidly adapting receptors by histamine is mediated by histamine H1-receptors.

Animals↗
PubMed1978

Effects of droperidol on activity of carotid body chemoreceptors in cat.

1 The effect of droperidol on the spontaneous activity of carotid body chemoreceptors and on their response to various stimuli was studied in 21 anaesthetized, paralyzed and artificially ventilated cats. Carotid body blood flow was controlled with a perfusion pump, and drugs were injected into the perfusion circuit. 2 In low doses, droperidol transiently increased the rate of spontaneous chemoreceptor activity, but in higher doses it depressed chemoreceptor activity after an initial stimulation. 3 Droperidol reduced or abolished the normal increase in chemoreceptor activity produced by stagnant asphyxia. This effect did not depend solely on the ability of droperidol to suppress spontaneously occurring impulses. Chemoreceptor responses to sodium cyanide, and to dopamine were also inhibited. 4 Dopamine antagonists other than droperidol were also studied for their effect on chemocreceptor activity. Chlorpromazine depressed spontaneous chemoreceptor activity and also reduced the chemoreceptor responses to sodium cyanide and dopamine, as did pimozide. The effects of these dopamine antagonists were much briefer and less marked than those of droperiodol. 5 Although the influence that we have shown droperidol to have on peripheral chemoreceptor activity has an uncertain basis, it may have important implications in human and veterinary medicine.

Animals↗