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Biomedical subjects

A Huszczuk

Publications and source records attributed to A Huszczuk.

At least 19 recordsLinked to original sources
PubMed1995

Vascular distension in muscles contributes to respiratory control in sheep.

It has recently been proposed that afferent fibers from skeletal muscle could sense the state of the microvascular circulation, linking ventilation to the degree of peripheral perfusion or vascular distension (Huszczuk et al., Respir. Physiol., 91:207-226, 1993). Ventilatory and circulatory responses to manipulation of peripheral vascular pressures in the hind limbs of anaesthetized (sodium thiopental) sheep were examined. Inflatable balloons were placed at the caudal ends of the abdominal aorta and the vena cava (Vc). Aortic (Ao) occlusion induced a consistent normocapnic decrease in minute ventilation (VE). In contrast, VE increased significantly during vena cava obstruction, leading to hypocapnia. Small changes in systemic blood pressure were observed (+7 mmHg for Ao occlusion and -12 mmHg during Vc obstruction). Moreover, inflation of the caval balloon superimposed on a previously established Ao occlusion, preventing venous drainage of anastomotic inflow, resulted in a significant rise in distal vascular pressures with trivial changes in systolic blood pressure. This led to a gradual rise of VE, despite further reduction of the CO2 flux to the lungs. The subsequent deflation of the aortic balloon, exposing the hindlimb vasculature to aortic pressure, resulted in an even more profound hypocapnic hyperpnea. The concurrent arterial blood pressure changes were too small to possibly involve the ventilatory component of the arterial baroreflex. We therefore hypothesize, that perfusion-related afferent signals within the muscles could contribute to respiratory homeostasis by maintaining ventilation of the lungs commensurate with the circulatory state of the muscular apparatus.

Afferent Pathways↗
PubMed1991

Role of the carotid bodies in the respiratory compensation for the metabolic acidosis of exercise in humans.

1. In response to an acute exercise-induced metabolic acidosis, the fall of arterial pH is constrained by the magnitude of the compensatory hyperventilation. To determine the role of the carotid bodies in this regulatory process, subjects performed prolonged (24 min) square-wave cycle ergometry from a background of unloaded cycling at inspired oxygen fractions (FI,O2) of 0.12 O2 (high carotid body gain), 0.21 O2 (normal carotid body gain) and 0.80 O2 (low carotid body gain). The work rates were selected to provide the same exercise intensity, despite the different inspirates; i.e. resulting in a constant increase in arterial blood [lactate] (delta [L-] approximately 4 mequiv l-1. 2. Ventilatory and pulmonary gas exchange variables were computed breath-by-breath and arterial blood was sampled at intervals throughout the tests and analysed subsequently for [lactate], [pyruvate], arterial partial pressures of oxygen and carbon dioxide (PO2, PCO2), pH, [bicarbonate] and [potassium]. 3. Hypoxia markedly reduced, and hyperoxia magnified, the transient decrease in arterial pH following exercise onset. However, there was a slow acid-base compensatory component, even when carotid chemosensitivity was suppressed by hyperoxia. We therefore conclude that, in humans, carotid body chemosensitivity plays a dominant role in constraining variations of arterial pH in response to the acute metabolic acidosis of heavy exercise, but that secondary-presumably central chemosensory-mechanisms subserve a slower compensatory role.

Acidosis↗
PubMed1990

Ventilatory control during exercise in calves with artificial hearts.

To determine the role of cardiac reflexes in mediating exercise hyperpnea, we investigated ventilatory responses to treadmill exercise in seven calves with artificial hearts and seven controls. In both groups, the ventilatory responses were adequate for the metabolic demands of the exercise; this resulted in regulation of arterial PCO2 and pH despite the absence of cardiac output increase in the implanted group. In this group, there was a small but significant reduction of arterial PO2 by 4 +/- 3 Torr and a rise of blood lactate by 1.1 +/- 1 mmol/l. When cardiac output was experimentally increased in the implanted calves to a level commensurate with that spontaneously occurring in the control calves, ventilation was not affected. However, experimental reductions of cardiac output led to an immediate augmentation of exercise hyperpnea by 4.56 +/- 4.3 l/min and a further significant lactate increase of 1.2 +/- 1.22 mmol/l that was associated with a significant decrease in the exercise O2 consumption (0.32 +/- 0.13 l/min). These observations indicate that neither cardiac nor hemodynamic effects of increased cardiac output constitute an obligatory cause of exercise hyperpnea in the calf.

Animals↗
PubMed1990

A respiratory gas exchange simulator for routine calibration in metabolic studies.

We have developed a method for simulating respiratory gas exchange for on-line calibration of metabolic measurement systems. It utilizes a pump which intakes a mixture of atmospheric air and a known flow of precision-analysed calibration gas (21% CO2, 79% N2). It expels the resulting mixture with flow wave form and profiles of gas concentration which closely resemble those of normal expiration. Control of the calibration mixture's inflow allows the investigator to set any desired metabolic rate regardless of the minute ventilatory rate. This separation of metabolic from ventilatory rates provides a stringent test of the computational performance of the respiratory gas exchange measurement systems. The apparatus can reproduce any range of respiratory and metabolic performance (currently ranging from 0.2-5 l.min-1 O2 uptake and CO2 output) with accuracy +/- 2%.

Calibration↗
PubMed1989

Respiration during recovery from exercise: effects of trapping and release of femoral blood flow.

To investigate the contribution of vascular and metabolic stimuli to the sustained hyperpnea after exercise, the respiratory effects of obstructing and then releasing the femoral blood flow were recorded in 15 normal volunteers during recovery from steady-state cycle exercise (80 W). Obstruction was achieved using cuffs around the upper thighs, inflated for the first 2 min of recovery to a pressure of 200 mmHg. Cuff inflation significantly reduced ventilation during recovery compared with control (P less than 0.001); the subsequent release of pressure was accompanied by an increase in ventilation (averaging 3.2 l/min), which began on the first breath after release. This preceded a rise in end-tidal CO2 (maximum 8.3 Torr increase), which first became significant on the fourth breath after release and led to a further rise in ventilation. The first-breath increase in ventilation after cuff release persisted, although slightly attenuated (averaging 2.5 l/min), in additional experiments with inspired O2 fraction of 1.0. The pattern of ventilatory response was also similar when the experiments were performed with 5% CO2 in air as the inspirate. The immediate rise in ventilation on cuff release, together with the persistent response on 100% O2, suggests that the vascular changes resulting from cuff release exert an influence on ventilation independent of the effects of released metabolites on the known chemoreceptors. The persistence of the response on 5% CO2 indicates that CO2-sensitive lung afferents do not have a major role in these responses.

Adolescent↗
PubMed1988

Intra-arterial and cuff blood pressure responses during incremental cycle ergometry.

Brachial intra-arterial blood pressure [systolic (AS) and diastolic (AD)] and cuff blood pressure [systolic (CS) and fourth- and fifth-phase diastolic (CD)] were simultaneously measured by a single observer in 13 middle-aged men during 1-min incremental cycle exercise. On the average, the mean AS exceeded the mean CS by 10 to 11 mm Hg, while the mean AD exceeded the average fourth and fifth CD by 5 and 13 mm Hg, respectively. During incremental exercise, AS, CS, AD, and fourth-phase CD increased, while fifth-phase CD decreased. We also measured intra-arterial blood pressure in nine young adult men smokers during 1-min incremental cycle exercise. In both groups, the average intra-arterial blood pressures increased in a relatively linear fashion from rest to maximal exercise: AS change = 74 +/- 5 mm Hg (SE) and AD change = 28 +/- 3 mm Hg for young men; AS change = 59 +/- 5 mm Hg and AD change = 12 +/- 3 mm Hg for middle-aged men. In this population of middle-aged smokers, intra-arterial mean blood pressure during exercise approximated diastolic plus 2/5 pulse pressure for intra-arterial measures or diastolic plus 1/2 pulse pressure for cuff measures rather than the traditional formula of diastolic plus 1/3 pulse pressure.

Adult↗
PubMed1986

Ventilatory responses to partial cardiopulmonary bypass at rest and exercise in dogs.

We determined the role of blood flow-induced changes in CO2 load to the lungs on ventilatory control, at rest and in the steady-state of electrically induced exercise, in the anesthetized dog. A portion of the vena caval blood was diverted to the descending aorta following "arterialization" through an extracorporeal gas exchanger. Ventilation typically decreased, both at rest and during exercise (i.e., at 2 different levels of mixed venous CO2), in proportion to the CO2 loss; arterial PCO2 was consequently regulated. There were concomitant increases of the pulmonary and peripheral vascular resistance. Bilateral cervical vagosympathectomy markedly attenuated the ventilatory response at rest, thus disrupting arterial PCO2 homeostasis, but not so during exercise. The results therefore provide evidence for and support the suggestion of CO2 flow-related hyperpnea both at rest and during muscular exercise.

Animals↗
PubMed1982

Cardiac output as a controller of ventilation through changes in right ventricular load.

Ventilatory responses to changes in right ventricular (RV) load were studied in spontaneous breathing anesthetized dogs. Moving average RV pressure leads to (PRV) was used as an index of the RV strain. RV load was changed in two ways: 1) cardiac output (Q) was increased by infusion of isoproterenol (0.7-1.2 micrograms/min) and reduced by infusion of vasopressin (0.3-0.5 U/min); and 2) RV pressure was increased independently on Q by partial balloon obstruction of the RV outflow. When Q was changed by drug infusion there was a linear correlation between leads to PRV and Q (avg r = 0.04). Well-correlated linear relationships were found between expired minute ventilation (VE) and leads to PRV (avg r greater than 0.03), the slopes and intercepts of which were not significantly different whether leads to PRV was changed by altering Q, partial obstruction of RV outflow, or combining both procedures. Bilateral vagotomy did not alter the VE/leads to PRV slope resulting from RV balloon inflations. It is suggested that the RV strain may act as a controller of ventilation and provide a link between Q and VE.

Animals↗
PubMed1982

[Usefulness of posterior electrorhinomanometry in the study of nasal and nasopharyngeal resistance in children aged 5 to 10].

Nasal passages constitute the physiologic airway. Impaired nasal breathing leads to various disease states. History taking and rhinoscopic examination are not sufficient for the complete evaluation of nasal respiratory patency. The authors present a case for introduction of posterior rhinomanometry (own modification) as an objective method in studying nasal patency in children, 127 healthy children (aged 5-10 years) were examined. Nasal resistance to air flow was measured. Posterior rhinomanometry was used in 198 children with impaired nasal patency of various causes. The results obtained in this study are reproducible and in accord with data in the literature. Children between 5 and 10 years of age cooperate well with the examiner. The authors find posterior rhinomanometry suitable for examination of children within this age group.

Adenoids↗
PubMed1981

Hypoventilation and elevation of end-expiratory pressure release a substance which relaxes isolated arteries and disaggregates platelets in the presence of cyclooxygenase inhibitors.

A prostacyclin-like substance was detected by bioassay in the blood of dogs and cats during hypoventilation and increased end-expiratory pressure. This biologically active material, most likely originating from lungs, relaxed isolated vascular strips and disaggregated platelets. Its release was not prevented by indomethacin or aspirin. Biological activity was not abolished by 10 min incubation of blood at 38 degrees C. Although the identity of the substance has not been established the release of a biologically active prostacyclin-like material might play a role in circulatory adaptation to disturbed ventilatory function.

Animals↗
PubMed1978

Lung reflexes in rabbits during pulmonary stretch receptor block by sulphur dioxide.

Anaesthetized rabbits were given 200 ppm sulphur dioxide to breathe for 10 min. This abolished activity in 23 of 26 pulmonary stretch receptors, while leaving that of lung irritant receptors unimpaired. The Breuer-Hering reflex was abolished and breathing became deeper and slower. Inspiratory time (tI) was increased and expiratory time (tE) decreased. Subsequent vagotomy increased tidal volume (VT), tI and tE. In animals with stretch receptors blocked, injections of phenyl diguanide and histamine still increased breathing frequency and decreased VT, indicating that reflexes from lung irritant and J-receptors were intact. Inhalation of 8% CO2 caused a bigger increase in frequency and tidal volume in rabbits with stretch receptor block compared with controls or those after vagotomy. Induction of pneumothorax with stretch receptor block transiently prolonged tI and shortened tE; removal of the pneumothorax also transiently shortened tE and usually also decreased tI. The results suggest that lung irritant receptors reflexly shorten tE in all our experimental conditions, but have various effects on tI which may depend on the timing of the irritant receptor discharge and refractoriness of the inspiratory response.

Animals↗
PubMed1977

Studies on reflex control of breathing in pigs and baboons.

In 8 pigs and 4 baboons, spontaneously breathing, anaesthetized with halothane, Hering-Breuer reflex was tested by means of a total obstruction of the airway preventing either inspiration or expiration. Subsequently animals were paralysed and maintained on phrenic nerve driven servo-respirator. The response of phrenic motoneurone output to various degree of lung inflation, introduced for one breath only, was then carefully studied. This was achieved by varying the gain of servorespirator. Additionally in baboons, identical series of gain manoeuvres was performed against a background of different levels of the initial gain setting. Changes in both inspiratory time and peak amplitude of phrenic signal were monoexponentially dependent on gain of servorespirator and linearly dependent on tidal volume (all negatively correlated). The relationship between inspiratory time T(1) and subsequent expiratory duration T(E )existed only within a range of growing T(1). Vagal positive feedback phenomenon was apparent in pigs and negligible in baboons. It is postulated that inspiratory cut-off mechanism terminates inspiration when excitatory function are outbalanced by their integral.

Animals↗
PubMed1975

The effect of varying tidal volume on the associated phrenic motoneurone output:studies of vagal and chemical feedback.

Two groups of dogs were anaesthetised, paralysed and artificially ventilated using a respirator driven by the phrenic motoneurone output, electrically processed to resemble transpulmonary pressure. In one group, blood gases were maintained constant with closed-chest cardiopulmonary bypass; the second group were studied without "bypass". Therefore it was possible to determine the relative contributions of vagal and chemial feedback to the effect of altering the depth of an inspiration on the associated phrenic motoneurone output. Mono-exponential regressions between change of respirator gain and changes in both inspiratory time and peak amplitude of the processed phrenic signal were found for all dogs. The rate of rise of the processed phrenic signal usually changed in the direction of the change in respirator gain, suggesting the presence of vagal positive feedback during eupnoeic breathing. After vagotomy, all responses were absent in the "bypass" group and small in the "non-bypass" group. These experiments quantitate the role of pulmonary vagal afferent discharge, in phase with inspiration, in the regulation of phrenic motoneurone output in a closed-loop situation.

Animals↗
PubMed1973

Studies on the central effects of Hering-Breuer reflexes.

In our previous experiments performed with rabbits, it was found out that the strength of both inflation and deflation Hering-Breuer reflexes depends on the level of anaesthesia and ventilation as correlative factors in spontaneously and artificially ventilated animals, though this dependence was quantitatively and qualitatively different in these two groups. On the basis of the recent evidence pointing to the rapidly conducting fibres and thus indirectly the pulmonary stretch receptors as the pathway along which both Hering-Breuer reflexes are transmitted, an attempt has been made to show how both parameters of ventilation are centrally controlled in response to afferent information concerning such mechanical factors as resistance and compliance of the respiratory system. The results presented seem to allow the following conclusions: (i) An important role may be ascribed to the pulmonary stretch receptors in transmission of both Hering-Breuer reflexes. (ii) In quiet breathing the central mechanisms of the Hering-Breuer inflation reflex are set to regulate tidal volume on the basis of analysis of the compliance of the respiratory apparatus at the given moment. Their role to the control of the respiratory frequency is of minor importance. (iii) The contribution of the pulmonary stretch receptors to the control of respiratory frequency is based on information about the resistance of the airways. This parameter influences the ratio of duration of the activity phase to silent phase in discharges of pulmonary stretch receptors.

Anesthesia↗
PubMed1973

Studies on central respiratory activity in artificially ventilated rabbits.

The level of integrated phrenic nerve activity (C3 root) has been studied under various forms of impairment of respiratory muscle function, such as paralysis (gallamine), pneumothorax and phrenectomy. Experiments were performed in two groups of rabbits artificially ventilated by means of the conventional respirator and the phrenic nerve driven respirator. It was found that both paralysis and bilateral pneumothorax were very strong stimuli exciting central inspiratory activity despite the constancy of ventilation. Under the same conditions phrenectomy caused only slight persistent excitation of the activity studied. It is worth noting that activity in the C3 root contralateral to the cut phrenic nerve trunk was as a rule more strongly stimulated. As artificial ventilation preceded by administration of gallamime is commonly applied in physiological experiments, the possibility of its effect on central respiratory activity will be discussed.

Animals↗