Distention of venous structures in muscles as a controller of respiration.
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Animals↗
Biomedical subjects
A Huszczuk
Publications and source records attributed to A Huszczuk.
Lack of causal link between muscle [H+] and ventilation during exercise.
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Exercise↗
Ventilatory and gas exchange response during walking in severe peripheral vascular disease.
It has long been recognized that at the onset of a dynamic muscular exercise the ventilatory and the circulatory (blood flow) responses appear to be matched, thereby maintaining arterial blood gas homeostasis. Such a coupling has recently been suggested to rely upon ventilatory reflex triggered by mechanoreceptors encoding changes in muscle blood flow or, more likely, blood volume. The aim of this study was to investigate whether patients with severe peripheral blood flow limitation to the lower extremities have a normal ventilatory response during a light intensity exercise. The ventilatory and gas exchange temporal response characteristics were studied during a 6 min walking test in seven patients with severe ischemic peripheral vascular disease and in six normal age-matched subjects. The magnitude of the overall ventilatory and Vo2 increment at the end of the tests was similar in both groups. However, in contrast to the control subjects, who presented an almost rectangular response, the patients had a considerably slowed response dynamics (t50 = 33 +/- 4 vs. 9 +/- 3 sec for Vo2 and 37 +/- 5 vs. 10 +/- 8 sec for VE) with a dramatic reduction in the magnitude of the initial 20 sec of the responses. Although the slow Vo2 dynamics in patients presumably reflected the impeded perfusion of the working muscles. the accompanying sluggishness of the V1 course implies that either muscular ischemia actually inhibits ventilatory response to exercise or, more likely, that this response is strongly linked to the magnitude of the hyperemia in the exercising muscles.
Heart Rate↗
Papaverine injection into the hindlimb circulation stimulates ventilation in sheep.
To test the hypothesis, previously suggested by Huszczuk et al. (1993), that distention of the peripheral microvascular network could, per se, stimulate ventilation, the ventilatory effects of papaverine-induced muscular vasodilation were studied in ten anaesthetized sheep. Because systemic action of papaverine may involve the arterial baro- and chemoreceptors, the animals were surgically prepared for a reversible isolation of the hindlimb circulation. Papaverine injection (1-2 mg/kg) into the arterial inflow of the isolated limbs provoked a 13 +/- 6 sec-delayed increase in VE by 1.8 +/- 0.2 L min-1 (p < 0.01) with a concomitant decrease in peripheral vascular resistance and no decrease in the systemic arterial blood pressure. Identical control injection into a jugular vein prior to the hindlimb circulatory separation yielded an increase of VE by 4.95 +/- 0.58 L min-1 with a latency of 21 +/- 2 sec and a coinciding moderate decrease of the systemic arterial pressure. The present data suggest that papaverine injection into the hindlimb circulation can stimulate ventilation independently of its possible effects on the arterial baro- or chemoreceptors, supporting the hypothesis that muscular vasodilation could contribute to the control of breathing through a neural link.
Animals↗
Muscle perfusion and control of breathing. Is there a neural link?
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Animals↗
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↗
Femoral vascular occlusion and ventilation during recovery from heavy exercise.
Ventilation and cardiac output subside gradually following cessation of exercise, which is commonly linked to the slow wash-out of materials from the recovering muscles. The effect of hindering the removal of the metabolic products of heavy cycle exercise on the kinetics of ventilation and gas exchange was studied in 5 subjects by occluding the femoral circulation with cuffs during the first 2 min of recovery (15 tests). Fifteen undisturbed recoveries served as controls. Compared to spontaneous recovery, circulatory obstruction induced an immediate (from the first breath) decrease in minute ventilation (VE), while end-tidal CO2 (PETCO2) as well as lactate and K+ in venous blood at forearm did not change significantly. A ventilatory deficit of 27 +/- 9 L was observed from the 2 min of occlusion. Following cuff deflation, VE rose 2-3 breaths after PETCO2 began to increase in every subject. The mechanisms of the normocapnic reduction of VE during occlusion, as well as the rise of ventilation following cuff release, are still unclear. However, these results argue against any significant role for hyperpnea-inducing intramuscular chemoreception, or point to muscular perfusion as a prerequisite of such a mechanism to operate.
Adult↗
Role of muscle perfusion and baroreception in the hyperpnea following muscle contraction in dog.
The influence of impeding muscle perfusion on the time course of ventilatory decline during recovery from electrically induced hindlimb contractions has been studied in 14 anesthetized dogs. When intravascular balloons, placed in abdominal aorta and inferior vena cava just rostral to the iliac bifurcation, were inflated at the cessation of contraction bout, minute ventilation (VE) was significantly reduced during recovery compared with control. The subsequent restoration of iliac circulation rapidly augmented VE, which peaked at the fifth breath after release, by an average of +4.97 L.min-1; VE then returned exponentially to resting (pre-contraction) level. Breathing 100% O2 did not affect the VE recovery pattern neither during iliac occlusion nor immediately after its release (the peak average delta VE = +4.42 L.min-1). When a local anesthetic (5% Lidocaine) was applied bilaterally to the regions of carotid bifurcation, systemic blood pressure was significantly increased and the VE response to both iliac occlusion and release were nearly abolished. The VE response to inhalation of 5% CO2 in air was not affected by this procedure, whereas the stimulation of VE with 2 mg i.v. bolus of NaCN was attenuated. When the local anesthetic was thoroughly washed out (and systemic blood pressure had returned to control level) the previously observed VE responses to iliac occlusion and release were restored. These results and analysis of the VE response timing (transits and latencies) suggest that the vascular rather than humoral effects or tissue 'metaboreception' modulate ventilatory recovery from muscular contractions; baroreception appears to be important in this process.
Animals↗
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↗
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↗
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↗
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↗
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↗
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↗
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↗
[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↗
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↗
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↗