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PubMed1966

The effects of hyperventilation on the reflex cardiac response from the carotid bodies in the cat.

1. Cats were anaesthetized with chloralose and urethane, and ventilated by an artificial intermittent negative pressure applied to the thorax. The carotid body chemoreceptors were isolated and perfused with oxygenated blood. They were stimulated by substituting hypoxic blood obtained from a donor animal.2. Stimulation of the carotid bodies during constant ventilation caused a bradycardia. When an artificial hyperventilation was induced during carotid body stimulation the heart rate increased.3. The increase in heart rate during hyperventilation, and while the carotid bodies were being stimulated, was due to at least two mechanisms, first a reflex from the lungs and secondly a fall in arterial blood P(CO) (2), both of which accompany the hyperventilation.

Animals↗
PubMed1971

Maternal hyperventilation and foetal hypocapnia in sheep.

1. In anaesthetized foetal lambs near term, hypocapnia induced by maternal hyperventilation abolished the rise of arterial pressure and femoral vasoconstriction caused by hypoxaemia. This is consistent with interaction of P(CO2) and P(O2) on the foetal aortic bodies.2. In immature lambs (0.6-0.77 of term) maternal hyperventilation caused a fall in foetal carotid P(CO2) commensurate with that in the maternal blood. In mature lambs (at 0.9 or more of term) the fall in foetal carotid P(CO2) was less than that in maternal blood, whether the foetus was exteriorized or in utero.3. The mean transplacental gradient for P(CO2) (maternal arterial-umbilical vascular), when the foetus was replaced with a mechanical pump recirculating foetal blood, was 6.3 mm Hg. This is attributed to placental CO(2) production, and is nearly half the mean P(CO2) gradient (maternal artery-foetal carotid) of about 14 mm Hg during normal maternal ventilation.4. The mean maternal-umbilical transcotyledonary venous gradients (avoiding vascular shunts through the myometrium and intercotyledonary chorion) were for P(CO2) 1.7 mm Hg and for P(O2) 13.4 mm Hg.5. Maternal hyperventilation (P(a, CO2) approximately 20 mm Hg) caused a small fall in mean foetal carotid P(O2) (5 mm Hg), which was readily reversible with no evidence of progressive acidaemia.

Animals↗
PubMed2004

Is lactic acidosis a cause of exercise induced hyperventilation at the respiratory compensation point?

OBJECTIVES: The respiratory compensation point (RCP) marks the onset of hyperventilation ("respiratory compensation") during incremental exercise. Its physiological meaning has not yet been definitely determined, but the most common explanation is a failure of the body's buffering mechanisms which leads to metabolic (lactic) acidosis. It was intended to test this experimentally. METHODS: During a first ramp-like exercise test on a cycle ergometer, RCP (range: 2.51-3.73 l x min(-1) oxygen uptake) was determined from gas exchange measurements in five healthy subjects (age 26-42; body mass index (BMI) 20.7-23.9 kg x m(-2); Vo(2peak) 51.3-62.1 ml x min(-1) x kg(-1)). On the basis of simultaneous determinations of blood pH and base excess, the necessary amount of bicarbonate to completely buffer the metabolic acidosis was calculated. This quantity was administered intravenously in small doses during a second, otherwise identical, exercise test. RESULTS: In each subject sufficient compensation for the acidosis, that is, a pH value constantly above 7.37, was attained during the second test. A delay but no disappearance of the hyperventilation was present in all participants when compared with the first test. RCP occurred on average at a significantly (p = 0.043) higher oxygen uptake (+0.15 l x min(-1)) compared with the first test. CONCLUSIONS: For the first time it was directly demonstrated that exercise induced lactic acidosis is causally involved in the hyperventilation which starts at RCP. However, it does not represent the only additional stimulus of ventilation during intense exercise. Muscle afferents and other sensory inputs from exercising muscles are alternative triggering mechanisms.

Acidosis, Lactic↗
PubMed1984

Bronchial responsiveness to hyperventilation in children with asthma: inhibition by ipratropium bromide.

Isocapnic hyperventilation dose response curves were constructed for 11 asthmatic children before and after pretreatment with placebo or ipratropium bromide, 40-1500 micrograms given by inhalation, on three separate days. The response before and after placebo was highly reproducible (within subject coefficient of variation 7.5%, 18%, and 22% for intervals of two hours, within two weeks, and over two weeks). It was independent of baseline lung function. Complete protection against hyperventilation induced asthma was achieved by ipratropium bromide 40 micrograms in six children and by 200 micrograms or more in a further four. The remaining child was unaffected by any dose of ipratropium up to 1500 micrograms. The dose of ipratropium required for protection was better related to the subjects' requirement for regular medication than to their sensitivity to hyperventilation or baseline lung function.

Adolescent↗
PubMed1985

Differences in responsiveness to hyperventilation and methacholine in asthma and chronic bronchitis.

In a previous study on 27 patients with chronic bronchitis we found that only three developed bronchoconstriction in response to hyperventilation of cold, dry air despite an increased responsiveness to methacholine inhalation. We therefore investigated bronchial responsiveness to hyperventilation with cold, dry air and methacholine in 27 patients with stable asthma who had a similar range of baseline FEV1 values but who developed bronchoconstriction that could be reversed to give an FEV1 more than 70% of the predicted value. Baseline FEV1 was 0.88-3.98 l (37-114% predicted). All but one subject developed bronchoconstriction in response to hyperventilation. There was a linear relationship between baseline FEV1 and response to methacholine (r2 = 0.37, p less than 0.001) and the relationship was significantly different from that found in the bronchitic subjects (F2.50 = 24.94, p less than 0.001). In general, the response to methacholine was greater in the asthmatic than in the bronchitic subjects for any baseline FEV1. The results suggest that there are different mechanisms underlying the increased responsiveness to methacholine in asthma and chronic bronchitis.

Adolescent↗
PubMed2006

Volitional hyperventilation during ramp exercise to exhaustion.

The purpose of this study was to determine whether volitional hyperventilation at 20 L x min(-1) above normal exercise values affected exercise duration while performing ramp exercise to exhaustion. Nine healthy subjects performed a ramp exercise test to exhaustion. On a subsequent test they hyperventilated, with the aid of visual and audio feedback, at 20 L x min(-1) greater than their initial test. Ramp exercise time to exhaustion was substantially reduced from 771.6 +/- 85.2 s to 726.6 +/- 86.6 s (p < 0.002) with the additional hyperventilation. Subjects underwent 2 more ramp exercise tests and performed a 5 s maximum voluntary ventilation or a forced vital capacity test at work rates corresponding to rest, below lactate threshold (LT), above LT, immediately after exercise, and 3 min recovery. Generally, the flow rates were not affected by exercise below LT and were enhanced during above-LT exercise, exhaustion, and recovery. This indicated a change in pulmonary function that is dependent on exercise intensity. In spite of this increased ability to generate high flow rates, exercise performance was diminished when respiratory muscle work was increased volitionally by 20 L x min(-1), indicating a strong coupling between respiratory muscle work and fatigue during ramp exercise in normal subjects.

Adult↗
PubMed1996

Augmented hyperventilation via normoxic helium breathing does not prevent exercise-induced hypoxemia.

The purpose of this study was to determine if augmented hyperventilation produced via normoxic helium breathing would reduce exercise-induced hypoxemia (EIH). Seven highly trained endurance athletes with a mean maximum oxygen uptake of 65 ml.kg-1.min-1, performed two cycle ergometer tests to volitional exhaustion. During one of the tests the subjects breathed ambient air, while during the other they breathed normoxic helium (21% O2, 79% He). Mean maximum expired ventilation significantly (p < .05) increased from 139 L.min-1 during the ambient trial to 168 L.min-1 while breathing normoxic helium. Mean arterial oxygen saturation obtained at maximum exercise, however, was not significantly different for the two trials (ambient = 90%, helium = 89%). These results suggest that significantly augmenting exercise hyperventilation by 21% essentially had no effect on EIH in endurance athletes. Thus, the data do not support the hypothesis that inadequate hyperventilation is an important mechanism for arterial oxygen desaturation during graded exercise to exhaustion in highly trained individuals.

Adult↗
PubMed1985

Sympathetic rhythms during hyperventilation-induced apnea.

The effect of hyperventilation-induced apnea on the respiratory rhythmicity of sympathetic nerve activity was determined using spectral analysis of sympathetic nerve frequencies. Left phrenic, external intercostal, and inferior cardiac sympathetic nerves were recorded in alpha-chloralose-anesthetized, vagotomized, paralyzed, artificially ventilated cats. The respiratory modulation of sympathetic activity during normoventilation was indicated by spectral peaks of sympathetic activity coinciding with respiratory frequencies determined from the phrenic nerve activity of each cat. The spectral peaks of respiratory-related sympathetic activity disappeared during hyperventilation-induced apnea and then reappeared with the return of phrenic nerve activity when normoventilation was resumed. Although sympathetic activity lost its respiratory modulation during hyperventilation, baroreceptor-mediated bilateral carotid occlusion responses and electrocardiogram (R wave)-triggered computer summation of cardiac related sympathetic activity were unaffected. Hence central respiratory inputs on sympathetic pathways in the central nervous system best explain the origin of respiratory-related sympathetic rhythms. Independent sympathetic rhythms of apparent nonrespiratory origin may be due to artificial ventilator influences, baroreflex-autonomic oscillation loops, or Mayer waves.

Animals↗
PubMed1979

Dibutyryl cyclic GMP and hyperventilation promote rat lung phospholipid release.

Ventilation of rats at high inspiratory pressures raises lung tissue content of guanosine 3',5'-cyclic monophosphate (cGMP). Hyperventilation in rabbits augments release of phospholipid into lavage fluid. Can cGMP, in the absence of hyperventilation, increase lung phospholipid release? Sprague-Dawley rats are injected with [14C]palmitate, and after 1.5 h are anesthetized and ventilated for 20 min. Three groups are ventilated at peak inspiratory pressures (PIP) of 10 cmH2O, while saline, dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP), or dibutyryl cGMP (DBcGMP) is infused into the pulmonary artery. In a fourth group, saline is infused into the pulmonary artery, but ventilation is performed with PIP of 25 cmH2O. Lung tissue and lavage fluid are then analyzed for phospholipid (PL) content and for incorporation of [14C]palmitate into lavage and tissue PL fractions. Ventilation at increased pressure and infusion of DBcGMP are associated with increases in release of labeled PL into lavage fraction. The findings suggest that the increase in lavage PL release associated with hyperventilation is, at least in part, mediated by cGMP.

Animals↗
PubMed1980

Ventilatory response to transient hyperoxia in head injury hyperventilation.

We have measured breath-by-breath instantaneous minute ventilation (VIinst) before, during, and after the administration of 10 breaths of 100% oxygen to seven male patients with head injury hyperventilation. The patients were hypoxemic (PaO2 61.2 +/- 6.3) and hypocapnic (PaCO2 26.6 +/- 5.9) with a respiratory alkalosis (pH 7.53 +/- 0.06) while breathing air. Following the oxygen VIinst fell on the average by 40 +/- 12.7% from 16.06 +/- 3.75 1.min-1 to a minimum of 9.73 +/- 3.20 1.min-1 at 20.4 +/- 2.9 s after the first breath of oxygen. In the majority of our hyperventilating patients, almost all of the resting hyperventilation could be abolished transiently by 100% oxygen. This fall in ventilation represents the peripheral chemoreceptor contribution to resting ventilation and is increased in the head injury patients in comparison with normal subjects breathing air or hypoxic gas mixtures, altitude-acclimatized subjects and patients who are hypoxic because of chronic bronchitis or interstitial lung disease. We suggest that the increased reflex hypoxic drive to ventilation found in our patients is secondary to their cerebral injury, resulting in a reduction of descending cortical inhibitory influences on the medullary respiratory control centers.

Adolescent↗
PubMed1988

Intra-airway thermodynamics during exercise and hyperventilation in asthmatics.

To determine whether exercise and hyperventilation produce the same intrathoracic thermal events in asthmatics, we used a thermal probe to record airstream temperatures during both stimuli at multiple points within the tracheobronchial tree. From these data, the global and regionally distributed exchanges of water and heat that occurred throughout the respiratory tract were calculated. During each provocation, intra-airway temperatures fell equivalently, thereby producing similar intrathoracic water fluxes and heat transfers. Neither stimulus was associated with airway drying, and both resulted in similar distributed losses of thermal energy from the tracheobronchial tree despite small regional heat and water exchanges. The degree of airway obstruction was identical after both challenges; however, the onset of airway narrowing was earlier with hyperventilation and developed in association with more rapid rewarming. These data demonstrate that the hyperpnea of exercise and hyperventilation produce identical thermal consequences within the respiratory tract of asthmatics.

Adult↗
PubMed1990

Thyroarytenoid muscle activity during hypoxia, hypercapnia, and voluntary hyperventilation in humans.

Intramuscular electromyographic activity of the thyroarytenoid (TA) muscle, a vocal cord adductor, was recorded in nine normal adult humans during progressive isocapnic hypoxia and hyperoxic hypercapnia. Four of the nine subjects also performed voluntary isocapnic hyperventilation. During quiet breathing of room air, the TA exhibited phasic activity in expiration and often tonic activity throughout the respiratory cycle. Both phasic and tonic TA activity progressively decreased with either increasing hypoxia or hypercapnia. Tonic activity appeared to decrease more rapidly than phasic activity with increasing chemical stimulation. At comparable tidal volume increments, the relative decrease in phasic TA activity appeared to be greater under hypoxic than under hypercapnic conditions. During voluntary isocapnic hyperventilation, phasic TA activity decreased without significant change in tonic activity. At tidal volumes approximately double those of base line, the relative decrease in TA activity was similar during both hypercapnia and voluntary hyperventilation, although differences appeared at higher tidal volumes. The results, in combination with recent findings in humans regarding the posterior cricoarytenoid muscle, a vocal cord abductor, suggest that vocal cord position is dependent on the net balance of counteracting forces not only during quiet breathing but also during involuntary and voluntary hyperpnea.

Adult↗
PubMed1993

Effect of inspired CO2 on ventilation and perfusion heterogeneity in hyperventilated dogs.

We studied the effect of inspired CO2 on ventilation-perfusion (VA/Q) heterogeneity in dogs hyperventilated under two different tidal volume (VT) and respiratory rate conditions with the use of the multiple inert gas elimination technique. Dogs anesthetized with pentobarbital sodium were hyperventilated with an inspired fraction of O2 of 0.21 by using an increased VT (VT = 30 ml/kg at 18 breaths/min) or an increased respiratory rate (VT = 18 ml/kg at 35 breaths/min). The arterial CO2 tension (PaCO2) was varied to three levels (20, 35, and 52 Torr) by altering the inspired PCO2. The orders of type of ventilation and PaCO2 level were randomized. Compared with normocapnia, VA/Q heterogeneity was increased during hypocapnia induced by increased respiratory rate ventilation, which was indicated by an increase in dispersion indexes and arterial-alveolar inert gas partial pressure difference areas (P < 0.01). In contrast, VA/Q heterogeneity was not affected by hypocapnia when a large VT ventilation was used. Under the conditions of our study, hypercapnia did not result in statistically significant changes in VA/Q heterogeneity with either type of ventilation. Increased VT ventilation reduced dead space at all PaCO2 levels (P < 0.01) and reduced the log standard deviation of the ventilation distribution during normocapnia (P < 0.05) and hypocapnia (P < 0.01). We conclude that hypocapnia increased VA/Q heterogeneity when hyperventilation was achieved with a rapid respiratory rate. Therefore, a lack of improvement in VA/Q matching with inhaled CO2 may be associated with the use of a large VT. These data suggest that hypocapnic bronchoconstriction may be important in mediating hypocapnia-induced VA/Q inequality in dogs.

Administration, Inhalation↗
PubMed2000

Eicosanoid and muscarinic receptor blockade abolishes hyperventilation-induced bronchoconstriction.

This study was designed to test the hypothesis that hyperventilation-induced bronchoconstriction (HIB) results from the combined effects of prostanoid and leukotriene metabolism. A bronchoscope was used in anesthetized dogs to record peripheral airway resistance and HIB before and after combined treatment with inhibitors of cyclooxygenase (indomethacin) and 5-lipoxygenase (MK-0591). Bronchoalveolar lavage fluid (BALF) cells and mediators from hyperventilated and control airways were also measured. Pretreatment with MK-0591 and indomethacin significantly attenuated, but did not abolish, HIB. However, addition of atropine nearly eliminated the residual response. Blockade of eicosanoid metabolism markedly reduced the concentrations of eicosanoids recovered in BALF after hyperventilation. Positive correlations between posthyperventilation BALF prostanoid and epithelial cell concentrations are suggestive of mucosal injury-induced mediator production and release. We conclude that HIB is prevented in the presence of eicosanoid and muscarinic-receptor blockade and that both classes of eicosanoids contribute similarly to the development of HIB.

Animals↗
PubMed2006

Bicarbonate infusion and pH clamp moderately reduce hyperventilation during ramp exercise in humans.

To test the hypothesis that the decrease in plasma pH contributes to the hyperventilation observed in humans in response to exercise at high workloads, five healthy male subjects performed a ramp exercise [maximal workload: 352 W (SD 35)] in a control situation and when arterialized plasma pH was maintained at the resting level (pH clamp) by intravenous infusion of sodium bicarbonate [129 mmol (SD 23), beginning at 59% maximal workload (SD 5)]. Bicarbonate infusion did not modify O(2) consumption (Vo(2)) but significantly (P < 0.05) increased arterial Pco(2), plasma bicarbonate concentration, and respiratory exchange ratio (P < 0.05). At the three highest workloads, pulmonary ventilation (Ve) and Ve/Vo(2) were approximately 5-10% lower (P < 0.05) when bicarbonate was infused than in the control situation, and hyperventilation was reduced by 15-30%. These data suggest that the decrease in plasma pH is one of the factors that contribute to the hyperventilation observed at high workloads.

Acid-Base Equilibrium↗
PubMed2004

Hyperoxia, reactive oxygen species, and hyperventilation: oxygen sensitivity of brain stem neurons.

Hyperoxia is a popular model of oxidative stress. However, hyperoxic gas mixtures are routinely used for chemical denervation of peripheral O2 receptors in in vivo studies of respiratory control. The underlying assumption whenever using hyperoxia is that there are no direct effects of molecular O2 and reactive O2 species (ROS) on brain stem function. In addition, control superfusates used routinely for in vitro studies of neurons in brain slices are, in fact, hyperoxic. Again, the assumption is that there are no direct effects of O2 and ROS on neuronal activity. Research contradicts this assumption by demonstrating that O2 has central effects on the brain stem respiratory centers and several effects on neurons in respiratory control areas; these need to be considered whenever hyperoxia is used. This mini-review summarizes the long-recognized, but seldom acknowledged, paradox of respiratory control known as hyperoxic hyperventilation. Several proposed mechanisms are discussed, including the recent hypothesis that hyperoxic hyperventilation is initiated by increased production of ROS during hyperoxia, which directly stimulates central CO2 chemoreceptors in the solitary complex. Hyperoxic hyperventilation may provide clues into the fundamental role of redox signaling and ROS in central control of breathing; moreover, oxidative stress may play a role in respiratory control dysfunction. The practical implications of brain stem O2 and ROS sensitivity are also considered relative to the present uses of hyperoxia in respiratory control research in humans, animals, and brain stem tissues. Recommendations for future research are also proposed.

Animals↗
PubMed1981

Beta-blocker therapy with metoprolol in the hyperventilation syndrome.

16 patients suffering from a hyperventilation syndrome were treated with metoprolol 2dd 100 mg and an identical placebo in a double-blind, cross-over trial. Before therapy and after metoprolol and placebo therapy a ventilatory response to CO2 was taken, VC and FEV1, a hyperventilation provocation test, blood gas values, and the subjective experiences of the patients were documented. The ventilatory response to CO2 was described in terms of decrease or increase of ventilation: before therapy ventilation decreased in 10 out of 16 patients, after metoprolol ventilation decreased in 3 of 16 patients (p less than 0.01). The end tidal PCO2 increased with a mean of 3.86 mm Hg (p = 0.0005) after metoprolol as compared to placebo. No differences were found in respiratory frequency or depth, base excess, provocation test. It is concluded that the cardioselective beta-blocker metoprolol is a useful drug in the therapy of the hyperventilation syndrome.

Adult↗
PubMed1984

Maternal hyperventilation as a possible cause of fetal tachycardia sub partu. A clinical and experimental study.

Examination of 28 agitated, hyperventilating patients with fetal tachycardia showed that the mothers were in a hyperventilation-related state of hypocapnia and alkalosis. The mean maternal pCO2 was 17.48 +/- 6.79 mm Hg, the pH 7.54 +/- 0.14, which caused a reflex spasm of the umbilical veins, fetal acidosis and fetal tachycardia. Additional experiments on sheep revealed a similar correlation between maternal hyperventilation, hypocapnia, respiratory alkalosis and fetal tachycardia while the flow volume of the uterus showed no change.

Alkalosis, Respiratory↗