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PubMed1990

Affective responses to hyperventilation: a test of the cognitive model of panic.

A cognitive explanation of the association between acute hyperventilation and panic attacks has been proposed: the extent to which sensations produced by hyperventilation are interpreted in a negative and catastrophic way is said to be a major determinant of panic. Non-clinical subjects were provided with a negative or a positive interpretation of the sensations produced by equivalent amounts of voluntary hyperventilation. As predicted, there was a significant difference between positive and negative interpretation conditions on ratings of positive and negative affect. Subjects in the positive interpretation condition experienced hyperventilation as pleasant, and subjects in the negative interpretation condition experienced hyperventilation as unpleasant, even though both groups experienced similar bodily sensations and did not differ in their prior expectations of the affective consequences of hyperventilation. When the subjects were given a positive interpretation, the number of their sensations correlated with positive affect; when a negative interpretation was given, the number of bodily sensations correlated with negative affect. The results provide support for a cognitive model of panic and are inconsistent with the view that panic is simply a symptom of hyperventilation syndrome.

Adult↗

PubMed2000

Effect of hyperventilation on brain tissue oxygenation and cerebrovenous PO2 in rats.

Previous studies have shown that cortical tissue oxygenation is impaired during hyperventilation. However, it is important to quantify the effect of hyperventilation on brain tissue PO(2) and cerebrovenous PO(2) simultaneously especially since cerebral venous oxygenation is often used to assess brain tissue oxygenation. The present study was designed to measure the sagittal sinus PO(2) (PvO(2)), brain tissue PO(2) in the thalamus (PtO(2)), and brain temperature (Bt) simultaneously during acute hyperventilation. Isoflurane-anesthetized rats were hyperventilated for 10 min during which time the arterial carbon dioxide tension (PaCO(2)) dropped from 40.3+4.9 mmHg to 23.5+2.8 mmHg. PtO(2) declined from 26.0+/-4.2 mmHg to 14.8+/-5.2 mmHg (P=0.004) while brain temperature decreased from 36.5+0.3 degrees C to 36.2+0.3 degrees C (P=0.02). However, PvO(2) and arterial blood pressure (BP) did not change during hyperventilation. The maintenance of PvO(2) when perfusion is thought to decline and PtO(2) decreases suggests that there may be a diffusion limitation, possibly due to selective perfusion. Therefore, cerebrovenous PO(2) may not give a good assessment of brain tissue oxygenation especially in conditions of acute hyperventilation, and deeper brain regions other than the cortex also show impaired tissue oxygenation following hyperventilation.

Animals↗

PubMed2002

Panic disorder and obsessive compulsive disorder in a hyperventilation challenge test.

BACKGROUND: Stress-induced hyperventilation produces symptoms that people are prone to misinterpret as life-threatening if they are unaware of the consequences of overbreathing. Our aim was to observe the induction of panic attacks by a hyperventilation challenge test in a series of panic disorder and obsessive compulsive disorder (OCD) patients (DSM-IV). METHOD: We randomly selected 28 panic disorder patients, 21 OCD patients and 28 normal volunteers. All patients were drug free for a week. They were induced to hyperventilate (30 breaths/min) for 4 min. Anxiety scales were applied before and after the test. RESULTS: A total of 64.3% (n=18) panic disorder patients, 9.5% (n=2) OCD patients and 3.6% (n=1) of control subjects had a panic attack after hyperventilating (chi(2)=3.99, d.f.=2, P=0.026). LIMITATIONS: The hyperventilation challenge test has a low sensitivity for panic disorder. CONCLUSION: In this challenge test the panic disorder patients were more sensitive to hyperventilation than OCD patients and normal volunteers. The induction of panic attacks by voluntary hyperventilation may be an easy test for validating the diagnosis in certain panic disorder patients.

Adult↗

PubMed2000

Epileptiform EEG during sevoflurane mask induction: effect of delaying the onset of hyperventilation.

BACKGROUND: Hyperventilation during sevoflurane-N2O-O2 mask induction in adults is associated with a hyperdynamic circulatory response and epileptiform electroencephalogram (EEG). We tested the hypothesis that delaying onset of hyperventilation will prevent severe (periodic) epileptiform EEG and hyperdynamic response. METHODS: Thirty patients were randomized to receive either delayed (group D, n=15) or immediate (group I, n=15) onset of hyperventilation during sevoflurane (8% in N2O 50%) mask inhalation induction with single-breath method for unconsciousness. Fifteen patients were allowed to breathe spontaneously for 2 min after loss of consciousness and controlled hyperventilation (ETCO2 <4%) was started thereafter. In 15 patients controlled hyperventilation was started immediately after loss of consciousness. EEG was recorded, and mean arterial pressure (MAP) and heart rate (HR) registered. RESULTS: Epileptiform EEG patterns were seen in 13 patients in group I and in 9 patients in group D (n.s.). Periodic epileptiform discharges (PED) tended to occur more often in group I (P=0.07). Heart rate and MAP were higher in group I than in group D from 2 min to 3 min (P < 0.05), and both HR and MAP rose significantly from the baseline in group I. In group D, HR but not MAP rose significantly from baseline. CONCLUSION: Regardless of its timing, hyperventilation at a high sevoflurane concentration produced severe epileptiform EEG with a hyperdynamic response. PED tended to occur more often with immediate onset of hyperventilation.

Adult↗

PubMed2000

Regional cerebral blood flow during hyperventilation in patients with acute bacterial meningitis.

Mechanical hyperventilation is often instituted in patients with acute bacterial meningitis when increased intracranial pressure is suspected. However, the effect on regional cerebral blood flow (CBF) is unknown. In this study, we measured regional CBF (rCBF) in patients with acute bacterial meningitis before and during short-term hyperventilation. In 17 patients with acute bacterial meningitis, absolute rCBF (in ml/100 g min-1) was measured during baseline ventilation and hyperventilation by single-photon emission computed tomography (SPECT) using intravenous 133Xe bolus injection. Intravenous 99mTc-HMPAO (hexamethylpropyleneamine oxime) was subsequently given during hyperventilation. In 12 healthy volunteers, rCBF was measured by SPECT and 99mTc-HMPAO during spontaneous ventilation. Using standard templates to identify regions of interest (ROIs), we calculated rCBF in percentage of cerebellar (99mTc-HMPAO images) or mean hemispheric (133Xe images) flow for each ROI, the degree of side-to-side asymmetry for each ROI, and the anterior-to-posterior flow ratio. On 133Xe images, absolute rCBF decreased significantly during hyperventilation compared to baseline ventilation in all regions, but the relative rCBF did not change significantly from baseline ventilation (n=14) to hyperventilation (n=12), indicating that the perfusion distribution was unchanged. On 99mTc-HMPAO images (n=12), relative rCBF and the anterior-to-posterior flow ratio were significantly lower in patients than in controls in the frontal and parietal cortex as well as in the basal ganglia. Focal perfusion abnormalities were present in 10 of 12 patients. Regional cerebral blood flow abnormalities are frequent in patients with acute bacterial meningitis. Short-term hyperventilation does not enhance these abnormalities.

Adult↗

PubMed2001

Hyperventilation facilitates induction of supraventricular tachycardia: a novel method and the possible mechanism.

INTRODUCTION: Hyperventilation has been demonstrated to alter autonomic function. Sympathomimetic drugs (isoproterenol) and parasympatholytic drugs (atropine) may be needed to facilitate induction of supraventricular tachycardia (SVT). The aim of this study was to test the clinical utility and mechanisms of hyperventilation to facilitate SVT initiation. METHODS AND RESULTS: Fourteen patients with clinically documented SVT (9 AV nodal reentrant tachycardia and 5 AV reciprocating tachycardia) but noninducible during baseline electrophysiologic study were included. Immediately after hyperventilation test (at least 30 respirations/min) for 2 minutes, systolic blood pressure, sinus cycle length, anterograde and retrograde 1:1 conduction, and induced SVT were measured. Arterial blood gas, pH, and heart rate variability before and after hyperventilation were measured. Seven of nine patients with AV nodal reentrant tachycardia and 3 of 5 patients with AV reciprocating tachycardia could be induced immediately after the hyperventilation test. After hyperventilation, anterograde AV and retrograde VA 1:1 conduction were improved, sinus cycle length was decreased, and heart rate variability were decreased in both groups. CONCLUSION: Hyperventilation can facilitate induction of SVT. Improvement of conduction properties and changes of autonomic function are the possible mechanisms.

Accessory Nerve↗

PubMed1994

Hyperventilation in the treatment of metabolic acidosis does not adversely affect pulmonary gas exchange.

BACKGROUND: Hyperventilation has been recommended to increase blood pH during metabolic acidosis. However, hypocapnia may adversely affect arterial blood oxygenation, especially in the presence of lung disease. We therefore studied the effects of metabolic acidosis, with and without normalization of pH by hyperventilation, on pulmonary gas exchange in dogs with permeability pulmonary edema. METHODS: Six pentobarbital-anesthetized dogs were administered 0.06 ml/kg of oleic acid at least 150 min before study. Ventilation was set with an inspired O2 fraction of 0.90 and a tidal volume of 18 ml/kg, and the respiratory rate was adjusted to alter the arterial CO2 tension (PaCO2) per the experimental protocol. The protocol in random order was (1) normal pH (7.36 +/- 0.01)/normal PaCO2 (39 +/- 1 mmHg); (2) low pH 7.20 +/- 0.01)/normal PaCO2 (40 +/- 1 mmHg); (3) low pH (7.18 +/- 0.01)/hyperventilation with inspired CO2 (PaCO2 = 40 +/- 1 mmHg); and (4) normal pH (7.35 +/- 0.01)/hyperventilation with low PaCO2 (24 +/- 1 mmHg). In phases 2-4, the pH was slowly reduced by intravenous infusion of 2 N hydrochloric acid. The pH was normalized in phase 1 where necessary by infusion of sodium bicarbonate. The pH in phase 4 was normalized by reducing the PaCO2 by increasing the respiratory rate. Gas exchange was assessed by the multiple inert-gas elimination technique. RESULTS: The hemodynamic measurements remained constant throughout the protocol. Arterial O2 tension increased from 244 +/- 55 to 293 +/- 49 mmHg in the presence of metabolic acidosis (P < 0.05). Hyperventilation to normalize the pH during metabolic acidosis (phase 4), increased arterial O2 tension (313 +/- 44 mmHg, P < 0.05), and reduced shunt (from 20 +/- 5% to 12 +/- 3%, P < 0.05) compared with normal acid-base conditions (phase 1). No change in shunt was observed with hyperventilation compared with metabolic acidosis alone (phase 2). The decrease in pulmonary shunt was not attributable to the direct effects of hyperventilation, because shunt was increased (20 +/- 5%) when PaCO2 was normalized during hyperventilation by inspiration of CO2 (phase 3). CONCLUSIONS: Hyperventilation to normalize blood pH during hydrochloric acid-induced metabolic acidosis did not adversely affect pulmonary gas exchange in dogs with permeability pulmonary edema.

Acidosis↗

PubMed1998

Quantitative topographical analysis of EEG during nonstandardized and standardized hyperventilation.

The aim of this study was to compare the topographical quantitative EEG (qEEG) changes induced by nonstandardized hyperventilation and those induced by standardized hyperventilation (with the end-tidal PCO2 being maintained at 2 kPa [15 mm Hg]). We examined 18 healthy volunteers during nonstandardized and 20 during standardized hyperventilation. During nonstandardized hyperventilation, the mean spectral power density in this group significantly increased 1.9 fold within the delta-, 2.2 fold within the theta-, 1.8 fold within the alpha-, and 1.9 fold within the beta-frequency band. There was no significant change of the power ratio and was no topographic difference between 4 frequency bands investigated. During standardized hyperventilation, the mean spectral power density in the group significantly increased to 12.9 fold within the delta-, to 7.6 fold within the theta-, to 1.4 fold within the alpha-, and to 2.4 fold within the beta frequency band. The power ratio decreased significantly. Such a pronounced EEG slowing with delta and theta augmentation was never found during nonstandardized hyperventilation. We conclude that a consistent slowing of the qEEG in all leads including a constant topographical maximum can only be induced by standardized, sufficiently pronounced hyperventilation.

Adult↗

PubMed1998

Vestibular disease unmasked by hyperventilation.

Hyperventilation-induced dizziness is often thought to be psychogenic, but its effects in the presence of known vestibular disease have not been adequately examined. In this study hyperventilation was tested in two models of vestibular disease. These were, first, patients with profound unilateral vestibular deficit (prior translabyrinthine acoustic neuroma resection [postsurgery group]) and, second, patients with variable unilateral vestibular deficit (unoperated unilateral acoustic neuroma [presurgery group]). Patients were hyperventilated for 90 seconds. Using infrared videonystagmography, 100% of the 32 postsurgery patients and 82% of the 28 presurgery patients developed nystagmus with hyperventilation. Hyperventilation was more sensitive than head shake for eliciting nystagmus in these models. The false-positive rate for nystagmus in 29 normal volunteers was 3.5% for hyperventilation and 10% for head shake. Our results show that hyperventilation can unmask underlying vestibular disease.

Dizziness↗

PubMed1994

Central and regional blood flow during hyperventilation. An experimental study in the pig.

Mechanical hyperventilation not only reduces brain oedema after neurotrauma but also affects the central and systemic circulation. We have, in pigs, measured blood flow in the pulmonary artery, the portal vein and in the femoral artery, as well as estimated the splanchnic blood flow and studied the relative perfusion using the microsphere technique in normo- and hypocarbia during intermittent positive pressure ventilation. A normoventilated control group did not change in cardiac output, portal vein blood flow, splanchnic blood flow and femoral arterial blood flow. Hyperventilation was performed to a PCO2 of 3.0 +/- 0.1 kPa. We found that in pigs ventilated with high tidal volume skeletal muscle blood flow did not change during the first 60 min of hyperventilation but gradually decreased thereafter. Blood flow to the cerebellum decreased soon after the induction of hyperventilation, whereas the cerebral blood flow did not decrease until the second hour of hyperventilation. Cardiac output, splanchnic perfusion and portal vein blood flow all decreased. Myocardial perfusion and arterial blood flow to spleen and kidney decreased while pancreatic and liver arterial blood flows were unaffected. It is concluded that mechanical hyperventilation with low frequency and large tidal volumes reduces the flow to most tissues, where the relative decrease according to microsphere measurements is most pronounced in skeletal muscles, heart muscle and cerebellum. However, the changes in cardiac output and splanchnic blood flow were not observed when hyperventilation was induced by increased frequency, keeping the tidal volume constant.

Animals↗

PubMed2007

Effects of bronchodilators on dynamic hyperinflation following hyperventilation in patients with COPD.

BACKGROUND AND OBJECTIVE: The present study was performed to examine the occurrence of dynamic hyperinflation following hyperventilation in COPD patients and former smokers without COPD, and the efficacy of short-acting anticholinergic agents (SAAC) and beta2-agonists (SABA) for lung hyperinflation following metronome-paced hyperventilation in COPD. METHODS: Fifty-nine patients with COPD, 20 ex-smokers without COPD and 20 healthy subjects who had never smoked were examined for dynamic hyperinflation by metronome-paced hyperventilation with respiratory rate increasing from 20 to 30 and 40 tidal breaths/min. Dynamic hyperinflation was evaluated as the decrease in inspiratory capacity (IC) following hyperventilation, and the effects of SAAC and SABA on dynamic hyperinflation were assessed. RESULTS: COPD patients showed a significant increase in end-expiratory lung volume and a decrease in IC following hyperventilation, and ex-smokers without COPD also showed mild but significant dynamic hyperinflation. Multiple stepwise linear regression analysis revealed that the carbon monoxide transfer coefficient (DLco/VA) and RV/TLC were significant and independent determinants of dynamic hyperinflation in COPD. Treatment with SAAC and SABA significantly increased IC at each respiratory rate, independently of the increases in FEV1. Furthermore, SABA significantly inhibited the decrease in IC due to hyperventilation. CONCLUSIONS: These findings suggest that lung hyperinflation following hyperventilation may be a useful method for detecting dynamic hyperinflation observed not only in patients with COPD but also in ex-smokers without COPD, and both SAAC and SABA are effective in reducing dynamic hyperinflation in COPD.

Administration, Inhalation↗

PubMed1995

Hyperventilation, central autonomic control, and colonic tone in humans.

Symptoms attributable to hyperventilation are common among patients with the irritable bowel syndrome (IBS); indeed, some have suggested that hyperventilation may exacerbate the alimentary symptoms of IBS. Hyperventilation changes haemodynamic function through central and peripheral mechanisms; its effects on colonic motor function, however, are unknown. The aim of this study, therefore, was to assess the effects of hyperventilation on colonic tone and motility and on cardiovascular autonomic activity, and to discover if hypocapnia was critical to elicit the response. Phasic and tonic motility of the transverse and sigmoid colon, end tidal PCO2, pulse rate, and beat to beat pulse variability were assessed before, during, and after a five minute period of hypocapnic hyperventilation in 15 healthy volunteers; in seven other subjects, effects of both eucapnic and hypocapnic hyperventilation were evaluated. Hypocapnic but not eucapnic hyperventilation produced an increase in colonic tone and phasic contractility in the transverse and sigmoid regions and an increase in pulse rate and pulse interval variability. The findings are consistent with inhibition of sympathetic innervation to the colon or direct effects of hypocapnia on colonic smooth muscle, or both. These physiological gut responses suggest that some of the changes in colonic function are caused by altered brain or autonomic control mechanisms.

Adult↗

PubMed1988

Role of cooling and drying in hyperventilation induced asthma.

Respiratory heat loss has been proposed as a mechanism of exercise induced asthma. Whether the predominant stimulus is airway drying or cooling remains unclear. We have measured changes in FEV1 after isocapnic cold air hyperventilation (CAH) (-23.4 degrees (SD 0.43 degrees) C) and dry ambient air hyperventilation (AAH) (18.7 degrees (0.52 degrees)C) in seven asthmatic patients (mean age 31 (SD 9) years and baseline FEV1 3.2(0.9)1) and in seven normal subjects (age 28(6) years and FEV1 3.6(0.7)1). The inspired water content in both cases was 0.3 mg/l air. The rate of respiratory heat exchange per breath was calculated in watts (W) with microcomputer based equipment. Cold air hyperventilation caused a fall in FEV1 almost twice that of ambient air hyperventilation at each level of ventilation: CAH v AAH (% fall) 8.0 (5.1) v 3.9 (4.0) at 15 l/min, 11.6 (7.8) v 7.0 (4.4) at 30 l/min, and 20.7 (10.9) v 12.4 (6.3) at 60 l/min. Identical latent heat loss (evaporative drying) was imposed on the airway during the two challenges. Sensible heat loss (convective cooling) in cold air hyperventilation was 41 W at 15 l/min, 63 W at 30 l/min, and 114 W at 60 l/min; whereas in ambient air hyperventilation the loss was 6, 13, and 23 W respectively. It is concluded that the rate of cooling of the upper airway is the predominant stimulus in hyperventilation induced asthma.

Adult↗

PubMed1991

Effect of inhaled budesonide on bronchial reactivity to histamine, exercise, and eucapnic dry air hyperventilation in patients with asthma.

BACKGROUND: It has been suggested that inhaled corticosteroids may provide greater protection against constrictor stimuli that act indirectly such as exercise than those that act directly such as histamine. METHODS: The effects of six weeks treatment with inhaled budesonide (800 micrograms twice daily) on bronchial reactivity to histamine, exercise, and eucapnic voluntary hyperventilation of dry air were compared in a double blind, placebo controlled, non-crossover study in 40 subjects with asthma. Change in bronchial reactivity to histamine and eucapnic hyperventilation over the six weeks was measured as change in the provocative dose of histamine or dry air causing a 20% fall in FEV1 (PD20 histamine and PV20 eucapnic hyperventilation (EVH) of dry air); this was not possible for exercise because of the development of refractoriness. To enable the change in response to all three stimuli to be compared, the response (percent fall in FEV1) to a fixed dose was measured for all three challenge tests. RESULTS: After budesonide there was an increase in PD20 histamine from 0.48 to 2.81 mumol and in PV20 EVH from 364 to 639 litres, and a significant correlation between the changes in PD20 histamine and PV20 EVH (r = 0.63). The median percentage fall in FEV1 in response to eucapnic hyperventilation, exercise, and histamine was similar before budesonide (25.5%, 26.6%, and 24.5%); the reduction in the percentage fall in FEV1 with budesonide was also similar for the three challenges (18.9%, 17.5%, and 16.6%), and all differed significantly from the changes following placebo. There was a significant correlation between change in percentage fall in FEV1 after budesonide with the three stimuli (histamine v exercise: r = 0.48; histamine v eucapnic hyperventilation: r = 0.46; exercise v eucapnic hyperventilation: r = 0.63). CONCLUSION: The similar magnitude of change in bronchial reactivity to all three stimuli after budesonide and the within subject correlation obtained between these changes suggest that corticosteroids act by a common mechanism to protect against eucapnic hyperventilation, exercise, and histamine.

Administration, Inhalation↗

PubMed1982

Effects of hyperventilation on pulmonary blood flow and recirculation time of humans.

We used direct invasive techniques to measure the effects of hyperventilation on the pulmonary blood flow (Q) and on recirculation time of helium and of carbon dioxide in humans. The subjects hyperventilated with a tidal volume of 1.5 liters (BTPS) and a frequency of 20 or 30 breaths/min. There was no significant change in Q from control at either level of hyperventilation. Helium first appeared in the pulmonary artery within 12 s from the onset of hyperventilation and increased by approximately 0.7% of its equilibrium arterial value per second at both levels of hyperventilation. In contrast, the PVCO2 remained at base-line level until 43 s from the onset of hyperventilation. We conclude that hyperventilation at 30 or 45 l/min with constant tidal volume does not significantly affect the value of Q and that the amount of recirculation of the two gases does not result in underestimation of Q when this variable is measured by indirect respiratory rebreathing techniques.

Adult↗

PubMed1987

Effect of cold and warm dry air hyperventilation on canine airway blood flow.

Tracheobronchial blood flow increases with cold air hyperventilation in the dog. The present study was designed to determine whether the cooling or the drying of the airway mucosa was the principal stimulus for this response. Six anesthetized dogs (group 1) were subjected to four periods of eucapnic hyperventilation for 30 min with warm humid air [100% relative humidity (rh)], cold dry air (-12 degrees C, 0% rh), warm humid air, and warm dry air (43 degrees C, 0% rh). Five minutes before the end of each period of hyperventilation, tracheal and central airway blood flow was determined using four differently labeled 15-micron diam radioactive microspheres. We studied another three dogs (group 2) in which 15- and 50-micron microspheres were injected simultaneously to determine whether there were any arteriovenous communications in the bronchovasculature greater than 15 micron diam. After the last measurements had been made, all dogs were killed, and the lungs, including the trachea, were excised and blood flow to the trachea, left lung bronchi, and parenchyma was calculated. Warm dry air hyperventilation produced a consistently greater increase in tracheobronchial blood flow (P less than 0.01) than cold dry air hyperventilation, despite the fact that there was a smaller fall (6 degrees C) in tracheal tissue temperature during warm dry air hyperventilation than during cold dry air hyperventilation (11 degrees C), suggesting that drying may be a more important stimulus than cold for increasing airway blood flow. In group 2, the 15-micron microspheres accurately reflected the distribution of airway blood flow but did not always give reliable measurements of parenchymal blood flow.

Animals↗

PubMed1994

Bronchial reactivity to isocapnic hyperventilation: results in an unselected population of outpatients with known or suspected asthma.

Isocapnic hyperventilation with dry air is nearly as effective as with dry cold air, and appears to be a valuable screening test for bronchial hyperresponsiveness. However some incidental factors such as prechallenge bronchoconstriction, level of hyperventilation, age and smoking habits have barely been examined or were investigated in small samples of either normals or well-characterised asthmatics. In an inhomogeneous population of 186 outpatients with known asthma, 286 with suspected asthma and 32 normals, a single isocapnic hyperventilation challenge of 6-min duration was performed. There was a weak, but significant correlation between the degree of prechallenge airway function and the bronchial response, assessed by the change in forced expiratory volume in 1 s (r = 0.27, p = 0.000) in known asthmatics, but not in patients with suspected asthma and in normals. No significant relation was found between the level of hyperventilation and the bronchial response when comparing the bronchial response to the single-dose hyperventilation test between the subjects (NS). Increasing age appears to be associated with an attenuation of the response in known asthmatics (r = 0.21, p = 0.004), but not in patients with suspected asthma. Smoking habits did not affect the bronchial response in this study. In conclusion, the main finding is that there is a weak correlation between baseline airway obstruction and the subsequent response to isocapnic hyperventilation, a slow decline in response with age and no increase in responsiveness in smokers. Hence, isocapnic hyperventilation is a relatively robust test for assessing bronchial reactivity in an inhomogeneous population of outpatients like ours.

Adolescent↗

PubMed1985

Hyperventilation-induced bronchoconstriction in guinea pigs.

The purpose of this study was to investigate the pulmonary effects of hyperventilation in anesthetized, mechanically ventilated guinea pigs. Airway resistance (Raw), dynamic lung compliance (CDyn), blood pressure (BP), heart rate (HR), arterial blood gases (PaO2, PaCO2), pH and arterial plasma HCO3- were measured before and after a 10-min period of hyperventilation produced by increasing the respiratory rate from 60 to 120 breaths/min while maintaining tidal volume at 4 ml. There was a significant increase in Raw and decrease in CDyn lasting up to 20 min after hyperventilation was stopped with no change in BP and HR. PaO2 was reduced from 109 +/- 3 mm Hg before to 53 +/- 7 mm Hg at 5 min after hyperventilation. The Raw and CDyn changes were prevented and reversed with the bronchodilators salbutamol and aminophylline indicating that reversible bronchospasms are induced in guinea pigs following a period of hyperventilation. Additional studies demonstrated that the pulmonary mechanical responses to hyperventilation were not changed by vagotomy, ventilation with high CO2 or by pretreatment with chlorpheniramine, methysergide, atropine, indomethacin, FPL 55712 or calcium-influx blockers. These results indicate that neither vagal reflexes, airway hypocapnia, receptors of histamine, serotonin, acetylcholine nor the products of arachidonic acid metabolism were involved in hyperventilation-induced bronchospasm in guinea pigs.

Airway Resistance↗