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PubMed1991

Effects of tromethamine and hyperventilation on brain injury in the cat.

The metabolic brain acidosis after trauma has been thought to be harmful and to contribute to neurological deterioration. Amelioration of the brain acidosis either by systemic buffering agents or by hyperventilation has been proposed as a method of treatment. The objective of this study was to explore with magnetic resonance (MR) spectroscopy the metabolic changes in brain that occur with the use of hyperventilation, THAM (tromethamine; tris[hydroxymethyl]aminomethane), and a combination (THAM and hyperventilation) therapy in experimental fluid-percussion injury. Brain lactate, brain pH, inorganic phosphate (Pi), and adenosine triphosphate levels were measured by 1H and 31P MR spectroscopy. Arterial and cerebrovenous lactate and water content in brain tissue was determined in 29 cats using the specific gravimetric technique. Following injury, the phosphocreatine (PCr)/Pi ratio, which is an index of cerebral energy depletion, decreased to 76% in four untreated animals, to 79% in 11 THAM-treated animals, to 68% in seven animals receiving hyperventilation, and to 66% in seven animals with combination THAM and hyperventilation therapy. The PCr/Pi ratio returned to a normal level in 8 hours in animals treated with THAM and THAM in combination with hyperventilation. The brain lactate index increased to 157% in the hyperventilation group after trauma. In cats receiving THAM plus hyperventilation, the brain lactate index was reduced to 142%, while the minimum rise of 126% was associated with treatment of THAM alone. In the THAM-treatment and combination-treatment groups, the water content of the white and gray matter was significantly decreased compared with that in untreated cat brains. Prolonged hyperventilation provided relative ischemia in brain tissue and promoted more production of brain lactate, no recovery of the PCr/Pi ratio, and no decrease in brain edema. On the other hand, administration of THAM decreased production of brain lactate and brain edema and promoted the recovery of cerebral energy dysfunction. It was found that THAM ameliorates the deleterious effects of hyperventilation by minimizing energy disturbance and that it also decreases brain edema. The authors conclude that THAM may be effective in reducing brain tissue acidosis and helpful as a metabolic stabilizing agent following severe head injury.

Acidosis, Lactic↗

PubMed1989

Hyperventilation and ergonovine tests in Prinzmetal's variant angina pectoris in men.

Hyperventilation and ergonovine tests were carried out in a group of 30 patients with variant angina to assess the sensitivity of the 2 tests and to correlate the response with spontaneous disease activity. Hyperventilation produced a positive response in 83% (25 of 30) and ergonovine in 93% (28 of 30) of the patients. After hyperventilation 22 of 25 showed ST-segment elevation, 2 ST depression and 1 T-wave pseudonormalization; after ergonovine ST-segment elevation developed in 23 patients, ST depression in 4 and T-wave pseudonormalization in 1. In all cases the electrocardiographic changes occurred in the same leads as during the spontaneous attacks. The incidence of chest pain and ventricular arrhythmias was similar during both tests; spontaneous remission of ischemia, however, was more frequent (48 vs 14%) after hyperventilation than after ergonovine. Acute ischemia developed at a mean of 218 +/- 112 seconds after the end of hyperventilation in 19 of 25 positive tests; at that time double product was not significantly different from basal values. The sensitivity of hyperventilation was similar (95 vs 100%) to ergonovine in the patients with greater than or equal to 1 daily attack, while in those with less than 1 daily attack the sensitivity of hyperventilation decreased to 55% compared to 77% with ergonovine. Thus, in variant angina the sensitivity of both tests correlates with disease activity. Hyperventilation is a safe provocative test with a sensitivity similar to ergonovine in patients with active disease; however, in patients with sporadic attacks hyperventilation has a lower sensitivity than ergonovine and therefore a limited diagnostic value.

Adult↗

PubMed1990

Waning of panic sensations during prolonged hyperventilation.

Recent theories about panic emphasize that a hyperventilatory positive feedback loop is involved in panic: catastrophic misinterpretation of bodily sensations may trigger anxiety, anxiety may stimulate hyperventilation, hyperventilation may promote the salience of feared sensations etc. Such models leave unexplained how and when panics come to an end. It was hypothesised that panic with hyperventilation may end because pronounced hyperventilation becomes, in the course of time, less powerful in generating perceivable bodily sensations. Twenty healthy subjects hyperventilated forcefully and experienced clear panic symptoms as defined by DSM IIIR. When pCO2 was kept 55% below base line for 90 min, panic symptoms waned. The mean intensity of the symptoms declined as did the number of symptoms occurring. No panic symptoms were observed in the control group (n = 20) who ventilated normally. In so far as hyperventilation is involved in the positive feedback loops that characterize panic, panic attacks may be time-limited because sensations induced by hyperventilation become less salient even if massive hyperventilation continues. As to the explanation of the reported phenomenon, it is suggested that, apart from habituation, local physiological changes due to prolonged hyperventilation may produce a decrease in interoceptive input.

Adult↗

PubMed1991

Hyperventilation-induced panic attacks in panic disorder with agoraphobia.

Eight minutes of hyperventilation to an end-tidal PCO2 of less than 20 mmHg led to a panic attack in 7 of 12 patients with panic disorder with agoraphobia and only 1 of 12 normal controls. Patients experienced greater increases in panic symptoms than controls during hyperventilation. Patients who reported more distress from somatic symptoms of hyperventilation during the preceding week were more likely to panic during hyperventilation. Patients who panicked during hyperventilation exhibited a delayed recovery of normocapnia following hyperventilation. Hyperventilation by this protocol is an effective means of inducing panic attacks in the laboratory. A hyperventilation challenge may identify a subgroup of patients for whom hyperventilation symptoms are frequently associated with panic.

Adult↗

PubMed1987

Provocative testing with prolonged hyperventilation and ergometrine in patients suspected of coronary artery spasm: a comparative study.

We induced coronary vasoconstriction by hyperventilation for 6 minutes (arterial pH = 7.6 +/- 0.06) and ergometrine (0.4 mg) in 24 patients suspected of coronary vasospasm. ST deviation greater than or equal to 1 mm was induced in 12 patients by hyperventilation and in 10 by ergometrine. Using spontaneous ST deviation as the independent reference the sensitivity of hyperventilation was 86% and the sensitivity of ergometrine 77%. Ergometrine caused sinus bradycardia and hypotension in 3 patients; hyperventilation caused no untoward reactions. In 12 of the patients coronary angiogram and wedge pressure were obtained during provocative testing. A computer-assisted analysis of coronary diameters in 43 arterial segments (3-4 per patient) showed a 16 +/- 12.6% and 14 +/- 16.7% reduction after hyperventilation and ergometrine, respectively. The maximal coronary diameter reduction induced by hyperventilation and ergometrine was 26 +/- 13.9% and 28 +/- 15.0%, respectively, and showed a significant correlation between the two tests (r = 0.77, N = 12, P less than 0.01). The wedge pressure increase induced by hyperventilation correlated to the maximal coronary diameter reduction (r = 0.63, N = 12, P less than 0.05), while no such correlation was found by ergometrine testing. We conclude that hyperventilation leading to arterial pH about 7.6 has essentially the same potency as 0.4 mg ergometrine, but the hyperventilation test appears to be safer.

Angiography↗

PubMed1990

Hyperventilation-induced EEG changes in humans and their modulation by an anticonvulsant drug.

Surface-negative DC shifts, arising from depolarization of apical dendrites of cortical pyramidal cells, represent excitability of cortical neuronal networks. Hyperventilation, used in epilepsy diagnosis to provoke epileptiform discharges, is thought to increase excitability of neuronal tissue; correspondingly, hyperventilation produces negative DC shifts. Extreme negative DC shifts, accompanying epileptiform EEG patterns, have been observed in epileptic patients during hyperventilation. Anticonvulsants, supposed to dampen cortical excitability, should inhibit the development of overexcitability and, hence, also of pronounced negative DC shifts. The present study examined DC shifts induced by hyperventilation in healthy human subjects under the influence of the benzodiazepine, clonazepam, which is used as anticonvulsant. In a double-blind setting, 36 male student volunteers received 4.5 mg clonazepam or the equivalent amount of placebo. DC-EEG and respiration rate were measured during 3 periods each of 3 min: baseline, hyperventilation, and recovery. Compared to baseline, hyperventilation produced a negative DC shift of an average 36 +/- 8 microV under placebo conditions. Clonazepam reduced the hyperventilation-induced negativity to 13 +/- 5 microV. Negativity suppression became weakened with increasing blood plasma levels of the drug. Respiration depth and frequency, increasing under hyperventilation, did not differ among the groups. Clonazepam treatment gave rise to beta-waves and prevented the increase in alpha and theta activity that was found in placebo subjects during the recording period; this was only true, however, for low to moderate plasma concentrations of clonazepam. Results are consistent with the notion that a hyperventilation-induced increase in neuronal excitability can be measured by cortical DC shifts. The reduction of negative shifts under anticonvulsants might indicate dampening of cortical neuronal excitability which is intended by antiepileptic drugs.

Adult↗

PubMed1988

Hyperventilation in the awake state: potentially treatable component of Rett syndrome.

Hyperventilation, which occurs in some patients with severe mental handicap, is a prominent feature in the histories of most girls with Rett syndrome but its mechanism and effects have not been established. Respiratory function was therefore studied in 18 patients with Rett syndrome and 23 healthy controls. Ten of the patients (56%), but none of the controls, hyperventilated only when awake, and began doing so after a period of normal breathing without hypoxaemia. After hyperventilation was established it was interspersed with prolonged periods of apnoea (over 19 seconds) accompanied by Valsalva manoeuvres. Hypoxaemia (less than 90%) occurred in 47% of these periods of apnoea and five (50%) of the patients had oxygen saturation values of under 50%. During hyperventilation severe hypocapnia developed in every patient, and recorded arterial pH measurements ranged from 7.47 to 7.60. A further four patients (22%) did not hyperventilate, but had clear histories of hyperventilation when younger. All had frequent apnoeic pauses accompanied by Valsalva manoeuvres. The remaining four girls (22%) neither hyperventilated nor gave a clear history of doing so. Three had occasional apnoeic pauses associated with the Valsalva manoeuvres. All but one of the 18 patients had increased quantities of periodic apnoea compared with the control subjects. The hypocapnic alkalaemia and hypoxaemia resulting from hyperventilation may contribute to the cerebral impairment in Rett syndrome. Since the hyperventilation is 'primary', and not secondary to preceding apnoea, it is potentially treatable. Further studies will determine if treatment is practical and of benefit.

Adolescent↗

PubMed1989

Effect of magnesium on anginal attack induced by hyperventilation in patients with variant angina.

To examine whether or not magnesium suppresses coronary spasm, the effect of magnesium infusion on anginal attacks induced by hyperventilation was studied in 20 patients with variant angina. In all patients, anginal attacks associated with ischemic ST segment changes on the electrocardiogram were repeatedly induced by hyperventilation. The study was performed in the early morning successively for 3 days. On days 1 and 3 (control studies), 50 minutes before the hyperventilation test, a 5% glucose solution was infused as a placebo. On day 2 (magnesium study), 50 minutes before the hyperventilation test, magnesium sulfate (0.27 mM/kg body wt) was infused during a 20-minute period. During the control studies, anginal attack was induced by hyperventilation in all 20 patients, whereas during the magnesium study, anginal attack was induced by hyperventilation in only six (30%) of the 20 patients (p less than 0.001 vs. control studies). The changes in arterial blood pH and PCO2 caused by hyperventilation were not significant between the control study and the magnesium study. Mean serum magnesium concentration increased from 2.2 +/- 0.2 to 6.0 +/- 0.5 mg/dl immediately after infusing magnesium and was 4.5 +/- 0.6 mg/dl before the hyperventilation test during the magnesium study. We conclude that magnesium suppresses anginal attacks induced by hyperventilation in patients with variant angina.

Aged↗

PubMed1985

[Cerebral angiography following hyperventilation in moyamoya disease--in reference to the "re-build up" phenomenon on EEG].

It is a well known fact that ischemic symptoms are apt to be induced after hyperventilation in child case of Moyamoya disease. We have previously noted that characteristic EEG findings are seen after hyperventilation in this disease. Among these findings, characteristic slow waves which appear after the disappearance or attenuation of ordinary build up have been labelled as "re-build up". Since this phenomenon is highly pathognomonic, we have been evaluating EEG records as an important screening test for childhood Moyamoya disease. Sequential angiograms were taken to understand the nature and pathophysiology of the "re-build up" phenomenon. We now report some interesting findings thought to be related to the particular hemodynamics and pathology of childhood Moyamoya disease. Hyperventilation angiography was performed in 17 patients with Moyamoya disease (7 children, 5 adults whose onset was in childhood and 5 adults). A control study was performed in 5 patients (one child and 4 adults) who were angiographically normal. In each patient, the presence or absence of the "re-build up" phenomenon in the EEG was determined within 1 month prior to the angiographical examination. Angiography was performed prior to 3 minutes of hyperventilation and in the period of "re-build up" under the same conditions with respect to position, site of the catheter tip, volume and the rate of injected contrast media and timing of angiography. In control cases and those cases which did not show "re-build up," angiography was performed 1 minute after termination of hyperventilation. During examination, serial arterial blood sampling was carried out for blood gas analysis. In two cases of Moyamoya disease, hyperventilation under inhalation of 8% CO2 was also performed. In patients with Moyamoya disease who showed the "re-build up" phenomenon, angiographical vascular changes such as decrease in the size of basal Moyamoya and decrease in the diameter of cortical arteries appeared together with "re-building up." These vascular changes are thought to be closely related to the "re-build up" phenomenon. In control cases and adult patients, these findings were not observed. Since these vascular changes did not occur in patients with the "re-build up" phenomenon after hyperventilation of 8% CO2, this phenomenon is thought to be initiated as a direct result of decreased arterial CO2 tension. Although during hyperventilation PaO2 increased, after hyperventilation it decreased significantly while the EEG showed "re-build up".(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

PubMed1985

The effect of verapamil and inspired CO2 on the bronchoconstriction provoked by hyperventilation in normal humans.

Two groups of eight normal subjects were investigated in separate studies to demonstrate the effects of changes in end-tidal PCO2, and of pretreatment with the calcium antagonist drug verapamil, on bronchoconstriction provoked by voluntary hyperventilation. Total respiratory resistance (Ros) was measured by the forced oscillation technique before and after 90 s voluntary hyperventilation. End-tidal PCO2 during hyperventilation was varied by altering inspired CO2 concentration. When end-tidal PCO2 fell during hyperventilation, there was a rise in Ros. This did not occur if end-tidal PCO2 was controlled at a normal resting level during hyperventilation. Specific conductance (sGaw) was measured before and after 90 s voluntary hyperventilation of air. Subjects were treated with oral verapamil or placebo for 2 1/2 days and the effect of hyperventilation on sGaw was reassessed. Verapamil reduced significantly the fall in sGaw caused by hyperventilation. Placebo had no effect. In normal humans, bronchoconstriction provoked by hyperventilating air at ambient temperature and humidity is mediated by the fall in PCO2, and is also reduced by verapamil.

Adult↗

PubMed1988

Mechanisms of the haematological changes induced by hyperventilation.

During voluntary hyperventilation an increase in the lymphocyte and thrombocyte counts occurs, paralleled by an increase in plasma epinephrine and norepinephrine. All these changes are rapidly reversible after hyperventilation and are followed by an increase in the neutrophil granulocyte count. The pathophysiological mechanisms of these changes were investigated by comparison of the hyperventilation-induced changes of the blood picture in 11 normal, 9 splenectomized and 12 beta-blocked volunteers. Splenectomy did not affect the hyperventilation-induced mobilization of lymphocytes and neutrophils but totally suppressed the change in the thrombocyte count. beta-blockade by 80 mg propranolol did not suppress the hyperventilation-induced increase in neutrophils. It reduced the absolute increase of lymphocytes and thrombocytes by half, but it also increased the baseline counts of these cells. The study shows that hyperventilation mobilizes thrombocytes from the spleen but not from extralienal pools, and that lymphocytes and neutrophils are mobilized from extralienal pools. Whereas neutrophil mobilization is not suppressed by beta-blockade, the reduction of hyperventilation-induced mobilization of lymphocytes and thrombocytes may be due to a reduction in the size of the mobilizable cell pools, and therefore cannot be interpreted as a sure indication that adrenergic mechanisms are involved in their hyperventilation-induced mobilization.

Adult↗

PubMed1989

The hyperventilation syndrome in panic disorder, agoraphobia and generalized anxiety disorder.

The symptom complex of panic disorder and generalized anxiety disorder suggests an etiological role for hyperventilation. The present study investigates the overlap between DSM-III-R panic disorder, panic disorder with agoraphobia and generalized anxiety disorder with hyperventilation syndrome (HVS). The anxiety disorder diagnoses were based on a structured interview, and HVS syndrome (HVS). The anxiety disorder diagnoses were based on a structured interview, and HVS determined by the so-called hyperventilation provocation test (a brief period of voluntary hyperventilation with recognition of symptoms). The overlap rates with HVS were: 48% for panic disorder, 83% for panic disorder with agoraphobia and 82% for generalized anxiety disorder. However, a pilot study on transcutaneous monitoring of carbon dioxide tension leads us to question the validity of the voluntary hyperventilation method that we used to determine HVS-status. It is unclear whether hyperventilation plays an important role in panic and general anxiety, as our overlap findings suggest. For patients who recognize the symptoms induced by voluntary hyperventilation, the hyperventilation provocation procedure provides a therapeutic means of exposure to feared bodily sensations.

Adult↗

PubMed1971

[Electrical picture of the brain under increased respiration in children. Studies on the structure of hyperventilation and its value as a provocation method in clinical electroencephalography in a model of multivariate analysis using electronic data processing].

In clinical electroencephalography, hyperventilation is the most used method of activation. However, knowledge of the conditions of hyperventilation with regard to their effects on the EEG is so far rather undifferentiated. For this reason the effects of hyperventilation in 1109 children are examined in this paper based on clinical and electroencephalographic parameters of a data configuration with a large number of criteria and the results obtained are calculated with the aid of electronic data processing. The statistical methods of examination were frequency and significance investigations by chi 2 tests, multifactorial analysis of variance, multiple regression analysis of influencing quantities, and determination of the reliability of the quantitative method of evaluation. New knowledge on group-statistical validity was obtained with this multivariant analysis and it was thus possible to extend the value of hyperventilation as a method of provocation in clinical electroencephalography. The increase in knowledge is based in particular on the facts that the hyperventilation effects are practically independent of sex, they do not require the consideration of certain age related development modalities of the EEG, they are diagnostically significant as regards unspecific changes of the bioelectrical activity, and they make a differentiated consideration with reference to their strength necessary, which results in 4 types of forms of changing the EEG spectrum. In addition to this, a recurrence of EEG changes was observed after the HV effect proper had faded, and the term "Reprise" is suggested for this and its clinico-encephalographic importance discussed. It was also found that occipital maxima dominate and that changes in frequency and amplitude require separate consideration. The influence of respiratory rate, tidal volume minute volume, alveolar CO2 tension, blood sugar and body weight on the strength of the effect of hyperventilation is not very significant. Mean controlled hyperventilation has proved useful to standardise arbitrary hyperventilation; an improvement could be achieved at the most by norming the respiratory rate. It was possible to prove that the applied method of non-mechanical quantitative EEG analyses had a high degree of accuracy and is consequently suitable for scientific investigations.

Adolescent↗

PubMedDate not supplied

[Pharmacotherapy of the hyperventilation syndrome].

Hyperventilation may be induced by several organic factors. The HVS-hyperventilation and symptoms such as hypertonia and pain-hypocapnia and disturbance of the acid-base balance--other symptoms--anxiousness--hyperventilation--etc. In the adaptation-hyperventilation and symptoms such as hypertonia and pain,-hupocapnia and disturbance of the acid-base balance-other symptoms--anxiousness--hyperventilation--etc. In the adaptation process one distinguishes the load, the strain and a tension or counterforce (stress). In the cause and effect relationship between the adaptation process and a specific pathology, it is obvious that the strain is the only element capable of eliciting the specific pathology or syndrome. Stress is a compensation for the strain and is therefore beneficial to the organism. The strain is associated with, amongst other things, anxiety and changes in the pyridoxine-L-tryptophan metabolism (nicotinic acid-ribonucleotide synthesis). Stress depends to a large extent on the intact serotonergic transmission in the cerebrum. But serotonin synthesis is critically dependent on the pyridoxine-L-tryptophan metabolism. Benzodiazepines improve the hyperventilation, anxiousness and strain, if these are of the free-floating anxiety type. Tricyclic preparations improve anxiousness in as much as it assumes the character of fear, phobia or an anxiety attack. They are active against strain when that reveals itself as an anxiety attack. Pyridoxine and L-tryptophan as serotonergic agonists, improve the hyperventilation, have a beneficial effect on symptoms such as hypertonia and pain, are effective against anxiousness and anxiety and potentiate the stress. In addition they directly correct the property of strain, i.e. the disturbance of the nicotinicacid-ribonucleotide synthesis. Clomipramine is the most potent serotonergic agonist available. That substance has a favourable effect on hyperventilation, hypertonia and pain, on anxiousness that expresses itself as fear, phobia or an anxiety attack. It favours stress. Further investigation is desirable, in particular of the new serotonergic agonists that have recently been made available or are still to come.

Adrenergic beta-Antagonists↗

PubMed1982

Protective effect of CO2-induced hyperventilation on the hepatotoxicity elicited by carbon tetrachloride.

Following oral intake or inhalation, halogenated hydrocarbons are metabolized to hepatotoxic intermediates in the liver to only a small extent, the major part being eliminated via the lungs without biochemical transformation. Following intoxication, increased pulmonary elimination of hydrocarbons can be achieved in patients by treatment with CO2-induced hyperventilation. To investigate the efficacy of this new therapy under exact experimental conditions, female Wistar rats received 2.5 ml CCl4/kg BW by gastric intubation and were then treated with CO2-induced hyperventilation. In comparison to untreated animals, hyperventilated rats showed only a few signs of hepatic injury by histological evaluation, whereas massive centrolobular necroses and fatty infiltrations were observed in non-hyperventilated animals. By biochemical assessment, significant decreases of GOT, GPT and GDH activity were observed in the serum, when hyperventilated rats were compared to untreated animals. Moreover, the LD50 for CCl4 was almost trebled after hyperventilation compared to the non-hyperventilated animals. The increased LD50, and the biochemical and histological results therefore substantiate the usefulness of CO2-induced hyperventilation therapy in the treatment of intoxications by hydrocarbons under standardized experimental conditions.

Alanine Transaminase↗

PubMed1983

Comparison of airway reactivity induced by histamine, methacholine, and isocapnic hyperventilation in normal and asthmatic subjects.

In an investigation of a rapid screening test for airway reactivity using isocapnic hyperventilation with room air and cold air the results of this test were compared with the airway response to histamine and methacholine challenge. Twelve non-atopic, non-smoking normal subjects and 11 subjects with stable asthma who had an FEV1 above 74% of the predicted value were studied. In the normal subjects isocapnic hyperventilation with room air (75 l/min; 22 degrees C (SEM 0.2 degrees); 10 mg H2O/l air) and isocapnic hyperventilation with cold air (77 l/min; -10 degrees C (0.9 degrees); 2.4 mg H2O/l air) produced no significant change in FEV1. In the asthmatic subjects, hyperventilation with room air (71 l/min; 22 degrees C (0.8 degrees); 10 mg H2O/l air) caused a mean fall in FEV1 of 11.7%; cold air hyperventilation (70 l/min; -10 degrees C (0.9 degrees); 2.4 mg H2O/l air) caused a mean fall in FEV1 of 20.4%. Cold air hyperventilation produced greater separation between normal and asthmatic subjects than room air. The provocative concentration of histamine required to reduce the FEV1 by 20% (PC20) correlated closely with the PC20 for methacholine (r = 0.95; p less than 0.001). Both tests separated normal from asthmatic subjects. PC20 for both histamine and methacholine correlated with the fall in FEV1 after cold air hyperventilation (r = 0.93, p less than 0.001; r = 0.87, p less than 0.001 respectively). We conclude that the results of a rapid screening test based on hyperventilation with cold air correlate well with a standard pharmacological challenge.

Adult↗

PubMed1990

Relationship between the airway response to inhaled sulfur dioxide, isocapnic hyperventilation, and histamine in asthmatic subjects.

To determine whether bronchoconstriction induced by sulfur dioxide can be predicted by the airway response to inhaled histamine, we exposed on two days 46 patients with asthma to air or 0.5 ppm SO2. The exposure protocol consisted of 10 min of tidal breathing followed by 10 min of isocapnic hyperventilation at a rate of 30 l/min. Airway response was measured before (baseline) and after hyperventilation in terms of specific airway resistance, SRaw. Exposure to air increased baseline mean (SD) SRaw from 6.27 (2.12) to mean (SD) maximum post-hyperventilation SRaw of 9.10 (4.38) cmH2O*s (P less than 0.0001). Exposure to SO2 increased mean (SD) baseline SRaw from 6.93 (3.29) to mean (SD) maximum post-hyperventilation SRaw of 18.21 (18.69) cmH2O*s (P less than 0.0001). Mean (SD) effect of SO2 defined as difference between maximum post-hyperventilation SRaw after SO2 versus air was 9.11 (16.14) cm H2O*s. When evaluated individually, 26 and 34 of the 46 patients showed an airway response to hyperventilation of air and SO2, respectively. Airway response to histamine was determined as the histamine concentration necessary to increase specific airway resistance by 100%, PC100SRaw. The airway response after SO2 and PC100SRaw showed a weak but significant correlation (R = -0.48), whereas the responses to hyperventilation and SO2 did not correlate. We suggest that the mechanisms by which histamine and SO2 exert their bronchomotor effects are different and that in asthmatic patients the risk of pollutant-induced asthmatic symptoms can be poorly predicted by histamine responsiveness.

Administration, Inhalation↗

PubMed1989

Does acute hyperventilation provoke cerebral oligaemia in comatose patients after acute head injury?

In 27 comatose patients with acute head injury, 45 paired studies of regional cerebral blood flow (rCBF) were performed before and after hyperventilation. In total 676 regions were studied, and rCBF was calculated as initial slope index using the intracarotid washout technique of 133 Xe. The tests were applied from one day to three weeks after the acute trauma. In total hyperventilation from PaCO2 averaging 4.8 to 3.5 kPa increased the frequency of regions with oligaemia defined CBF less than 20 ml/100 g/min from 5 to 16%. Before hyperventilation oligaemia was observed in 11 of 45 studies (9 of 27 patients); after hyperventilation the frequency increased to 21 studies (15 patients). The frequency of severe oligaemia (CBF less than 15 ml) increased from 0.1 to 3% of all regions, or from 2 to 8 of all studies (from 2 to 9 patients). The increased frequency of oligaemia after hyperventilation was correlated to a poor outcome (dementia, vegetative survival or death), where it was observed in 21% of all regions, in 16 of 26 studies and 11 of 15 patients, whereas the frequency in patients with a good recovery was found to be 7% of all regions and observed in 5 of 19 studies (4 of 12 patients). The high frequency of oligaemia after hyperventilation was associated to a low hemispheric CBF before hyperventilation, but not to the level of PaCO2, the level of intracranial pressure, cerebral perfusion pressure or CSF-pH or lactate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗