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At least 613 records · Page 34Linked to original sources
PubMed1990

Hyperventilation stimulates the release of prostaglandin I2 and E2 from lung in humans.

It has been reported that hyperventilation (HV) increases the release of vasodilative prostaglandins (PGs) from animal lungs. However, it has not yet been clarified whether or not the results obtained from animal experiments are applicable to humans. To confirm this point, we performed this study. Healthy male volunteers, aged 22-28 years, were divided into two groups. Group I (n = 11) breathed room air and showed respiratory alkalosis. Group II (n = 11) breathed room air containing 5% CO2 and maintained normal arterial blood pH. Each subject hyperventilated voluntarily and vigorously for 10 min. The mean values of respiratory rates, tidal volumes and minute volumes during HV were 42.1 +/- 6.2 breaths/min, 1390 +/- 280 ml and 58.5 +/- 15.2 l/min, respectively. Arterial and venous blood samples were drawn simultaneously before and after HV from brachial artery and medial cubital vein, respectively. Plasma 6-keto PGF1 alpha, a metabolite of PGI2, and PGE2 were measured by radioimmunoassay (RIA). After HV, concentrations of 6-keto PG F1 alpha and PGE2 in both arterial and venous blood were increased significantly. There were no significant differences in the levels of 6-keto PGF1 alpha and PGE2 between two groups, nor between arterial and venous blood either before or after HV. We concluded that voluntary HV stimulates the release of PGI2 and PGE2 from lung in humans and respiratory alkalosis has no significant effect on the release of PGs.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Simplified eucapnic voluntary hyperventilation challenge.

A simplified scheme for eucapnic voluntary hyperventilation ( EVH ) is described that requires only that a source of dry gas containing 5% CO2, 21% O2, and 74% N2 be hyperventilated at 40 L/min or greater. Refrigeration or measurement of end tidal CO2 is not required. When the ventilation pattern of a standardized treadmill exercise challenge in a group of exercise-sensitive asthmatics breathing dry air was matched according to this EVH procedure, the magnitude of the resultant bronchospasm and the exclusive nature of the postchallenge refractory period were similar, since patients in both cases were still fully responsive to methacholine. It is concluded that such an EVH challenge may be used to reproduce the bronchial heat and water fluxes that occur with exercise challenge as well as the consequential challenge-specific refractoriness that follows.

Air↗
PubMed1986

Airway responses to hyperventilation of cold dry air: duration of protection by cromolyn sodium.

The magnitude and duration of the inhibitory effect of three doses of cromolyn sodium on the airway response to hyperventilation of cold dry air was examined in a double-blind, randomized controlled trial. Eight subjects with well controlled asthma were studied. On 4 separate days, doses of either 2 mg, 10 mg, 20 mg, or placebo were administered by metered-dose inhaler. Twenty minutes, 2 hours, and 4 hours after each medication, airway responsiveness to isocapnic hyperventilation of cold dry air was measured by use of a standardized dose-response method. At 20 minutes, all three doses inhibited bronchoconstriction, and there was no evidence of any difference in the magnitude of the inhibition between the doses. All three doses progressively provided less protection with time. By 2 hours, the inhibition induced by 2 mg was no longer different from placebo, and by 4 hours, only 20 mg still provided significant protection. The results demonstrate that, although the initial magnitude of inhibition may not be different between 2 mg and 20 mg, the rate at which the protective effect wears off is dose related.

Adolescent↗
PubMed1987

Type A behaviour, borderline hyperventilation and psychological, psychosomatic and neuroendocrine responses to mental task load.

Psychological, psychosomatic and neuroendocrine (in blood) responses to mental task load were investigated in relation to Type A behaviour and borderline hyperventilation. For this purpose 32 apparently healthy, male volunteers were classified on the basis of their scores on the Jenkins Activity Survey (JAS) and on a questionnaire assessing hyperventilation related symptoms (HRS). The subjects performed a memory search task in which a monetary bonus could be won or lost. At rest higher HRS scores were related to increased acute psychosomatic symptom scores and higher JAS scores to higher prolactin levels. Task performance caused an increase of state anxiety, acute psychosomatic symptoms, adrenaline and cortisol, whereas prolactin decreased. Higher JAS scores were related to greater cortisol responses and higher HRS scores to smaller adrenaline responses.

Adult↗
PubMed1990

Transcranial pulsed Doppler measurements of blood flow velocity in the middle cerebral artery: reference values at rest and during hyperventilation in healthy children and adolescents in relation to age and sex.

Transcranial pulsed Doppler (TCD) measurement of blood flow velocity in the middle cerebral artery was performed in 76 healthy children and adolescents (age 2-19 years), to obtain normative reference data, both at rest and during hyperventilation (from 10 years on). The Mean Flow Velocity (MFV) decreased with increasing age. Girls of 10 years or older showed a tendency for higher MFV values than boys of the same age. In combination with a previous study, this suggests that females in their reproductive years have higher maximal MFV values than males. The MFV values, during hyperventilation, were higher in girls than in boys. This gender difference, as in adults, disappeared gradually at lower levels of pCO2. At the lowest pCO2 levels, systolic minus diastolic blood flow velocity was more sensitive to vascular changes than MFV. With TCD measurements, age, sex, and pCO2 have to be taken into account, for a correct interpretation of the data obtained.

Adolescent↗
PubMed1995

Attenuation of pain-related hyperventilation in adjuvant arthritic rats with adrenal medullary transplants in the spinal subarachnoid space.

The adjuvant arthritic rat model has been utilized for the study of chronic pain, as polyarthritic rats present a variety of symptoms similar to those seen in human chronic pain conditions. In particular, hyperventilatory responses are notable in both and may more accurately reflect basal ongoing pain than do evoked noxious stimuli. To assess whether adrenal medullary transplants in the spinal subarachnoid space can alleviate basal arthritic pain, respiratory parameters were determined using whole body plesthmography in polyarthritic rats. Arthritis was induced by inoculation with an intradermal injection of complete Freund's adjuvant. Steady-state ventilation was monitored at weekly intervals in arthritic animals with adrenal medullary or control striated muscle transplants. Results revealed that adjuvant arthritis produced significant hyperventilation in animals with control transplants, as indicated by increased tidal volumes and minute ventilation, which paralleled the progression of the inflammatory process. In contrast, this hyperventilation was eliminated by adrenal medullary transplants. A role for catecholamines and opioid peptides released from the transplants was suggested by the reversal of these effects with phentolamine and naloxone. In addition, the retardation in weight gain normally observed in polyarthritic animals was markedly attenuated by adrenal medullary, but not control transplants. These findings indicate that adrenal medullary transplants in the spinal subarachnoid space can alleviate basal chronic pain as assessed in adjuvant arthritis.

Adrenal Medulla↗
PubMed1988

Hyperventilation-induced simultaneous multivessel coronary spasm in patients with variant angina: an echocardiographic and arteriographic study.

Left ventricular wall motion abnormalities during an attack of coronary spasm induced by hyperventilation were examined with use of two-dimensional echocardiography in 27 patients with variant angina. Transient abnormal wall motion (asynergy) confined to one coronary artery region was found in 18 of the 27 patients and transient abnormal motion extending over more than one coronary artery region in the remaining 9 patients. Spasm of more than one major coronary artery was demonstrated separately by coronary arteriography during an attack induced by injection of acetylcholine or ergonovine in seven of the nine patients who manifested asynergy in more than one coronary artery region. In one patient, spasm was demonstrated in one major coronary artery, and the other coronary arteries were severely stenosed or occluded organically. In the remaining patient, acetylcholine was not injected into both arteries; however, the attack was sometimes associated with ST segment elevation in the anterior leads and at other times in the inferior leads. Therefore, simultaneous multivessel coronary spasm seems to have occurred in eight of the nine patients who exhibited asynergy in more than one coronary artery region. The 8 patients with simultaneous multivessel coronary spasm had a higher degree and longer duration of ST segment elevation and a higher incidence of arrhythmias during the attack induced by hyperventilation than did the 19 patients with single vessel coronary spasm, and all of them had no significant organic stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris, Variant↗
PubMedDate not supplied

Hyperventilation and anxiety: alcohol withdrawal symptoms decreasing with prolonged abstinence.

We previously presented evidence that hyperventilatory and anxiety symptoms are the result of physically dependent alcohol use rather than a premorbid condition. The purpose of the present study was to examine the effect of prolonged abstinence versus resumption of dependent drinking on those symptoms. Two questionnaires (a hyperventilation complaint checklist and Spielberger's Anxiety Inventory) were presented twice to 15 ss, once during an inpatient treatment and once after a median followup period of 17 months. Six ss were abstinent for the entire period, 3 were abstinent with 1 or 2 slips and 6 ss were drinking in a dependent way again for at least 6 months. In the abstinent or abstinent-with-slips group, a significant decrease over time in hyperventilatory symptoms and trait (but not state) anxiety could be found, whereas in the dependent drinking group there was a significant increase in hyperventilatory symptoms and state (but not trait) anxiety. An extended followup in 5 abstinent ss showed a continued decrease in those symptoms. These results provide further evidence for the hypothesis that hyperventilation and anxiety are part of a subacute alcohol withdrawal syndrome.

Adult↗
PubMed2004

BOLD-contrast functional MRI signal changes related to intermittent rhythmic delta activity in EEG during voluntary hyperventilation-simultaneous EEG and fMRI study.

Differences in the blood oxygen level dependent (BOLD) signal changes were studied during voluntary hyperventilation (HV) between young healthy volunteer groups, (1) with intermittent rhythmic delta activity (IRDA) (N = 4) and (2) controls (N = 4) with only diffuse arrhythmic slowing in EEG (normal response). Subjects hyperventilated (3 min) during an 8-min functional MRI in a 1.5-T scanner, with simultaneous recording of EEG (successful with N = 3 in both groups) and physiological parameters. IRDA power and average BOLD signal intensities (of selected brain regions) were calculated. Hypocapnia showed a tendency to be slightly lighter in the controls than in the IRDA group. IRDA power increased during the last minute of HV and ended 10-15 s after HV. The BOLD signal decreased in white and gray matter after the onset of HV and returned to the baseline within 2 min after HV. The BOLD signal in gray matter decreased approximately 30% more in subjects with IRDA than in controls, during the first 2 min of HV. This difference disappeared (in three subjects out of four) during IRDA in EEG. BOLD signal changes seem to depict changes, which precede IRDA. IRDA due to HV in healthy volunteers represent a model with a clearly defined EEG pattern and an observable BOLD signal change.

Adult↗
PubMed2004

Role of L-glutamate in the locus coeruleus of rats in hypoxia-induced hyperventilation and anapyrexia.

Locus coeruleus (LC) is a noradrenergic nucleus in the pons which has been reported to play an inhibitory role in the ventilatory response to hypoxia. Since LC contains glutamatergic receptors and L-glutamate is known to participate in the ventilatory and thermoregulatory responses to hypoxia, the effects of kynurenic acid (KYN, a glutamatergic receptor antagonist) microinjected into the LC in the hypoxic hyperventilation and anapyrexia (a regulated drop in body temperature [Tb]) were examined. Ventilation (V) and Tb were measured before and after a microinjection of KYN (10 nmol/0.1 microl) into the LC, followed by hypoxia. Control rats received a saline injection. Under normoxia, KYN treatment did not affect V or Tb. Typical hypoxia-induced hyperventilation and anapyrexia were observed after saline injection. KYN injection caused an increase in the ventilatory response, acting on tidal volume (Vt), but did not affect the anapyrexic response to hypoxia. These data suggest that L-glutamate in the LC is an excitatory neurotransmitter that activates an inhibitory pathway to reduce the hypoxic ventilatory response, similarly to the data reported for rostral ventrolateral medulla (VLM). The role of L-glutamate into the LC and VLM opposes its effect on other nuclei such as the nucleus of the solitary tract and ventromedullary surface, where the neurotransmitter participates in an excitatory pathway of the ventilatory response.

Animals↗
PubMed1996

The low specificity of the Hyperventilation Provocation Test.

The Hyperventilation Provocation Test (HVPT) has become a routine procedure in the diagnosis of hyperventilation syndrome (HVS). During an HVPT the patient voluntarily overbreathes for several minutes to produce hypocapnia. The test is considered positive if the induced symptoms are recognized by the patient as similar to those experienced in daily life. The present study tests the assumption that hypocapnia is the primary trigger for symptoms during an HVPT. In a randomized double-blind crossover design. 115 patients suspected of HVS and 40 healthy controls performed an HVPT and a placebo test (PT, isocapnic overbreathing). The HVPT induced more symptoms than the PT, especially more neuromuscular symptoms, cerebral symptoms, paresthesias, and temperature sensations. However, the absolute difference between the number of symptoms induced by the HVPT and PT was small. In patients, the PT induced 66% of symptoms induced by the HVPT. In the control group this percentage was 60%. The low specificity of the HVPT implies that symptom recognition during the HVPT is invalid as a diagnostic criterion for HVS.

Adult↗
PubMed2003

The nucleus raphe magnus modulates hypoxia-induced hyperventilation but not anapyrexia in rats.

The nucleus raphe magnus (NRM) is one of the brainstem cell groups involved in physiological responses to hypoxia. Thus, we tested the hypothesis that the NRM modulates hypoxia-induced hyperventilation and anapyrexia. To this end, we assessed the participation of NRM in the respiratory and thermoregulatory responses to hypoxia using ibotenic acid lesions produced in the NRM of rats. Our results demonstrated that, under resting breathing, NRM plays no role in ventilation or body temperature. Hypoxia caused hyperventilation and anapyrexia in all groups. NMR lesions elicited an increased ventilatory response to hypoxia due to a higher tidal volume (V(T)) but did not affect hypoxia-induced anapyrexia. Therefore, we conclude that NRM exerts an inhibitory modulation of breathing during hypoxia, acting on V(T), but plays no role in the hypoxia-induced anapyrexia.

Animals↗
PubMed1993

Hyperventilation-induced seizures in mentally impaired children.

Two children with profound development delay and medically intractable seizures were found to have hyperventilation-induced seizures. Following detection of this precipitating factor the parents, teachers and caretakers were taught to modify the childrens' breathing when they began to hyperventilate. In both patients this technique resulted in a dramatic decrease in seizure frequency.

Anticonvulsants↗
PubMed2003

Lactate as a modulator of hypoxia-induced hyperventilation.

In the present study, we tested the hypothesis that lactate, which is a classic companion of hypoxic stress in mammals, is a modulator of hypoxia-induced hyperventilation. To this end, pulmonary ventilation (V(E)) of male Wistar rats was measured by whole body plethysmograph, and dichloroacetate (DCA, 100 mg/kg) was used to inhibit lactate production. Plasma lactate levels, arterial pH (pHa), arterial carbon dioxide partial pressure (PaCO(2)), arterial oxygen partial pressure (PaO(2)), plasma bicarbonate (HCO3(-)) and oxygen consumption (VO(2)) were determined as well. In normoxia, intraperitoneal DCA elicited a decrease only in plasma lactate levels. Hypoxia caused an increase in V(E), pHa and plasma lactate levels and parallel to decreases in PaCO(2), PaO(2) and VO(2) in the control group. DCA administration markedly reduced the ventilatory response to hypoxia by acting on tidal volume (V(T)). This reduced ventilatory response caused by DCA was independent of VO(2). In conclusion, the present study indicates that lactate contributes to the initiation and maintenance of hypoxia-induced hyperventilation in rats, modulating the adjustments in V(T).

Acidosis, Lactic↗
PubMed1989

Fear talk versus voluntary hyperventilation in agoraphobics and normals: a controlled study.

Twenty-three drug-free patients with agoraphobia and panic disorder (DSM-III criteria) had, at rest, lower mean end-tidal PCO2 (32 v. 36 mmHg) and higher mean heart rate (92 v. 83 bpm) than did 18 controls. During 5 min of listening to fear talk, only eight (35%) patients and three (16%) controls panicked, but panic was associated with marked physiological changes in only two patients and one control. Patients said that breathlessness began slightly more often before than after panic. In 59% of patients the symptoms from voluntary hyperventilation (VHV) were very similar or identical to those of their usual panics. Compared with the remainder, these patients felt more unpleasant during hyperventilation (HV); in such patients HV may aggravate somatic symptoms. Agoraphobics with panic differed from controls in having higher baseline arousal, but were not more reactive than controls to HV or fear talk.

Agoraphobia↗
PubMed2001

Compulsory hyperventilation and hypocapnia of patients with Leigh syndrome associated with SURF1 gene mutations as a cause of low serum bicarbonates.

Experimental data show that elevation of intracellular pH leads to severe lesions of brain cells. Acidification of intracellular fluid by accumulation of lactate may compensate the effect of respiratory alkalosis. Increased serum pH, and low PCO2, associated with hyperlactataemia (sometimes incorrectly called 'acidosis') have been reported in children with Leigh syndrome (LS). The aim of the study was to determine whether respiratory alkalosis is characteristic of patients with LS due to SURF1 mutations. All venous blood gas data (88 samples) of 18 spontaneously breathing LS patients with recently established SURF1 mutations, hospitalized during 1986-2000, were retrospectively reviewed. The data of an affected boy who survived on a respirator for more than 3 months (79 daily samples) were analysed separately. In spontaneously breathing patients, the data indicated that the patients had compensated or partially compensated respiratory alkalosis (pH 7.388+/-0.060, Pco2 29.2+/-5.7 mmHg, HCO3- 17.4+/-3.0 mmol/L, BE -6.7+/-3.2 mmol/L). Bicarbonate excretion was detected in urine of two examined LS cases in spite of decreased serum HCO3-. In the affected child maintained on a respirator, simple manipulation of the inspired CO2 tension to establish a normal pressure of 35-45 mmHg automatically caused an increase of serum HCO3- concentration to a normal value of 26.3+/-2.9 mmol/L (and BE to +2.2+/-3.1 mmol/L), in spite of cytochrome oxidase (COX) deficiency due to a confirmed SURF1 mutation. We suggest that respiratory alkalosis (hypocapnia) of Leigh syndrome patients with SURF1 mutations results from compulsory hyperventilation and speculate that hypocapnia may contribute to Leigh-like brain damage in the SURF1-deficient patients as well as in other patients presenting with Leigh-like syndrome. The supposition that accumulation of lactate may protect the brain of LS patients from alkalosis-related damage requires further study. Avoidance of any factors stimulating hyperventilation of LS patients and caution when attempting to correct low plasma bicarbonate are suggested.

Alkalosis, Respiratory↗
PubMed1994

Fear of physical sensations and trait anxiety as mediators of the response to hyperventilation in nonclinical subjects.

Three studies were conducted to compare the ability of a measure of fear of physical sensations (Anxiety Sensitivity Index; ASI) and a measure of trait anxiety (State-Trait Anxiety Inventory; STAI) to predict response to hyperventilation. In the first study subjects (N = 43) were selected who differed in scores on the ASI but were equated on levels of trait anxiety. Two other studies were conducted in which subjects (ns = 63 and 54) varied randomly on ASI and STAI scores. The results indicate that scores on the ASI account for a significant proportion of variance in the response to hyperventilation that is not accounted for by scores on the STAI.

Adult↗