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Query: UMLS:C0085383 (hypocapnia)
1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The human pharmacology of anxiety disorders, including panic disorder, is detailed. The major theories center around the role of benzodiazepine receptor, noradrenergic and serotonergic dysfunction. The contribution that challenge tests with lactate, hyper- and hypocapnia, beta- and alpha-2-adrenoceptor agonists, peptides, pentylenetetrazol, and caffeine make to our understanding of the biological basis of anxiety and these major theories are described and discussed.
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PMID:The pharmacology of human anxiety. 197 44

The role of carbon dioxide (CO2) is underestimated in the pathomechanism of neuropsychiatric disorders, though it is an important link between psyche and corpus. The actual spiritual status also influences respiration (we start breathing rarely, frequently, irregularly, etc.) causing pH alteration in the organism; on the other hand the actual cytosolic pH of neurons is one of the main modifiers of Ca2+-conductance, hence breathing directly, quickly, and effectively influences the second messenger system through Ca2+-currents. (Decreasing pCO2 turns pH into alkalic direction, augments psychic arousal, while increasing pCO2 turns pH acidic, diminishes arousal.) One of the most important homeostatic function is to maintain or restore the permanence of H+-concentration, hence the alteration of CO2 level starts cascades of contraregulation. However it can be proved that there is no perfect compensation, therefore compensational mechanisms may generate psychosomatic disorders causing secondary alterations in the "milieu interieur". Authors discuss the special physico-chemical features of CO2, the laws of interweaving alterations of pCO2 and catecholamine levels (their feedback mechanism), the role of acute and chronic hypocapnia in several hyperarousal disorders (delirium, panic disorder, hyperventilation syndrome, generalized anxiety disorder, bipolar disorder), the role of "locus minoris resistentiae" in the pathomechanism of psychosomatic disorders. It is supposed that the diseases of civilization are caused not by the stress itself but the lack of human instinctive reaction to it, and this would cause long-lasting CO2 alteration. Increased brain-pCO2, acidic cytosol pH and/or increased basal cytosolic Ca2+ level diminish inward Ca2+-current into cytosol, decrease arousal--they may cause dysthymia or depression. This state usually co-exists with ATP-deficiency and decreased cytosolic Mg2+ content. This energetical- and ion-constellation is also typical of ageing-associated and chronic organic disorders. It is the most important link between depression and organic disorders (e.g. coronary heart disease). The above-mentioned model is supported by the fact that H+ and/or Ca2+ metabolism is affected by several drugs (catecholemines, serotonin, lithium, triaecetyluridine, thyroxine) and sleep deprivation, they act for the logically right direction.
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PMID:The role of carbon dioxide (and intracellular pH) in the pathomechanism of several mental disorders. Are the diseases of civilization caused by learnt behaviour, not the stress itself? 2012 95

Blood-injection-injury (BII) phobia is an anxiety disorder that may be accompanied by vasovagal fainting during confrontation with the feared stimuli. The underlying pattern of autonomic regulation has been characterized as a diphasic response, with initial increases in heart rate and blood pressure that are typical of a fight-flight response, and subsequent drops in blood pressure and/or heart rate that may precipitate vasovagal fainting. Tensing skeletal muscles of the arms, legs, and trunk (applied tension) has been proposed as a technique to cope with this dysregulation. This review critically examines the empirical basis for the diphasic response and its treatment by applied tension in BII phobia. An alternative perspective on the psychophysiology of BII phobia and vasovagal fainting is offered by focusing on hypocapnia that leads to cerebral blood flow reductions, a perspective supported by research on neurocardiogenic and orthostatically-induced syncope. The evidence may indicate a role for respiration-focused coping techniques in BII phobia.
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PMID:The psychophysiology of blood-injection-injury phobia: looking beyond the diphasic response paradigm. 2057 5

Recent clinical trial research suggests that baseline low end-tidal CO2 (ETCO2, the biological marker of hyperventilation) may predict poorer response to cognitive-behavioral therapy (CBT) for anxiety-related disorders. The present study examined the predictive value of baseline ETCO2 among patients treated for such disorders in a naturalistic clinical setting. Sixty-nine adults with a primary diagnosis of a DSM-5 anxiety disorder, obsessive-compulsive disorder, or posttraumatic stress disorder completed a 4-min assessment of resting ETCO2, and respiration rate (the first minute was analyzed). Lower ETCO2 was not associated with a diagnosis of panic disorder, and was associated with lower subjective distress ratings on certain measures. Baseline ETCO2 significantly predicted treatment dropout: those meeting cutoff criteria for hypocapnia were more than twice as likely to drop out of treatment, and ETCO2 significantly predicted dropout beyond other pre-treatment variables. Weekly measurement suggested that the lower-ETCO2 patients who dropped out were not responding well to treatment prior to dropout. The present results, along with previous clinical trial data, suggest that lower pre-treatment ETCO2 is a negative prognostic indicator for CBT for anxiety-related disorders. It is suggested that patients with lower ETCO2 might benefit from additional intervention that targets respiratory abnormality.
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PMID:Low pre-treatment end-tidal CO2 predicts dropout from cognitive-behavioral therapy for anxiety and related disorders. 2796 95