Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:[Pharmacotherapy of the hyperventilation syndrome]. 614 57

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

Vasovagal reactions are conventionally understood as resulting from systemic changes in cardiovascular activity; however, there exists a complementary perspective focused on specific changes in cerebral vasoconstriction associated with hyperventilation-induced hypocapnia. The present study investigated the role of cardiovascular and respiratory activity in self-reported pre-syncopal vasovagal reactions to a surgery video in a sample of 49 healthy women. Participants who indicated more previous real-life episodes of dizziness reported experiencing significantly more symptoms in the laboratory consistent with a vasovagal response. They also showed lower total peripheral resistance and higher pre-ejection period in general, suggesting lower sympathetic nervous system activity. Significant decreases in end-tidal carbon dioxide (PETCO2) occurred during the surgery video among susceptible participants, without significant increases in respiration rate. Further, participants who experienced reductions from the neutral video in PETCO2, systolic blood pressure, or both, reported vasovagal symptoms during the surgery video. The results suggest that patterns of respiration associated with decreases in PETCO2 may contribute to vasovagal symptoms reported in non-clinical groups as well as those with blood-injection-injury phobia and are associated with susceptibility to dizziness.
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PMID:Respiratory and hemodynamic contributions to emotion-related pre-syncopal vasovagal symptoms. 2845 64