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

23% of all septic patients develop septic encephalopathy which is associated with an increased mortality rate. Symptoms such as agitation, confusion and disorientation ranging from stupor to coma often develop in early sepsis. Severe hypotension is significantly associated with the development of septic encephalopathy. Several other factors which may play a role are also discussed: effects of inflammatory mediators on the brain, inadequate cerebral perfusion pressure, blood-brain barrier derangements, disturbances of the cerebral microcirculation, cerebral ischemia e.g. due to hypocapnia,metabolic changes, altered amino acid levels, transmitter imbalances, liver insufficiency, multiple organ failure and infections of the CNS, respectively. Compared to patients with an isolated infection,patients in septic shock have increased levels of aromatic amino acids such as phenylalanine and tryptophan in the plasma and brain as well as decreased levels of branched chain amino acids. Patients who died had higher levels of aromatic amino acids than the survivors. The correlation between aromatic amino acids and the APACHE II score was significant. The tryptophan metabolite quinolinic acid which can be synthesized in activated macrophages could act as an excitatory transmitter on the N-methyl-D-aspartate (NMDA) -receptor. Observations from experimental models indicate that activated NMDA receptors activate the neuronal isoform of the NO-synthase and other calcium dependent enzymes. This releases free radicals which may damage the DNA and activate the nuclear enzyme Poly-ADP-ribose-synthetase (PARS), resulting in energy depletion and cell death. Sepsis is the main cause of metabolic encephalopathies in critically ill patients. The differential diagnoses include hepatic, renal,hypoxic-ischemic or cardiovascular encephalopathies as well as encephalopathies,metabolic disorders and organ dysfunctions of other origin. Therapeutic interventions are numerous,however, so far only investigated in few controlled studies. The primary therapeutic goal is to maintain an adequate perfusion pressure and to prevent hypoxia and hypocapnia. Although the infusion of branched chain amino acids is controversial, experimental investigations demonstrated improvements improvements in an animal model with septic encephalopathy. Further investigations with respect to glutamate receptor antagonists, new radical scavengers, NO- and PARS-inhibitors may show whether these substances are suitable for the prophylaxis or early therapy of septic encephalopathy.
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PMID:[Septic encephalopathy. Diagnosis und therapy]. 1275 14