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

The treatment of cerebral edema has changed during recent years. On the one hand, knowledge of the pathophysiology of brain swelling has expanded; on the other, the analysis of biodata such as intracranial pressure, cerebral blood flow, and blood volume has become routine. The methods of measuring intracranial pressure (nowadays without risk due to the use of microtipepidural probes, e.g. Gaeltec) in particular, make it possible to monitor the effects of therapy and enable us to evaluate the different therapeutic measures individually for each patient. Regarding drug treatment, osmotherapy deserves first mention, especially the polyvalent alcohols mannitol and sorbitol, but in spite of possible side effects, glycerin as well. Knowledge of the mechanism of osmotic therapy leads to the proper concept of treatment with bolus administration under control of serum osmolarity and intracranial pressure. Corticosteroids only effectively influence the cerebral edema caused by tumor. The treatment of posttraumatic (and postoperative) cerebral edema is described controversally in the literature. As the side-effects of cortisone therapy are under control, corticosteroids may also be included in the treatment of therapy-resistant cerebral edema. Acting together with sedative drugs, procaine derivatives help to reduce intracranial pressure peaks during intensive care measures. Barbiturates are used as sedatives or in a loading dose until burst suppression is seen in the EEG. The risk of hemodynamic side effects such as reduced cardiac output and cerebral perfusion pressure is decreased by measuring pulmonary arterial pressure and the use of catecholamines. The acidotic impairment of cerebral autoregulation can be regulated using THAM (thrometamine) and the response of the vascular system to hypocapnia can be improved.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Current status of treatment of the cerebral edema]. 311 35

As it was previously reported that Tris-elevated pH acutely activated extracellular regulated protein kinase (ERK) in rat aorta smooth muscle cells, this study tested whether this finding could be extended to endothelial cells and, moreover, the relevance of this finding in brain microvascular endothelial cells with respect to respiratory-induced hypocapnic alkalosis. Exposure of bovine brain microvascular endothelial cells to pH 7.90 due to Tris for 15 and 30 min activated ERK twofold. In contrast, pH elevated to 7.75 and 7.90 by lowered percent CO2 failed to activate ERK (15, 30, and 60 min). These results suggest that respiratory alkalosis due to hypocapnia does not activate ERK in brain microvascular endothelial cells. The ability of Tris to activate ERK suggests a novel pathway, possibly independent of pH elevation, whereby Tris activates ERK.
 ...
PMID:Alkaline pH-induced extracellular regulated protein kinase activation in brain microvascular endothelial cells: differential effects of Tris and lowered CO2. 1709 Apr 3