Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.11.18 (MAP)
 7,412 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cerebral effects of alterations in plasma osmolality (Osm) and colloid oncotic pressure (COP) were examined in normocarbic, normothermic, pentobarbital-anesthetized rabbits that had been subjected to cryogenic brain injury. Monitored variables in all animals included mean arterial, right atrial, and intracranial pressures (MAP, CVP, and ICP), electroencephalographic (EEG) recordings, and cerebral blood flow (CBF). When surgical preparation was complete, a left parietal lesion was produced with liquid nitrogen. Group 1 (control, n = 8) animals subsequently received only maintenance fluids [lactated Ringer's solution (LR)]. One hour after injury, 3 other groups of animals underwent 45 minutes of plasmapheresis, carried out by arterial phlebotomy (packed red cells returned), with separated plasma being replaced by one of three fluids given in amounts sufficient to maintain MAP and CVP at baseline values. The three fluids were 1) 6% hetastarch in hypo-osmotic LR [Group 2 (Hypo-Osm), n = 6; COP = 21 mm Hg, Osm = 130 mOsm/kg]; 2) iso-osmotic LR [Group 3 (Hypo-COP), n = 8; COP = 0; Osm = 305]; and 3) 6% hetastarch in iso-osmotic LR [Group 4 (Iso-Osm/COP), n = 8; COP = 21, Osm = 310]. The animals were killed by exsanguination 25 minutes after completion of plasmapheresis. The brain was removed, the hemispheres separated, weighed, and sliced, and the specific gravities (SpGr) of the regional tissue determined. There were no differences in MAP, CVP, regional CBF, or EEG activity among the groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute effects of changing plasma osmolality and colloid oncotic pressure on the formation of brain edema after cryogenic injury. 271 75

The effects of an 8-h period of reduced colloid oncotic pressure (COP) on cerebral edema formation following cryogenic brain injury were studied in 24 normothermic, normocarbic rabbits. Anesthesia was induced with halothane and catheters inserted to permit the monitoring of arterial, right atrial, and intracranial pressures (MAP, CVP, and ICP, respectively). When surgery was complete, halothane was discontinued, 40 mg/kg of pentobarbital was given iv, and ventilation continued with 66% N2O/balance O2. A left parietal cryogenic injury was then produced using liquid N2, and the animals assigned to one of three groups. In group 1 (Control, n = 8), only maintenance lactated Ringer's solution (LR) was given for the remainder of the study. Beginning 30 min after injury, animals in the other two groups (n = 8 each) underwent 45 min of plasmapheresis (arterial phlebotomy, with packed cells returned). In group 2 (Iso-COP) separated plasma was replaced with 6% hetastarch in LR, while in group 3 (Hypo-COP), plasma was replaced with LR alone. In both groups, the volume of fluid given was adjusted to maintain MAP and CVP at baseline values. After plasmapheresis, animals subsequently received only maintenance LR. Eight and one-half hours after the injury (8 h after the start of plasmapheresis), animals were killed and the brains removed. Regional tissue specific gravities (SpGr) and water contents (%H2O) were measured respectively by microgravimetry and drying. In addition, the %H2O of samples of skeletal muscle and small bowel were determined to assess peripheral edema formation. There were no important intergroup differences in MAP, CVP, ICP, blood gases, or osmolality at any time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prolonged reduction in colloid oncotic pressure does not increase brain edema following cryogenic injury in rabbits. 280 12

The influence of aniso-osmolarity on the activity of the MAP kinases Erk-1 and Erk-2 was studied in C6 glioma cells. Hypo-osmotic treatment (205 mosmol/l) led to an increased activity of Erk-1 and Erk-2 within 3 min, which became maximal at 10 min and returned to basal level within 120 min. In contrast, Erk activity was reduced under hyper-osmotic conditions (405 mosmol/l), compared to the normo-osmotic control (305 mosmol/l). Erk activation was accompanied by a mobility shift of Raf-1. Hypo-osmotic exposure increased the cytosolic Ca2+ concentration ([Ca2+]i). Absence of extracellular Ca2+ largely abolished the [Ca2+]i response to hypo-osmolarity, whereas Erk activation following hypo-osmotic stimulation remained unaffected, suggesting a Ca2+ independence of the osmosignalling pathway to the MAP kinases. Both the Ca2+ response as well as the Erk activation following hypo-osmotic exposure were maintained in the presence of the phospholipase C inhibitor U73122. Application of 8-CPT cAMP, forskolin/isobutylmethylxanthine or isoproterenol blocked Erk activation following hypo-osmotic treatment of the cells, suggesting a role of the Ras/Raf pathway upstream from Erk-1 and Erk-2. Protein kinase C (PKC) is unlikely to play a role in the hypo-osmolarity- induced signalling towards MAP kinases, as revealed by inhibition of PKC with Go6850. Inhibition of pertussis- or cholera toxin-sensitive G-proteins as well as inhibition of tyrosine kinases with genistein and of PI3 kinase by wortmannin had no effect on the Erk response to hypo-osmolarity. It is concluded that osmosignalling in C6 glioma cells differs upstream of the MAP kinases from that observed in primary rat astrocytes, H4IIE rat hepatoma cells and isolated rat hepatocytes.
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PMID:Osmosignalling in C6 glioma cells. 900 90