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Seite 1 von 453 Ergebnisse
Prostaglandins modulate alterations of microvascular permeability, blood flow, edema and serotonin levels following spinal cord injury: an experimental study in the rat.
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The possibility that prostaglandins influence edema formation, microvascular permeability increase and reduction of blood flow following spinal cord trauma was examined in a rat model. In addition, the influence of prostaglandins on serotonin metabolism of the traumatized spinal cord was evaluated.
Antidepressant activity of beta-lactam antibiotics and their effects on the severity of serotonin edema.
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Injection of beta-lactam antibiotics (reterpen, ceftazidime, and thienam) to mice in doses equivalent to the mean therapeutic doses for humans led to shortening of the duration of behavioral despair in the hanging by the tail test, modified the resistance to serotonin edema, and intensified the
Ankle edema after administration of selective serotonin reuptake inhibitors.
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Clinical manifestations of drug-induced skin reactions include a wide range of symptoms, from mild drug-induced exanthemas to dangerous and life-threatening generalized systematic reactions. Drug-induced skin reactions to psychotropic medication are usually associated with antiepileptic drugs.
Histamine paw edema of mice was increased and became H2-antagonist sensitive by co-injection of nitric oxide forming agents, but serotonin paw edema was decreased.
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Nitric oxide (NO) surprisingly caused the opposite effect on histamine and serotonin edema. The local injection of acidified nitrite (0.3-30 micrograms/paw which correspond 10 micrograms-1 mg/kg) increased histamine edema of mice up to 45 +/- 4% and suppressed serotonin edema to 90 +/- 3%. Other
Role of serotonin and prostaglandins in brain edema induced by heat stress. An experimental study in the young rat.
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The possibility that serotonin and prostaglandins participate in edema formation following heat stress (HS) was examined in young rats. Exposure of conscious young animals (8-9 weeks old) to heat at 38 degrees C in a biological oxygen demand (BOD) incubator (relative humidity 50-55%; wind velocity
Zinc protoporphyrin IX attenuates closed head injury-induced edema formation, blood-brain barrier disruption, and serotonin levels in the rat.
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The role of heme oxygenase (HO) in closed head injury (CHI) was examined using a potent HO and guanylyl cyclase inhibitor, zinc protoporphyrin (Zn-PP) in the rat. Blood-brain barrier (BBB) permeability to Evans blue and radioiodine, edema formation, and plasma and brain levels of serotonin were
Serotonin syndrome presenting as pulmonary edema.
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Serotonin syndrome (SS) is a potentially life-threatening condition resulting from excessive central and peripheral serotonergic activity. Clinically, it is a triad of mental-status changes, neuromuscular abnormalities, and autonomic disturbances. It can be caused by intentional self-poisoning,
Role of platelets in vasogenic brain edema. II. Contribution of platelet serotonin in brain edema.
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In this study of the function of platelets after CNS injury, platelets were treated with serotonin labeled with radioactive carbon (14C) in animals subjected to a freezing lesion of the cerebrum. The distribution of platelet serotonin was measured by counting the specific activity of 14C-labeled
Early accumulation of serotonin in rat spinal cord subjected to traumatic injury. Relation to edema and blood flow changes.
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Changes in the concentration of serotonin (5-hydroxytryptamine) in the early period after a focal traumatic injury to rat spinal cord were determined and related to the formation of edema and alterations in blood flow. A unilateral, 5-mm-long and 3-mm-deep traumatic injury located 2 mm from the
Participation of serotonin in capsaicin-induced mouse ear edema.
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We investigated the involvement of serotonin (5-HT) in mouse ear edema induced by topical application of capsaicin (250 micrograms/ear). Application of capsaicin to the ear caused degranulation of mast cells in skin connective tissue. Capsaicin-induced ear edema was significantly inhibited by
Depletion of endogenous serotonin synthesis with p-CPA attenuates upregulation of constitutive isoform of heme oxygenase-2 expression, edema formation and cell injury following a focal trauma to the rat spinal cord.
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The possibility that the upregulation of hemeoxygenase (HO) enzyme responsible for carbon monoxide (CO) formation in the spinal cord following trauma is involved in edema formation and cell damage was examined in a rat model. A focal trauma to the rat spinal cord by making an incision into the right
Unexpected Serotonin Syndrome, Epileptic Seizures, and Cerebral Edema Following 2,5-dimethoxy-4-bromophenethylamine Ingestion.
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4-bromo-2,5-dimethoxyphenethylamine (2C-B) is a designer drug. In Europe, 2C-B is easily obtained and used for recreational purposes. It is known for its stimulating effects similar to those of 3,4-methylenedioxymethamphetamine, although in higher doses it has more hallucinogenic effects. Here, we
A role for serotonin in alpha-naphthylthiourea-induced pulmonary edema.
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alpha-Naphthylthiourea (ANTU) damages the pulmonary capillary endothelium producing a marked pulmonary edema. Since the pulmonary microvasculature regulates the circulating levels of serotonin (5-HT), the role of 5-HT in the pathophysiology of ANTU-induced pulmonary edema was examined. Mice treated
S1-receptor participation in serotonin-induced pulmonary edema in the dog.
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A canine lung-perfusion preparation was used to evaluate the role of serotonin receptor subtype in the development of serotonin-induced pulmonary edema. Ketanserin, an S2-receptor antagonist, blocked an increase in pulmonary arterial pressure caused by serotonin, but not the development of pulmonary
Opposite effect of superoxide dismutase, L-arginine analogues, methylene blue and desferal: suppression of histamine-induced and stimulation of serotonin-induced paw edema in mice.
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Endogenous nitric oxide (NO, endothelium-derived relaxing factor) was stimulatory for histamine- and suppressive for serotonin-induced paw edema of mice. This action was mediated by guanosine 3',5'-cyclic monophosphate production. Local injection of superoxide dismutase (SOD), catalase,
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