Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peritoneal adhesions were created in rats by brisk scrubbing of the terminal part of the ileum. Adhesions were graded by total number and the presence of small bowel obstruction. Adhesion prophylaxis was evaluated using dexamethasone, methylprednisolone sodium succinate, promethazine hydrochloride, and human fibrinolysin (Thrombolysin) in various combinations, doses, and routes of administration. Methylprednisolone and dexamethasone, depending on the route of administration, modified the total number of adhesions but did not modify their severity when compared to control animals. Promethazine by itself modified peritoneal adhesions in the rat. Used together, methylprednisolone and promethazine also modified adhesions, but were not substantially better than the combination of dexamethasone and promethazine. Methylprednisolone, promethazine, and human fibrinolyzin, when used in combination intraperitoneally, virtually eliminated adhesion formation.
 ...
PMID:Prevention of peritoneal adhesions in the rat. The effects of dexamethasone, methylprednisolone, promethazine, and human fibrinolysin. 12 75

Only limited therapeutic measures are currently available for the treatment of spinal cord injury. This review describes the pathologic mechanisms of trauma-induced spinal cord injury in rats, which will contribute to new understanding of the pathologic process leading to spinal cord injury and to further development of new therapeutic strategies. Spinal cord injury induced by trauma is a consequence of an initial physical insult and a subsequent progressive injury process that involves various pathochemical events leading to tissue destruction; the latter process should therefore be a target of pharmacological treatment. Recently, activated neutrophils have been shown to be implicated in the latter process of the spinal cord injury in rats. Activated neutrophils damage the endothelial cells by releasing inflammatory mediators such as neutrophil elastase and oxygen free radicals. Adhesion of activated neutrophils to the endothelial cell could also play a role in endothelial cell injury. This endothelial cell injury could in turn induce microcirculatory disturbances leading to spinal cord ischemia. We have found that some therapeutic agents that inhibit neutrophil activation alleviate the motor disturbances observed in the rat model of spinal cord injury. Methylprednisolone (MPS) and GM1 ganglioside, which are the only two pharmacological agents currently clinically available for treatment of acute spinal cord injury, do not inhibit neutrophil activation in this rat model. Taken together, these observations raise a possibility that other pharmacological agents that inhibit neutrophil activation used in conjunction with MPS or GM1 ganglioside may have a synergistic effect in the treatment of traumatic spinal cord injury in humans.
 ...
PMID:Spinal cord injury in the rat. 977 Feb 43