Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0026827 (hypotonia)
 5,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A reduction of the arterial blood pressure of the muscles of the 4 tight fascial compartments of the shank may be initiated by: Trauma and operation of the lower extremities, spontaneous bleeding, occlusion of the arteries, general and local hypotonia due to elevation of the leg, as well as by drug abuse and increased stress of the muscles of the lower extremities. This is followed by an increased swelling and tension of the tissue with ischemia and consecutive paralyses of the nerves and muscles in the presence of almost simultaneous muscle contractures. We may encounter a double insult, a "rebound" effect, if f.i. following removal of a two thigh bandage of the shank the compartment again becomes too narrow due to a postischemic swelling. The anterior tibial syndrome is frequently caused by an increased exertion in sports and in the military service. The dorsal syndromes are often accompanied by Sudeck's dystrophy in the late stages. In treatment the early and extensive longitudinal incision of the respective fasciae is imperative in order to prevent the typical equino-varus deformity and hallux flexus.
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PMID:[Compartment syndromes of the lower extremities (author's transl)]. 710 62

GHB is a naturally occurring compound in the central nervous system (CNS) whose tissue concentration are highly increased during drug abuse and in the inherited deficiency of succinic semialdehyde dehydrogenase (SSADH) activity. SSADH deficiency is a neurometabolic-inherited disorder of the degradation pathway of gamma-aminobutyric acid (GABA). It is biochemically characterized by increased concentrations of gamma-hydroxybutyric acid (GHB) in tissues, cerebrospinal fluid (CSF), blood and urine of affected patients. Clinical manifestations are variable, ranging from mild retardation of mental, motor, and language development to more severe neurological symptoms, such as hypotonia, ataxia and seizures, whose underlying mechanisms are practically unknown. In the present study, the in vitro and in vivo effects of GHB was investigated on some parameters of oxidative stress, such as chemiluminescence, thiobarbituric acid-reactive substances (TBA-RS), total radical-trapping antioxidant potential (TRAP), total antioxidant reactivity (TAR), as well as the activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in homogenates from cerebral cortex of 15-day-old Wistar rats. In vitro, GHB significantly increased chemiluminescence and TBA-RS levels, while TRAP and TAR measurements were markedly diminished. In contrast, the activities of the antioxidant enzymes SOD, CAT and GPX were not altered by GHB in vitro. Acute administration of GHB provoked a significant enhance of TBA-RS levels and a decrease of TRAP and TAR measurements. These results indicate that GHB induces oxidative stress by stimulating lipid peroxidation and decreasing the non-enzymatic antioxidant defenses in cerebral cortex of young rats. If these effects also occur in humans, it is possible that they might contribute to the brain damage found in SSADH-deficient patients and possibly in individuals who consume GHB or its prodrug gamma-butyrolactone.
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PMID:Gamma-hydroxybutyric acid induces oxidative stress in cerebral cortex of young rats. 1719 55