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Titolo:
SPINAL-CORD EVOKED-POTENTIALS AND EDEMA IN THE PATHOPHYSIOLOGY OF RATSPINAL-CORD INJURY - INVOLVEMENT OF NITRIC-OXIDE
Autore:
WINKLER T; SHARMA HS; STALBERG E; BADGAIYAN RD; ALM P; WESTMAN J;
Indirizzi:
UPPSALA UNIV,CTR BIOMED,DEPT ANAESTHESIA,LAB NEUROANAT,BOX 571 S-75123 UPPSALA SWEDEN UNIV UPPSALA HOSP,DEPT CLIN NEUROPHYSIOL S-75185 UPPSALA SWEDEN UNIV LUND HOSP,DEPT PATHOL S-22185 LUND SWEDEN
Titolo Testata:
Amino acids
fascicolo: 1-3, volume: 14, anno: 1998,
pagine: 131 - 139
SICI:
0939-4451(1998)14:1-3<131:SEAEIT>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
INHIBITOR; TRAUMA;
Keywords:
NITRIC OXIDE; SPINAL CORD EVOKED POTENTIALS; EDEMA; CELL CHANGES; P-CPA; DIAZEPAM; IMMUNOHISTOCHEMISTRY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
15
Recensione:
Indirizzi per estratti:
Citazione:
T. Winkler et al., "SPINAL-CORD EVOKED-POTENTIALS AND EDEMA IN THE PATHOPHYSIOLOGY OF RATSPINAL-CORD INJURY - INVOLVEMENT OF NITRIC-OXIDE", Amino acids, 14(1-3), 1998, pp. 131-139

Abstract

The possibility that nitric oxide is somehow involved in the early bioelectrical disturbances following spinal cord injury in relation to the later pathophysiology of the spinal cord was examined in a rat model of spinal cord trauma. A focal trauma to the rat spinal cord was produced by an incision of the right dorsal horn of the T 10-11 segments under urethane anaesthesia. The spinal cord evoked potentials (SCEP) were recorded using epidural electrodes placed over the T9 and T12 segments of the cord following supramaximal stimulation of the right tibial and sural nerves in the hind leg. Trauma to the spinal cord significantly attenuated the SCEP amplitude (about 60%) immediately after injury which persisted up to 1h. However, a significant increase in SCEP latency was seen at the end of 5h after trauma. These spinal cord segments exhibited profound upregulation of neuronal nitric oxide synthase (NOS) immunoreactivity, and the development of edema and cell injury. Pretreatment with a serotonin synthesis inhibitor drug p-chlorophenylalanine (p-CPA) or an anxiolytic drug diazepam significantly attenuatedthe decrease in SCEP amplitude, upregulation of NOS, edema and cell injury. On the other hand, no significant reduction in SCEP amplitude, NOS immunolabelling, edema or cell changes were seen after injury in rats pretreated with L-NAME. These observations suggest that nitric oxide is somehow involved in the early disturbances of SCEP and contribute to the later pathophysiology of spinal cord injury.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/07/20 alle ore 15:11:47