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Titolo:
Infusion of prostacyclin following experimental brain injury in the rat reduces cortical lesion volume
Autore:
Bentzer, P; Mattiasson, G; McIntosh, TK; Wieloch, T; Grande, PO;
Indirizzi:
Univ Lund, Dept Physiol Sci, SE-22362 Lund, Sweden Univ Lund Lund SwedenSE-22362 , Dept Physiol Sci, SE-22362 Lund, Sweden Univ Lund Hosp, Wallenberg Neurosci Ctr, Div Expt Brain Res, S-22185 Lund,Sweden Univ Lund Hosp Lund Sweden S-22185 v Expt Brain Res, S-22185 Lund,Sweden Univ Penn, Sch Med, Dept Neurosurg, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 Neurosurg, Philadelphia, PA 19104 USA
Titolo Testata:
JOURNAL OF NEUROTRAUMA
fascicolo: 3, volume: 18, anno: 2001,
pagine: 275 - 285
SICI:
0897-7151(200103)18:3<275:IOPFEB>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
FOCAL CEREBRAL-ISCHEMIA; MISSILE HEAD-INJURY; CAT SKELETAL-MUSCLE; VASCULAR-PERMEABILITY; NEURONAL DEGENERATION; NITRIC-OXIDE; CELL LOSS; CONTUSION; ANALOG; ILOPROST;
Keywords:
brain contusion; endothelium; lateral fluid percussion; microvessels; prostacyclin; rat; traumatic brain injury;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
61
Recensione:
Indirizzi per estratti:
Indirizzo: Bentzer, P Univ Lund, Dept Physiol Sci, Solvegatan 19, SE-22362 Lund, Sweden Univ Lund Solvegatan 19 Lund Sweden SE-22362 2362 Lund, Sweden
Citazione:
P. Bentzer et al., "Infusion of prostacyclin following experimental brain injury in the rat reduces cortical lesion volume", J NEUROTRAU, 18(3), 2001, pp. 275-285

Abstract

Endothelial-derived prostacyclin is an important regulator of microvascular function, and its main actions are inhibition of platelet/leukocyte aggregation and adhesion, and vasodilation. Disturbances in endothelial integrity following traumatic brain injury (TBI) may result in insufficient prostacyclin production and participate in the pathophysiological sequelae of brain injury. The objective of this study was to evaluate the potential therapeutic effects of a low-dose prostacyclin infusion on cortical lesion volume,CA3 neuron survival and functional outcome following TBI in the rat. Anesthetized animals (sodium pentobarbital, 60 mg/kg, i.p.) were subjected to a lateral fluid percussion brain injury (2.5 atm) or sham injury. Following TBI, animals were randomized to receive a constant infusion of either prostacyclin (1 ng/kg . min(-l) i.v.) or vehicle over 48 h. All sham animals received vehicle (n = 6). Evaluation of neuromotor function, lesion volume, andCA3 neuronal loss was performed blindly. By 7 days postinjury, cortical lesion volume was significantly reduced by 43% in the prostacyclin-treated group as compared to the vehicle treated group (p < 0.01; n = 12 prostacyclin, n = 12 vehicle). No differences were observed in neuromotor function (48 h and 7 days following TBI), or in hippocampal cell loss (7 days following TBI) between the prostacyclin- and vehicle-treated groups. We conclude thatprostacyclin in a low dose reduces loss of neocortical neurons following TBI and may be a potential clinical therapeutic agent to reduce neuronal cell death associated with brain trauma.

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Documento generato il 31/03/20 alle ore 08:46:30