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Titolo:
Role of nitric oxide in the secondary expansion of a cortical brain lesionfrom cold injury
Autore:
Stoffel, M; Rinecker, M; Plesnila, N; Eriskat, J; Baethmann, A;
Indirizzi:
Univ Bonn, Dept Neurosurg, D-53105 Bonn, Germany Univ Bonn Bonn Germany D-53105 nn, Dept Neurosurg, D-53105 Bonn, Germany Univ Munich, Klinikum Grosshadern, Inst Surg Res, D-8000 Munich, Germany Univ Munich Munich Germany D-8000 Inst Surg Res, D-8000 Munich, Germany
Titolo Testata:
JOURNAL OF NEUROTRAUMA
fascicolo: 4, volume: 18, anno: 2001,
pagine: 425 - 434
SICI:
0897-7151(200104)18:4<425:RONOIT>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
FOCAL CEREBRAL-ISCHEMIA; L-ARGININE; MESSENGER MOLECULE; IMPACT INJURY; RAT; SYNTHASE; EDEMA; AMINOGUANIDINE; INHIBITION; MODEL;
Keywords:
aminoguanidine; cerebral contusion; lesion growth; L-arginine; N-G-nitro-L-arginine; nitric oxide synthase; traumatic brain injury;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Stoffel, M Univ Bonn, Dept Neurosurg, Sigmund Freud Str 25, D-53105 Bonn, Germany Univ Bonn Sigmund Freud Str 25 Bonn Germany D-53105 n, Germany
Citazione:
M. Stoffel et al., "Role of nitric oxide in the secondary expansion of a cortical brain lesionfrom cold injury", J NEUROTRAU, 18(4), 2001, pp. 425-434

Abstract

We have investigated the role of nitric oxide (NO) as mediator of the secondary growth of a traumatic cortical necrosis. For this purpose, a highly standardized focal lesion of the brain was induced in 46 Sprague-Dawley ratsby cold injury. Twenty-four hours later-the timepoint of maximal lesion spread-the animals were sacrificed and brains were removed for histomorphometry of the maximal necrosis area and volume. The animals were divided into five experimental groups. Group I received the NO donor L-arginine as i.v. bolus 10 min prior to trauma (300 mg/kg body weight; n = 10) and a second bolus of the same dosage intraperitoneally 1 h after trauma. Group II (n = 10)-serving as control of group I-was infused with an i.v. bolus of 1 mL/kg isotonic saline 10 min prior to and a subsequent bolus i.p. 1 h after trauma. Group III (n = 8) received 100 mg/kg b.w. of the inducible NOS (iNOS) inhibitor aminoguanidine (AG) 1 h before and 8 1 1 after trauma by intraperitoneal route. Group IV was administered with the nitric oxide synthase (NOS) inhibitor N-G-nitro-L-arginine (L-NNA; 100 mg/kg b.w., i.p.; n = 8); group V-the controls of group III and IV-was administered with isotonic saline (1mL/kg b.w, i.p.; n = 10) 1 h before and 8 h after trauma. In the control group with i.v./i.p. sham treatment (II), the focal lesion led to a corticalnecrosis with a maximum area of 3.1 +/- 0.3 mm(2) and a lesion volume of 5.7 +/- 0.5 mm(3) at 24 h after trauma. In animals with administration of L-arginine, the focal lesion had a maximum area of 3.1 +/- 0.3 mm(2) and a volume of 5.3 +/- 0.5 mm3. Hence, the NO donor did not affect the secondary growth of necrosis. Animals with i.p. sham treatment (group V) had a maximallesion area of 3.6 +/- 0.2 mm(2) and lesion volume of 6.2 +/- 0.4 mm(3). Administration of aminoguanidine afforded significant attenuation of the lesion growth. Accordingly, the maximal area of necrosis spread only to 2.8 +/- 0.2 mm(2) with a volume of 4.5 +/- 0.5 mm(3), respectively, at 24 h aftertrauma (p < 0.01 vs group V). On the other hand, administration of L-NNA did not influence the maximal lesion area (3.7 +/- 0.2 mm(2)) or lesion volume (6.5 +/- 0.5 mm(3)) evolving at 24 h after trauma. Thus, neither the enhancement of the formation of NO by L-arginine nor gross inhibition of the synthesis of NO by L-NNA did affect the secondary spread of the necrosis from a focal trauma. The marked attenuation of the posttraumatic necrosis growth by the iNOS inhibitor aminoguanidine strongly indicates an important role of iNOS product in this phenomenon. These findings, thus, demonstrate that the expansion of a primary necrotic focal lesion is a secondary process which can be therapeutically inhibited. Thereby, the growth of a focal tissue necrosis from trauma is clearly identified as a manifestation of secondary brain damage. This information is deemed important for the better understanding of the pathophysiology of traumatic brain injury and for the targeted development of specific treatment modalities.

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Documento generato il 05/04/20 alle ore 18:49:22