Effects of aminoguanidine administration on vascular hyporeactivity in thoracic aorta from endotoxaemic rats
Küçük Resim Yok
Tarih
2000
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Elsevier Science Bv
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
Overproduction of nitric oxide has been implicated in the pathogenesis of the vascular hyporesponsiveness of endotoxic shock. In this study, we investigated the effects of aminoguanidine, an inducible nitric oxide synthase inhibitor, on the decreased vascular responsive ness in endotoxic shock. Male albino rats were administered intraperitoneally aminoguanidine (25, 50 or 75 mg kg(-1)) 1 h after they received saline or lipolysaccharide (Escherichia coli serotype 055:B5). The thoracic aortas were removed 18 h after Lipopolysaccharide administration and suspended in organ baths containing Krebs solution, and tested for vascular reactivity. Contractile responses to phenylephrine and potassium chloride, and relaxant responses to acetylcholine were reduced in endotoxaemic animals. Aminoguanidine was ineffective in improving the vascular hypocontractility at 25 and 75 mg kg(-1) doses; but at 50 mg kg(-1) dose, it restored the decreased contractile responses toward normal values. Diminished relaxant responses to acetylcholine were restored by aminoguanidine at all three different doses. There were no significant differences in sodium nitroprusside induced relaxant responses between all groups. Administration of aminoguanidine in control animals did not change vascular responses to any agent. These data suggest that aminoguanidine treatment improves the vascular hyporesponsiveness to contractile- and endothelium-dependent relaxant agents observed in endotoxic shock. (C) 2000 Elsevier Science B.V. All rights reserved.
Açıklama
Anahtar Kelimeler
endotoxic shock, aminoguanidine, nitric oxide (NO), (Rat)
Kaynak
European Journal of Pharmacology
WoS Q Değeri
Q1
Scopus Q Değeri
Q1
Cilt
408
Sayı
2
