[The effect of bacterial lipopolysaccharide on the gastric emptying of rats: a pretreatment evaluation using Nw-nitro-L-arginine methyl ester (L-NAME)].
BACKGROUND
There is evidence that nitric oxide plays a role in the decrease in gastric emptying induced by bacterial lipopolysaccharide.


OBJECTIVE
To evaluate the effect of pretreatment with Nw-nitro-L-arginine methyl to ester, one competitive inhibitor of the nitric oxide synthases, on the gastric emptying delay induced by lipopolysaccharide.


METHODS
Male Wistar rats, SPF, were used after 24 h fast and 1 h-water withdrawn. The pretreatment was done intravenously with vehicle (saline) or N(w)-nitro-L-arginine methyl to ester in the doses of 0.5, 1, 2.5 e 5 mg/kg. After 10 min, the animals were treated iv with lipopolysaccharide (50 microg/kg) or received vehicle (saline). The gastric emptying was evaluated 1 h after the lipopolysaccharide administration. A saline solution containing phenol red was used as the test meal. The gastric emptying was indirectly assessed by the determination of percent gastric retention of the test meal 10 min after orogastric administration.


RESULTS
The animals pretreated with vehicle and treatment with lipopolysaccharide have significant rise of the gastric retention (average = 57%) in comparison with the controls receiving only vehicle (38.1%). The pretreatment with the different doses of N(w)-nitro-L-arginine methyl to ester did not modify per se the gastric retention in comparison with the animals pretreated with vehicle. Pretreatment with N(w)-nitro-L-arginine methyl to ester with the dose of 1 mg/kg determined a discrete but significant reduction in the gastric retention (52%) of animals treated with lipopolysaccharide in comparison with vehicle-pretreated rats. Paradoxically, animals pretreated with 2.5 or 5 mg of N(w)-nitro-L-arginine methyl to ester/kg followed by treatment with lipopolysaccharide displayed a significantly higher gastric retention (74.7% and 80.5%, respectively) as compared to their controls, pretreated with the same doses of the inhibitor and treated with vehicle (40.5% and 38.7%, respectively) and to those pretreated with vehicle and treated with the same toxin.


CONCLUSIONS
The pretreatment with N(w)-nitro-L-arginine methyl to ester at low dose (1 mg/kg) resulted in a discrete inhibition of the gastric emptying delay induced by lipopolysaccharide. Nevertheless, N(w)-nitro-L-arginine methyl to ester at higher doses (2.5 and 5 mg/kg) induced an enhancement of the lipopolysaccharide effect on gastric emptying, despite not interfering with the gastric emptying per se.
Collares
Edgard Ferro
EF
Centro de Investigação em Pediatria, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, SP. efcollares@hotmail.com
Vinagre
Adriana Mendes
AM
D000704:Analysis of Variance; D000818:Animals; D004195:Disease Models, Animal; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005746:Gastric Emptying / Q000187:drug effects*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D051381:Rats; D017208:Rats, Wistar
D004791:Enzyme Inhibitors; D008070:Lipopolysaccharides; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester