Intestinal preconditioning is mediated by a transient increase in nitric oxide.
The effect of ischemic preconditioning on the intestine, as well the implantation of nitric oxide and prostacyclin in this process has been evaluated. Thus, intestinal ischemia-reperfusion was induced in rats, and the protection conferred by previous preconditioning was evaluated. In addition, the effect of nitric oxide inhibition and the administration of nitric oxide were determined. Results show that the increases observed in LDH release after ischemia-reperfusion were prevented after preconditioning. Inhibition of nitric oxide synthesis abolished the protective effect of preconditioning, and nitric oxide administration replicated this effect. Also, an increased synthesis of nitric oxide has been detected after preconditioning. Increases in 6 keto PGF1 alpha were independent of nitric oxide. Altogether indicates that preconditioning is triggered by an initial increase in nitric oxide synthesis.
Hotter
G
G
Department of Medical Bioanalysis, IIBB-CSIC, Barcelona, Spain.
Closa
D
D
Prados
M
M
Fernández-Cruz
L
L
Prats
N
N
Gelpí
E
E
Roselló-Catafau
J
J
D000818:Animals; D011464:Epoprostenol / Q000096:biosynthesis*; D007422:Intestines / Q000098:blood supply*; D007511:Ischemia / Q000503:physiopathology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000517:prevention & control; D013997:Time Factors
D009569:Nitric Oxide; D011464:Epoprostenol; D007770:L-Lactate Dehydrogenase; D019001:Nitric Oxide Synthase