This study investigated the effect of vasopressin on portal-systemic collaterals in portal hypertensive rats and the influence of nitric oxide (NO) and prostaglandin on the responsiveness of collateral vessels to vasopressin. The vascular responsiveness to graded concentrations of vasopressin was te
Involvement of nitric oxide and prostaglandins in gastric mucosal hyperemia of portal-hypertensive anesthetized rats
✍ Scribed by María Casadevall; Julián Panés; Josep M. Piqué; Norma Marroni; Jaume Bosch; Brendan J. R. Whittle
- Publisher
- John Wiley and Sons
- Year
- 1993
- Tongue
- English
- Weight
- 857 KB
- Volume
- 18
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
✦ Synopsis
This study investigates the effects of inhibition of nitric oxide synthesis by NG-nitro-L-arginine methyl ester (L-NAME), the inhibition of prostaglandin synthesis with indomethacin and the combined effects on gastric mucosal hyperemia of ketamine-anesthetized rats with portal hypertension induced by partial portal vein ligation. The hydrogen gas-clearance technique was used for measurement of gastric mucosal blood flow. Blood pressure increased with L-NAME administration in a similar manner in portal-hypertensive and sham-operated rats. Low doses of L-NAME (1 and 3 mgkg, intravenously) caused a significant and dosedependent reduction in gastric mucosal blood flow in portal-hypertensive rats but had no effect on shamoperated animals. With a higher dose of L-NAME (13 mg/kg, intravenously), a significant decrease in gastric mucosal blood flow was observed in both portal-hypertensive and sham-operated rats. Indomethacin pretreatment (5 mg/kg, subcutaneously) caused a significant decrease in basal gastric mucosal blood flow of portal-hypertensive rats but did not modify this parameter in sham-operated animals. In sham-operated rats pretreated with indomethacin, the lower dose of L-NAME (3 mgkg) did not significantly modify basal gastric mucosal blood flow. Likewise, pretreatment with indomethacin in sham-operated rats did not augment the significant reduction in gastric mucosal blood Aow produced by the higher dose of L-NAME. In portal-hypertensive rats the significant dose-dependent reduction in gastric muaosal blood flow induced by L-NAME (3 and 13 m e g ) was not significantly altered by pretreatment with indomethacin. Portal pressure was higher in portal-hypertensive than in sham-operated rats, and no significant differences were observed in this parameter between portal-hy-
📜 SIMILAR VOLUMES
Systemic and especially splanchnic arterial vasodilation accompany chronic portal hypertension. Different soluble mediators causing this vasodilation have been proposed, the strongest evidence being for nitric oxide (NO). No data exist if structural vascular changes may partly account for this vasod
Anti-tumor necrosis factor ␣ (TNF-␣) treatment decreases nitric oxide (NO) synthesis and ameliorates the hyperdynamic circulation in portal hypertensive rats. We have recently demonstrated that nitric oxide synthase isoform 3 (NOS3) is overexpressed in portal hypertensive gastric mucosa and that res
receptors to adenylyl cyclase and K / channel opening. 24 The ton, DC. activation of inhibitory guanine nucleotide regulatory pro-
This study examined whether an increased activity of the endothelium-derived relaxing factor, nitric oxide, may account for the hyporesponsiveness to vasoconstrictors in portal hypertension. W e performed dose-response curves to methoxamine, an eadrenoceptor agonist, with and without N"dtr0-Larginin
sults suggest that vascular NO production is higher in Nitric oxide (NO) is postulated to play a role in the cirrhotic rats than in PVL rats. This increased producpathogenesis of arterial vasodilation in chronic portal tion may contribute to the more marked abnormalities hypertension. This present s