The role of portal pressure in the severity of bleeding in portal hypertensive rats
✍ Scribed by Beatriz Castañeda; Wilma Debernardi-Venon; Juan-Carlos Bandi; Victoria Andreu; Sofía Pérez-del-Pulgar; Eduardo Moitinho; Pilar Pizcueta; Jaime Bosch
- Publisher
- John Wiley and Sons
- Year
- 2000
- Tongue
- English
- Weight
- 236 KB
- Volume
- 31
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
✦ Synopsis
The aim of this study was to investigate the role of portal hypertension determining the severity of bleeding in portal hypertensive rats. The effects of section of branches of the ileocolic vein were studied in sham-operated (SO), partial portal vein-ligated (PPVL), and common bile duct-ligated (CBDL) rats. The ensuing hemorrhage was compared with that caused by section of femoral vein, where the portal hypertensive factor is excluded. In PPVL rats, section of branches of increasing size (divided into fourth, third, second, and first order) resulted in increasingly severe bleeding (arterial pressure: < ؎ 4%, <6 ؎ 12%, <15 ؎ 8%, and <28 ؎ 13%; P F .005; hematocrit <4 ؎ 2%, <6 ؎ 1%, <7 ؎ 2%, and <10 ؎ 4%; P F .005). Bleeding from first-order branches was mild in SO, moderate in PPVL, and severe in CBDL rats, as shown by increasing changes in arterial pressure (<3 ؎ 3%, <12 ؎ 16% and, <43 ؎ 23%; P F .01), hematocrit (<4 ؎ 1%, <12 ؎ 2%, and <32 ؎ 19%; P F .01), and mortality (0%, 0%, and 56%; P F .001). Greater blood loss in CBDL rats was associated with higher portal pressure (16.6 ؎ 2.7 vs. 13.1 ؎ 1.1 mm Hg in PPVL; P F .01) and more prolonged bleeding time (70 ؎ 4 vs. 35 ؎ 3 seconds in PPVL; P F .001). Vessels were similarly dilated in CBDL and PPVL (0.7 ؎ 0.2 and 0.7 ؎ 0.1 vs. 0.4 ؎ 0.1 mm in SO; P F .05). Section of femoral vein caused equal blood loss in SO, PPVL, and CBDL rats, assessed by falls in hematocrit (<8 ؎ 2%, <7 ؎ 1%, <8 ؎ 1%, respectively; NS) and by the blood loss (3.6 ؎ 0.7, 3.5 ؎ 0.9, and 3.8 ؎ 0.7 g; NS). The study shows that the degree of portal pressure elevation is a major determinant of the severity of portal hypertension-related bleeding in PPVL and CBDL rats. (HEPATOLOGY 2000;31:581-586.)
Variceal bleeding is the more frequent and severe complication of portal hypertension in patients with cirrhosis. Al-
📜 SIMILAR VOLUMES
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
Portal hypertension (PHT) is characterized by increased portal pressure caused in part by a reduction in mesenteric vascular resistance. The aim of this study was to evaluate the role of endothelin (ET) and specific ET receptors in maintaining the vasculopathy of PHT. PHT was created in Sprague-Dawl
receptors to adenylyl cyclase and K / channel opening. 24 The ton, DC. activation of inhibitory guanine nucleotide regulatory pro-
Reduced intrahepatic endothelial nitric oxide synthase (eNOS) activity contributes to the pathogenesis of portal hypertension (PHT) associated with cirrhosis. We evaluated whether asymmetric dimethylarginine (ADMA), a putative endogenous NOS inhibitor, may be involved in PHT associated with cirrhosi