Mechanical, morphological and pharmacological properties of oesophageal varices and small mesenteric veins in portal hypertensive rabbits

Abstract

The properties of isolated small oesophageal and mesenteric veins were investigated in a rabbit model subjected to a 4-week period of portal vein stenosis. The animals developed oesophageal varices and these together with the small mesenteric veins were mounted on a myograph. Compared with sham-operated controls portal hypertension resulted in an increased normalized inner radius and media thickness of the oesophageal veins resulting in a non-significant increase in the media to lumen ratio, while the inner radius decreased as media thickness increased in mesenteric veins resulting in a significant (P less than 0.01) increase in the media to lumen ratio. When activated, the active wall tension of both the oesophageal and mesenteric veins was increased following portal hypertension, but the active media stress was unchanged. The EC50 for noradrenaline and angiotensin II did not change in portal hypertensive vessels compared with controls and was equal in oesophageal and mesenteric vessels. The ability of isoprenaline and serotonin to relax pre-contracted vessels of both types was reduced by the portal hypertension. The results of these studies suggest that the development of oesophageal varices is not only due to increased portal venous pressure.

Length-tension relationships of small arteries, veins, and lymphatics from the rat mesenteric microcirculation

“…By the same approach, we determined the maximal active stress to be ϳ0.53-1.48 ϫ 10 5 N/m 2 in small mesenteric veins and ϳ0.38 -0.60 ϫ 10 5 N/m 2 in mesenteric lymphatics. There have been only a few measurements of maximal active stress reported for small veins (1,7,27). At least one of these (27) agrees quite closely (143 kN/m 2 ) with the present results (148 kN/m 2 ).…”

“…There have been only a few measurements of maximal active stress reported for small veins (1,7,27). At least one of these (27) agrees quite closely (143 kN/m 2 ) with the present results (148 kN/m 2 ). There are only a few previous reports (15, 16, 32) of maximal active tension and wall stress in lymphatics.…”

“…Mesenteric veins differ from their corresponding arteries in terms of wall morphology and contractile properties (42,47), even though they exhibit comparable expression levels of contractile proteins such as actin, myosin light chain, myosin heavy chain, and calponin (50). Maximal active tension and stress as a function of preload have been previously recorded in mesenteric veins (1,7,27). Because mesenteric lymphatics from rat (18) and cow (17,31) exhibit similar pressure-volume and pressure-radius relationships as peripheral veins (34,39), we hypothesized that mesenteric lymphatics would exhibit a contractile capacity similar to that of mesenteric veins.…”

Effects of portal hypertension on responsiveness of rat mesenteric artery and aorta

“…This difference may be due to differing susceptibilities to the actions of vasodilators such as glucagon. In other studies of portal hypertension, the contractile response to NA was reported to be increased in the aorta and decreased in the portal vein of portal hypertensive rats (Bomzon et al, 1991), unchanged in femoral artery (Villamediana et al, 1988) from cirrhotic rats, but increased in mesenteric veins from portal vein ligated rabbits (Jensen et al, 1987). Other studies of isolated blood vessels report no change in the contractile response to angiotensin II in aorta (Leehey, 1993) or femoral artery (Villamediana et al, 1989) from cirrhotic rats, and an increased contraction to 5-HT in mesenteric veins from portal hypertensive rats (Cummings et al, 1986).…”

“…Increased contractile response could be due to alterations in second messenger systems, or to alterations in smooth muscle mass. It has been previously reported that an increased maximum contraction to NA and angiotensin II in mesenteric veins from portal hypertensive rabbits was due to an increase in media thickness, and thus to an increase in smooth muscle (Jensen et al, 1987), presumably as an adaptive change to increased pressure. Similar hypertrophy of the portal vein has been reported in portal hypertensive rats, with concomitant increased contraction to KCl (Chao et al, 1992).…”