Low NO bioavailability in CCl4cirrhotic rat livers might result from low NO synthesis combined with decreased superoxide dismutase activity allowing superoxide-mediated NO breakdown: A comparison of two portal hypertensive rat models with healthy controls

Table 2 eNOS related parameters in rat livers: caveolin-1, endothelin-1, as well as SOD total activity and malondialdehyde levels.

	Normal	PPVL	CCl₄ cirrhosis
	(n = 9)	(n = 5)	(n = 9)
Body weight (g)	272 (10)	280 (13)	355 (58)*
Liver weight (g)	10.4 (0.8)	9.7 (0.9)	14.8 (5.6)
Portal venous pressure (mm Hg)	5.0 (1.1)	9.9 (1.5)*	11.0 (2.9)*
cDNA dilutions still detecting caveolin-1 by RT-PCR	128 [4–512]	32 [8–256]	384 [128–2048]
cDNA dilutions still detecting endothelin-1 by RT-PCR	8 [0–64]	13 [2–144]	310 [16–512]*
SOD total activity (U/mg protein)	15 (7)	14 (3)	10 (3)*
Malondialdehyde (pmol/mg liver)	15 [2–20]	8 [4–16]	26 [6–130]*

* p < 0.05 as compared with normal group. PPVL: partial portal vein ligation (= model of prehepatic portal hypertension). CCl₄ cirrhosis: carbon tetrachloride induced cirrhosis. Livers of normal and two types of portal hypertensive rats used for the study of eNOS related parameters: caveolin-1 and endothelin-1 as well as superoxide dismutase (SOD) activity and malondialdehyde levels. For cDNA dilutions see Methods. Data are expressed as mean (SD) for normally distributed data or median [range] for not normally distributed data.