Graphical depiction of adrenergic hypertone in cirrhotic rats, treated (G4) or not (G3) with diuretics.

<p>Early (G5) and late (G6) blunting of adrenergic function in cirrhotic rats receiving, respectively, clonidine or guanfacine, along with diuretics.</p

Hormonal status.

<p>Comparisons between means ± SD of PRA, plasma aldosterone, etc. taken on weeks 11–12 (Group GX_A) vs. weeks 13–14 (Group GX_B) or among different G1–G6 groups. In each group, worsening of clinical parameters <u>underlined</u>, improvements in <b>bold</b> print (weeks 13–14, Group GX_B, vs. weeks 11–12, Group GX_A).</p

Morphological analysis of chronic liver disease progression.

<p>13 weeks of CCl₄ (G3): development of liver cirrhosis (and ascites). The liver of rats receiving both CCl₄ and the chymase inhibitor was characterized by a significant prevention of fibrosis progression towards cirrhosis. This was maximal in animals treated with 20 mg/kg b.w. of the chymase inhibitor (G5). Prevention of fibrosis progression is clearly documented by either Gomori trichrome staining or Sirius Red.</p

Liver weight and function data, portal pressure, and hepatic tissue levels of Ang II and ET-1 in the different rat groups.

<p>Liver weight and function data, portal pressure, and hepatic tissue levels of Ang II and ET-1 in the different rat groups.</p

Renal distribution of chymase.

<p>Panel A: Indirect immunofluorescence staining of kidney sections from cirrhotic rats (G3 group). Panel B: Immunohistochemical staining for chymase in kidney sections from either control animals (G1) or cirrhotic rats (G3). In the kidney of cirrhotic rats, chymase was found in the wall of cortical arterioles (Panel A), in the wall of proximal convoluted tubules (Panel B, green arrows), in distal convoluted tubules (Panel B, red arrows), and at the vascular pole of the glomerulus (Panel B, black arrow).</p

Chymase immunohistochemical localization in resected samples of normal and cirrhotic human liver.

<p>Original magnification as indicated.</p

Morphological analysis of chronic liver disease progression through αSMA immunohistochemistry.

<p>Administration of chymase inhibitor to healthy rats (G2) did not affect normal liver morphology. 13 weeks of CCl₄ (G3): development of liver cirrhosis (and ascites). The liver of rats receiving both CCl₄ and the chymase inhibitor was characterized by a significant prevention of fibrosis progression towards cirrhosis. This, already appreciable in G4, was maximal in animals treated with 20 mg/kg b.w. of the chymase inhibitor (G5).</p