27 research outputs found
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
Renal function.
<p>Comparisons between means ± SD of FENa, kaliuresis, plasma Na, etc. taken on weeks 11–12 (Group GX<sub>A</sub>) vs. weeks 13–14 (Group GX<sub>B</sub>) 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<sub>B</sub>, vs. weeks 11–12, Group GX<sub>A</sub>).</p
Marked increase in PRA (concurrent with development of diuretic-unresponsive ascites) over CCL<sub>4</sub> weeks 13–14 in cirrhotic rats (G3, untreated, red line, and G4, receiving diuretics only, yellow line).
<p>Blunting of renin secretion in G5 (cirrhotic rats treated with diuretics plus clonidine, blue line) and G6 (cirrhotic rats treated with diuretics plus oral prodrug of guanfacine, green line). Further group depicted: G1 (untreated controls, black line). Mean measurements ± SD of three rats studied at a time in each group are depicted.</p
Transient natriuretic effects in G4 (cirrhotic rats treated with furosemide and potassium canrenoate, yellow line) and G5 (cirrhotic rats treated with diuretics plus clonidine, blue line) over CCl<sub>4</sub> weeks 11–12.
<p>Progressive natriuretic effects in G6 (cirrhotic rats treated with diuretics plus oral prodrug of guanfacine, green line). Further groups depicted: G1 (healthy controls, black line), G3 (untreated cirrhotic rats, red line). Mean measurements ± SD of three rats studied at a time in each group are depicted.</p
Hormonal status.
<p>Comparisons between means ± SD of PRA, plasma aldosterone, etc. taken on weeks 11–12 (Group GX<sub>A</sub>) vs. weeks 13–14 (Group GX<sub>B</sub>) 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<sub>B</sub>, vs. weeks 11–12, Group GX<sub>A</sub>).</p
Progressive weight gain of untreated cirrhotic rats (G3, red line) and of cirrhotic rats treated with diuretics (G4, yellow line) or with diuretics plus clonidine (G5, blue line).
<p>Further groups depicted: G1 (healthy controls, black line), G6 (cirrhotic rats treated with diuretics plus oral prodrug of guanfacine, green line). Mean measurements ± SD of three rats studied at a time in each group are depicted.</p
Both human activated, myofibroblast-like, hepatic stellate cells and human hepatoblastoma cells show basal expression of chymase mRNA and a considerable increase in its expression after stimulation with TGF-β1, earlier in HepG2 cells and later in activated stellate cells.
<p>Both human activated, myofibroblast-like, hepatic stellate cells and human hepatoblastoma cells show basal expression of chymase mRNA and a considerable increase in its expression after stimulation with TGF-β1, earlier in HepG2 cells and later in activated stellate cells.</p
Renal chymase indirect immunofluorescence staining.
<p>Enhanced tubular expression of chymase in cirrhotic rats. Goat polyclonal anti-chymase primary antibodies (Santa Cruz Biotechnology, Inc.) and anti-goat C3y-conjugated secondary antibodies (Amersham Biosciences, Braunschweig, Germany) were used.</p
Morphological analysis of chronic liver disease progression.
<p>13 weeks of CCl<sub>4</sub> (G3): development of liver cirrhosis (and ascites). The liver of rats receiving both CCl<sub>4</sub> 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