Abstract
ABSTRACTPurpose:To assess the biochemical, histological, histomorphometric and molecular effects of biliary duct ligation (BDL) induced liver cirrhosis in the heart and kidneys.Methods:Thirty-two weaning rats (21 days old, 50-70 g) underwent BDL and were divided in four groups (euthanasia after two, four, six, and eight weeks, respectively) and compared to control groups.Results:The animals’ hearts of group 3 were bigger than those of the control group (p=0.042), including thinner right ventricle wall, decreased internal diameter of ventricles, and increased perivascular collagen deposition in left ventricle, as well as increased interstitial collagen in right ventricle after six weeks. In the kidneys of groups 3 and 4, bilirubin impregnation in the tubules, hydropic degeneration, loss of nuclei and lack of plasmatic membrane limits were noted. Nitric oxide synthase (NOS) gene expressions were higher in group 1 (p=0.008), and endothelial nitric oxide synthase (eNOS) gene expressions were elevated in all experimental groups (p=0.008, p=0.001, p=0.022, and p=0.013, respectively). In the heart, a decreased expression of eNOS in group 1 (p=0.04) was observed.Conclusions:Liver cirrhosis leads to histological and histomorphometric alterations in the heart and kidneys, with changes in the NOS and eNOS gene expressions, that may suggest a role in the associated myocardial and renal manifestations.
Highlights
Liver cirrhosis results from progressive replacement of normal parenchyma by fibrosis, nodule formation and the development of signs and symptoms of portal hypertension and organ failure
Nitric oxide synthase (NOS) gene expressions were higher in group 1 (p=0.008), and endothelial nitric oxide synthase gene expressions were elevated in all experimental groups (p=0.008, p=0.001, p=0.022, and p=0.013, respectively)
All biliary duct ligation (BDL) animals showed dilation of the common biliary duct as a consequence of the distal obstruction that accentuated throughout time, with evident liver parenchyma alterations, ascites accumulation and splenomegaly
Summary
Liver cirrhosis results from progressive replacement of normal parenchyma by fibrosis, nodule formation and the development of signs and symptoms of portal hypertension and organ failure. It was verified that patients with portal hypertension have increased both circulating and endothelial vasodilators7—such as nitric oxide (NO)8—, owing to a combination of impaired hepatic function and escape of vasodilators through portosystemic shunts[9] This process contributes to the development of splanchnic arterial vasodilatation, leading to the development of a hyperdynamic syndrome with reduced central blood volume followed by baroreceptor-induced activation of the reninangiotensin-aldosterone system (RAAS) and the sympathetic nervous system (SNS)[10]. This activation phenomenon causes renal vasoconstriction, which is intrinsically related to the development of the hepato-renal syndrome[11]
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