Abstract
We tested the hypothesis that there is a topographical sympathetic activation in rats submitted to experimental cirrhosis. Baseline renal (rSNA) and splanchnic (sSNA) sympathetic nerve activities were evaluated in anesthetized rats. In addition, we evaluated main arterial pressure (MAP), heart rate (HR), and baroreceptor reflex sensitivity (BRS). Cirrhotic Wistar rats were obtained by bile duct ligation (BDL). MAP and HR were measured in conscious rats, and cardiac BRS was assessed by changes in blood pressure induced by increasing doses of phenylephrine or sodium nitroprusside. The BRS and baseline for the control of sSNA and rSNA were also evaluated in urethane-anesthetized rats. Cirrhotic rats had increased baseline sSNA (BDL, 102 vs control, 58 spikes/s; p<0.05), but no baseline changes in the rSNA compared to controls. These data were accompanied by increased splanchnic BRS (p<0.05) and decreased cardiac (p<0.05) and renal BRS (p<0.05). Furthermore, BDL rats had reduced basal MAP (BDL, 93 vs control, 101 mmHg; p<0.05) accompanied by increased HR (BDL, 378 vs control, 356; p<0.05). Our data have shown topographical sympathetic activation in rats submitted to experimental cirrhosis. The BDL group had increased baseline sSNA, independent of dysfunction in the BRS and no changes in baseline rSNA. However, an impairment of rSNA and HR control by arterial baroreceptor was noted. We suggest that arterial baroreceptor impairment of rSNA and HR is an early marker of cardiovascular dysfunction related to liver cirrhosis and probably a major mechanism leading to sympathoexcitation in decompensated phase.
Highlights
The cardiovascular autonomic dysfunction is well established in cirrhosis of different etiologies, with the degree of sympathetic activation strongly associated with the disease severity and poor prognosis [1, 2]
mean arterial pressure (MAP) and heart rate (HR) were measured in conscious rats, and cardiac baroreceptor reflex sensitivity (BRS) was assessed by changes in blood pressure induced by increasing doses of phenylephrine or sodium nitroprusside
We suggest that arterial baroreceptor impairment of renal sympathetic nerve activity (rSNA) and HR is an early marker of cardiovascular dysfunction related to liver cirrhosis and probably a major mechanism leading to sympathoexcitation in decompensated phase
Summary
The cardiovascular autonomic dysfunction is well established in cirrhosis of different etiologies, with the degree of sympathetic activation strongly associated with the disease severity and poor prognosis [1, 2]. Increased sympathetic nerve activity was observed in both patients and experimental animal models of liver cirrhosis, evidenced by increased plasma levels of norepinephrine or norepinephrine spillover from the neuroeffector junctions, compatible with the activation of the sympathetic nervous system [3,4,5,6,7,8,9,10]. PLOS ONE | DOI:10.1371/journal.pone.0152512 April 7, 2016
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