1998
DOI: 10.1016/s0168-8278(98)80022-6
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The sympathetic nervous system in liver disease

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Cited by 148 publications
(123 citation statements)
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References 121 publications
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“…However, the relative CBV was significantly lower in the cirrhotic group and a normal volume may be relatively reduced if the capacity of the vascular bed is enlarged. A key feature is that the effective blood volume is physiologically reduced and activates volume and baroreceptors, as reflected by the increased sympathetic nervous activity and activated renin-angiotensin-aldosterone system (9,25,27). This is also supported by the finding of an increased arterial central compliance in patients with cirrhosis, as recently reported by our group (8,10,18).…”
Section: Discussionsupporting
confidence: 59%
“…However, the relative CBV was significantly lower in the cirrhotic group and a normal volume may be relatively reduced if the capacity of the vascular bed is enlarged. A key feature is that the effective blood volume is physiologically reduced and activates volume and baroreceptors, as reflected by the increased sympathetic nervous activity and activated renin-angiotensin-aldosterone system (9,25,27). This is also supported by the finding of an increased arterial central compliance in patients with cirrhosis, as recently reported by our group (8,10,18).…”
Section: Discussionsupporting
confidence: 59%
“…Indeed in human cirrhosis, myocardial hypertrophy could be an adaptive response to chronically expanded blood volume, since these patients have sodium and water retention, starting at the pre-ascitic stage of the disease [24,49]: notably at this early stage neuroendocrine overactivity is slight, becoming increasingly more severe as the cirrhotic process progresses [30]. Nevertheless, in previous studies sympathetic nerve outflow has been documented to be already in- creased even in the compensated stage of disease [50,51]: then the sympathetic nervous system could play a key role in the development of left ventricular hypertrophy in cirrhosis, as already clearly reported in hypertension [52].…”
Section: Discussionmentioning
confidence: 99%
“…Diastolic dysfunction, characterized by an altered pattern of transmitral flow due to impaired diastolic relaxation of left ventricle, can be easily assessed by echocardiography and accordingly can be considered as a marker of this condition. As far as diastolic dysfunction is concerned, many etiological factors have been reliably advocated as potential pathogenic agents: notably substances as NO [18][19][20][21], TNF [22], reactive nitrogen species [23], neurohormones [24][25][26][27][28] may well affect heart structure and function along with circulatory overload [24,29] and overactivity of the SNS [30]. Thickening of heart parietal walls has been reported [12,14,17,31], nevertheless the nature of the structural changes underlying diastolic dysfunction has not been clarified so far.…”
Section: Introductionmentioning
confidence: 99%
“…Patients with LC have shown enhanced sympathetic nervous system activity, including increases in sympathetic nerve burst frequency and circulating catecholamine concentrations. 13 Because most LC patients do not have hypertension, changes in LC patients may be due to stimulation mediated by baroreceptors and volume receptors, resulting from low AP and reduced central blood volume. 13,14 Therefore, in LC patients, cardiac remodeling may be caused primarily by sympathetic overactivity together with the induction of an autonomic imbalance and relative parasympathetic withdrawal and, finally, with BRS impairment.…”
Section: Discussionmentioning
confidence: 99%