Hyperdynamic circulation in portal-hypertensive rats is dependent on central c-fos gene expression

Song, Daisheng; Liu, Hongqun; Sharkey, Keith A.; Lee, Samuel S.

doi:10.1053/jhep.2002.30417

Cited by 49 publications

(42 citation statements)

References 50 publications

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“…Though the reduction in peripheral resistance is slow, compensatory mechanisms play a pivotal role in maintaining and further worsening the hyperdynamic circulation ( Fig. 1) [12][13][14][15][16]. Plasma volume expansion is relevant in these cirrhotic patients, even if distribution between the central and peripheral vascular areas is often not balanced [6,17].…”

Section: Hemodynamic Changes Contributing To Hyperdynamic Syndromementioning

confidence: 99%

Clinical implications of the hyperdynamic syndrome in cirrhosis

Licata

Mazzola

Ingrassia

et al. 2014

European Journal of Internal Medicine

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The hyperdynamic syndrome is a late consequence of portal hypertension in cirrhosis. The principal hemodynamic manifestations of the hyperdynamic syndrome are high cardiac output, and increased heart rate and total blood volume, accompanied by reduced total systemic vascular resistance. Pathophysiology involves a complex of humoral and neural mechanisms that can determine hemodynamic changes, and lead to hyperdynamic circulation. In this review we focus our attention on the manifestations of the hyperdynamic syndrome. Some of these are well described and directly related to portal hypertension (varices, ascites, hepatic encephalopathy, and hepatorenal syndrome), while others, such as hepatopulmonary syndrome, portopulmonary hypertension, and cirrhotic cardiomyopathy, are less known as clinical manifestations related to cirrhosis and, therefore, merit further investigation.

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Section: Hemodynamic Changes Contributing To Hyperdynamic Syndromementioning

confidence: 99%

Clinical implications of the hyperdynamic syndrome in cirrhosis

Licata

Mazzola

Ingrassia

et al. 2014

European Journal of Internal Medicine

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show abstract

“…Besides NTS neuronal activations, increased Fos immunoreactivity was also observed in PBN neurons after IL-1b administration (Buller et al 2004), what confirms the involvement of PBN in inflammatory processes (Bellavance and Beitz 1996). Besides pro-inflammatory cytokines, other factors including changes in osmolality and haemodynamicity (Kobashi and Adachi 1986;Gu and Ju 1995;Krukoff et al 1995;Smith et al 1995;Morita et al 1997;Grindstaff et al 2000;Blair et al 2001;Song et al 2002), may induce Fos expression in both the abovementioned nuclei as well as in the SFO, LC, and A1/C1 regions and the magnocellular PVN and SON neurons. Actually, the portal vein contributes much more effectively to liver blood supplementation than hepatic artery (Nishida et al 2000) and portal triade clamping noticeably reduced the liver blood flow and temporary liver blood pressure after the reperfusion (Chávez-Cartaya et al 1994;Nishida et al 2000).…”

Section: Discussionmentioning

confidence: 54%

Effect of Liver Ischemia–Reperfusion Injury on the Activity of Neurons in the Rat Brain

et al. 2009

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Liver ischemia-reperfusion injury (LIRI) influences different body cells. Little is known about the effect of LIRI on the activity of neurons. Response of neurons to: (1) single ligation of hepatic artery (LIRIa) for 30 min and (2) combined ligation of portal triade (common hepatic artery, portal vein, common bile duct, LIRIb) for 15 min was investigated in Wistar rats. Ninety minutes, 5 h, and 24 h after liver reperfusion, alanine aminotransferase (ALT) and aspartate aminotransferase (AST), interleukin 1alpha (IL-1alpha), and tumor necrosis factor alpha (TNFalpha) serum levels were analyzed and Fos-immunolabeled cells counted in subfornical organ (SFO), suprachiasmatic (SCH), paraventricular (PVN), supraoptic (SON), arcuate (ARC), and ventromedial (VMN) hypothalamic nuclei, locus coeruleus (LC), nucleus of the solitary tract (NTS), and A1/C1 catecholaminergic cell groups. LIRIb increased ALT serum level after 90 min and 24 h while AST activity only after 24 h in all experimental groups. IL-1alpha serum level was increased only after 90 min of LIRIb while TNFalpha level did not change. Ninety minutes after surgeries more Fos-immunostained cells occurred in both LIRIs than sham-operated animals in all structures studied. More distinct Fos expression occurred after LIRIb than LIRIa in SON, PVN, VMN, and NTS. Five hours after both LIRIs, Fos increased in the parabrachial nucleus (PBN) and NTS. Twenty-four hours after both LIRIs Fos incidence decreased in all groups. Although the present data indicate that increased neuronal activity after both LIRIs is mainly a consequence of the liver damage itself partial impact of non-specific factors can not be excluded. However, the anatomical distribution of Fos occurrence detected after LIRIs gives great opportunity to perform a targeted phenotypic identification of the activated neurons by LIRIs in the subsequent experiments.

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“…This treatment completely blocked the development of the hyperdynamic circulation, i.e., abnormalities in cardiac output, mean arterial pressure and systemic vascular resistance were completely eliminated [45] . In normal control rats, c-fos antisense oligonucleotides had no effect [45] . These results indicate that central neural activation is a sine qua non for the development of the hyperdynamic circulation in portal hypertension.…”

Section: Central Neural Mechanismsmentioning

confidence: 99%

Cardiac and vascular changes in cirrhosis: Pathogenic mechanisms

Liu

Gaskari²,

Lee

2006

WJG

Self Cite

130

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Cardiovascular abnormalities accompany both portal hypertension and cirrhosis. These consist of hyperdynamic circulation, defined as reduced mean arterial pressure and systemic vascular resistance, and increased cardiac output. Despite the baseline increased cardiac output, ventricular inotropic and chronotropic responses to stimuli are blunted, a condition known as cirrhotic cardiomyopathy. Both conditions may play an initiating or aggravating pathogenic role in many of the complications of liver failure or portal hypertension including ascites, variceal bleeding, hepatorenal syndrome and increased postoperative mortality after major surgery or liver transplantation. This review briefly examines the major mechanisms that may underlie these cardiovascular abnormalities, concentrating on nitric oxide, endogenous cannabinoids, central neural activation and adrenergic receptor changes. Future work should address the complex interrelationships between these systems.

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Hyperdynamic circulation in portal-hypertensive rats is dependent on central c-fos gene expression

Cited by 49 publications

References 50 publications

Clinical implications of the hyperdynamic syndrome in cirrhosis

Clinical implications of the hyperdynamic syndrome in cirrhosis

Effect of Liver Ischemia–Reperfusion Injury on the Activity of Neurons in the Rat Brain

Cardiac and vascular changes in cirrhosis: Pathogenic mechanisms

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