Portal and arterial free and conjugated noradrenaline in two models of portal hypertension in rats

Gaudin, Christophe; Ruget, G; Braillon, Alain; Selz, Françoise; Cuche, Jean-Louis; Lebrec, Didier

doi:10.1016/0024-3205(89)90019-2

Cited by 21 publications

(14 citation statements)

References 18 publications

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“…However, this was not the aim of the current investigation and has to be addressed by further studies. Nonetheless, our data concur with previous indirect evidence of enhanced splanchnic NA release showing increased NA concentrations in portal venous as compared to arterial and/or peripheral blood samples in human [6] and experimental cirrhosis [5].…”

Section: Discussionsupporting

confidence: 93%

“…Es gibt deutliche Evidenz dafür, dass bei portaler Hypertension die systemischen NA-Plasmakonzentrationen hauptsächlich von der mesenterialen NA-Produktion abhängen [5]. Aber anders als bei systemischen NAKonzentrationen sind Daten zu lokaler splanchnischer Neurotransmitter-Produktion und -Sekretion sehr spärlich vorhanden und zudem kontrovers [6][7][8][9][10][11][12].…”

Section: Dysbalance In Sympathetic Neurotransmitter Release and Actiounclassified

“…Portal hypertension decreases afterwards due to the development of portosystemic collaterals, whereas compensatory SNS upregulation and altered NA release in cirrhosis emerge chronically [22]. In cirrhotic rats, systemic NA levels are higher than in PVL rats, indicating that enhanced sympathetic nerve activity depends on the development of cirrhosis [5]. Therefore, PVL rats were not used for NA measurement.…”

Section: Protocol I: Desensitization To Repetitive Pns and Neurotransmentioning

confidence: 99%

“…Upregulated sympathetic nervous system (SNS), acting as compensatory mechanism, reveals prognostic significance, namely increased serum levels of noradrenaline (NA), correlating with survival of cirrhotic patients [3,4]. In case of portal hypertension, systemic plasma NA levels could mainly depend on splanchnic NA production [5]. Besides systemic NA levels, data in terms of actual splanchnic synthesis/release of neurotransmitters are scarce and controversial [6][7][8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

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Dysbalance in sympathetic neurotransmitter release and action in cirrhotic rats: Impact of exogenous neuropeptide Y

Dietrich¹,

Moleda²,

Kees

et al. 2013

Journal of Hepatology

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Section: Discussionsupporting

confidence: 93%

Section: Dysbalance In Sympathetic Neurotransmitter Release and Actiounclassified

Section: Protocol I: Desensitization To Repetitive Pns and Neurotransmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Dysbalance in sympathetic neurotransmitter release and action in cirrhotic rats: Impact of exogenous neuropeptide Y

Dietrich¹,

Moleda²,

Kees

et al. 2013

Journal of Hepatology

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“…The cirrhotic patients 60,61,62 and in animal models of cirrhosis. 63,64 degree of motional freedom for lipid moieties in the memBaseline norepinephrine levels are positively correlated with brane has been termed ''fluidity,'' and this parameter can be the severity of cirrhosis. 16 Sustained increases in norepinephassessed by means of fluorescent probes, such as diphenylrine are known to cause myocardial injury 65 and b-adrenergic hexatriene, that can be incorporated into the plasma memreceptor desensitization.…”

Section: Cardiac Histology In Cirrhosismentioning

confidence: 99%

Cirrhotic cardiomyopathy: Getting to the heart of the matter

1996

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can lead to liver dysfunction and damage. How unexpected In cirrhosis, cardiac contractile function has been exand gratifying, therefore, to find a voice as eloquent as the tensively documented to be abnormal. At baseline, carlate Chilean Nobel laureate's to not only extoll the many diac output is increased, and this is one of the charactervirtues of the liver, but also remind us that sometimes the istics of hyperdynamic circulation. However, when liver takes precedence over the heart, i.e., that liver failure cirrhotic patients are challenged by pharmacological or can also lead to cardiac dysfunction. physiological stress, ventricular hyporesponsiveness is It has been known for more than four decades that hepatic revealed. Similar patterns have been noted in cirrhotic cirrhosis is associated with a host of cardiovascular abnoranimal models. This phenomenon has been termed ''cirmalities. The initial studies in the early 1950s documented rhotic cardiomyopathy.'' Although alcohol abuse may the existence of hyperdynamic circulation in cirrhosis, manicontribute to some cases of cirrhotic cardiomyopathy, it has been clearly documented to occur even in the ab-fested by increased cardiac output and reduced systemic vassence of alcohol ingestion. Diminished myocardial b-ad-cular resistance. This latter phenomenon, the peripheral varenergic receptor signal transduction function, possibly sodilatation, continues to fascinate investigators even up to caused by a persistent elevation in norepinephrine con-the present, and recent studies have examined the possible tent, has been shown to play an important role. Alter-role of nitric oxide and other endothelium-dependent factors ation in cardiac plasma membrane properties due to im-in mediating the vasodilatation. The heart itself was not expaired lipid metabolism is also crucial. Other possible amined until about three decades ago, and around that time pathogenic factors are reviewed, including accumula-studies of cardiac contractile function in patients with alcotion of cardiodepressant substances caused by hepato-holic-induced liver disease started consistently showing that cellular insufficiency, and ventricular overload sec-despite the increased baseline cardiac output, when ventricuondary to increased blood volume and hyperdynamic lar contractile responses were tested under conditions of circulation. Because the cardiac reserve function is bor-pharmacological or physiological stress, the heart behaved derline in patients with cirrhosis, cardiovascular status abnormally in a blunted manner. For many years, this was should be carefully monitored, especially when patients ascribed to the well-known direct toxic effects of alcohol on undergo stresses such as liver transplantation or porto-cardiac muscle, i.e., as a manifestation of latent or subclinical systemic shunting procedures. (HEPATOLOGY 1996;24: alcoholic cardiomyopathy, and relegated to the scientific 451-459.)backwaters as a clinically insignificant curiosity. However, recently several studies have emerged in both ...

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Plasma catecholamines in patients with presinusoidal portal hypertension: Comparison with cirrhotic patients and nonportal hypertensive subjects

et al. 1991

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During a hemodynamic study, plasma catecholamine concentrations were measured in the pulmonary artery and in the hepatic vein in 18 presinusoidal portal hypertensive patients. Results were compared with those in 15 nonportal hypertensive subjects and in 24 cirrhotic patients in good condition (grade A, according to Pugh's classification). Plasma norepinephrine concentrations in the pulmonary artery or in the hepatic vein were not significantly different between nonportal hypertensive subjects (mean +/- S.E.M.: 271 +/- 36 and 83 +/- 11 pg/ml, respectively) and presinusoidal portal hypertensive patients (273 +/- 33 and 84 +/- 11 pg/ml, respectively). These concentrations were, however, elevated in cirrhotic patients (408 +/- 47 and 256 +/- 45 pg/ml, p less than 0.05 in comparison with the two other groups). These differences suggest that increased sympathetic nervous activity in cirrhosis is associated with the presence of liver disease or increase in sinusoidal pressure. Differences in plasma epinephrine concentrations were not significant among the three groups of patients. However, the existence of a significant correlation between pulmonary artery plasma epinephrine concentration and cardiac index (r2 = 0.46, p less than 0.01) in patients with presinusoidal portal hypertension suggests that the adrenal medulla could play a role in the pathophysiology of the hyperkinetic syndrome of these patients.

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Portal and arterial free and conjugated noradrenaline in two models of portal hypertension in rats

Cited by 21 publications

References 18 publications

Dysbalance in sympathetic neurotransmitter release and action in cirrhotic rats: Impact of exogenous neuropeptide Y

Dysbalance in sympathetic neurotransmitter release and action in cirrhotic rats: Impact of exogenous neuropeptide Y

Cirrhotic cardiomyopathy: Getting to the heart of the matter

Plasma catecholamines in patients with presinusoidal portal hypertension: Comparison with cirrhotic patients and nonportal hypertensive subjects

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