Sustained Elevation in Circulating Catecholamine Levels During Polymicrobial Sepsis

Hahn, Peter Y.; Wang, Haichao; Tait, S. M.; Ba, Zheng F.; Reich, Stephen; Chaudry, Irshad H.

doi:10.1097/00024382-199510000-00007

Cited by 97 publications

(61 citation statements)

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“…Using a cecal ligation and puncture (CLP) model of rodent polymicrobial sepsis, we previously demonstrated that the up-regulation of pro-inflammatory cytokines, such as TNF-α, is caused by the increased release of NE from the gut during sepsis. This is evidenced by our studies (40) and others (41), which show that peripheral sympathetic activity increases during sepsis, resulting in the elevation of plasma levels of NE. Intraportal infusion of NE in vivo increased TNF-α release and was inhibited by co-infusion with yohimbine, a non-specific antagonist of the α 2 -adrenergic receptor.…”

Section: Direct Effect Of Ethanol On Kupffer Cell Activation By Norepsupporting

confidence: 78%

Alcohol and hepatocyte-Kupffer cell interaction (Review)

Ajakaiye

Jacob

et al. 2011

Mol Med Rep

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Abstract. Alcoholic liver disease accounts for 12,000 deaths per year in the United States and is the second leading indication for liver transplantation. It covers a spectrum of disease conditions ranging from steatosis and cirrhosis to hepatic malignancies. Epidemiological data clearly show a strong correlation between alcohol consumption and liver diseases. A large body of evidence has accumulated over the years in determining the molecular mediators of alcohol-induced liver injury. In this review, we provide an overview of such mediators, which include alcohol metabolites and reactive oxygen/ nitrogen species, endotoxin via bacterial translocation from the gut and TNF-α, and highlight the role of the sympathetic nervous stimuli, norepinephrine and the α 2A -adrenergic receptors in contributing to the deleterious effect observed in alcohol-induced hepatic dysfunction.

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Section: Direct Effect Of Ethanol On Kupffer Cell Activation By Norepsupporting

confidence: 78%

Alcohol and hepatocyte-Kupffer cell interaction (Review)

Ajakaiye

Jacob

et al. 2011

Mol Med Rep

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“…This is evidenced by our studies 8 and others 9 which show that peripheral sympathetic activity increases during sepsis resulting in the elevation of plasma levels of NE. In addition, enterectomy prior to onset of sepsis markedly reduced circulating levels of NE.…”

Section: -7supporting

confidence: 72%

Mechanism of the inhibitory effect of ghrelin in sepsis

Jacob

Zhou

et al. 2010

HMER

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Sepsis and septic shock are the leading causes of death in intensive care units. Approximately 40%-70% of the mortality is associated with severe sepsis and septic shock. Systemic antibiotic usage, surgical intervention, aggressive fluid resuscitation and careful monitoring are common measures currently used to treat sepsis. Despite the advances in the understanding of the pathophysiology of sepsis, very little progress has been made towards therapeutic interventions. Recently we have shown that ghrelin, a stomach-derived peptide which is an endogenous ligand for the growth hormone secretagogue receptor (GHSR-1a), is beneficial in attenuating the inflammatory response, organ injury and mortality in an experimental model of polymicrobial sepsis induced by cecal ligation and puncture (CLP). In this review, we describe the mechanism of action of ghrelin in sepsis, highlight the role ghrelin plays in attenuating the hepatic dysfunction induced by sepsis and septic shock and suggest in developing ghrelin as a potential therapy for sepsis.

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“…Septic patients are known to be exhibit increased levels of catecholamines (55,83,84). These findings have been confirmed in various animal studies (85,86). In a murine model of sepsis, decreased density of β-adrenoceptors on the myocardium was reported (87,88).…”

Section: β-Adrenergic Receptorsmentioning

confidence: 74%

Molecular Events in the Cardiomyopathy of Sepsis

Flierl

Rittirsch

Huber‐Lang

et al. 2008

Mol Med

108

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Septic cardiomyopathy is a well-described complication of severe sepsis and septic shock. However, the interplay of its underlying mechanisms remains enigmatic. Consequently, we constantly add to our pathophysiological understanding of septic cardiomyopathy. Various cardiosuppressive mediators have been discovered, as have multiple molecular mechanisms (alterations of myocardial calcium homeostasis, mitochondrial dysfunction, and myocardial apoptosis) that may be involved in myocardial dysfunction during sepsis. Finally, the detrimental roles of nitric oxide and peroxynitrite have been unraveled. Here, we describe our present understanding of systemic, supracellular, and cellular molecular mechanisms involved in sepsis-induced myocardial suppression. SYSTEMIC, SUPRACELLULAR MECHANISMS Decreased Coronary Blood FlowOne of the first suggestions was that reduced coronary perfusion in the septic heart might be responsible for a setting of global cardiac ischemia. This hypothesis was soon abandoned after direct measurements of coronary blood flow were obtained, showing no reduced, but rather increased, coronary blood flow (22,23). In later studies, however, increased levels of plasma troponin were observed and correlated with the severity of myocardial depression during sepsis and septic shock (24). Myocardial necrosis could not be observed in patients who died from septic shock (3,25), however, raising the question whether increases in troponin were due to cytokine-induced, transient increases in cardiomyocyte membrane permeability to troponin. To date, this remains to be determined. Alterations of MicrovasculatureThere is now increasing evidence that sepsis and septic shock leads to changes of the myocardial microvasculature. In a canine model of endotoxemia, maldistribution of heterogeneous coronary blood flow has been reported (26). These findings might be caused by endothelial swelling and nonocclusive intravascular fibrin deposits in the microvasculature (27). In parallel, activated cardiomyocytes from septic mice promoted transendothelial migration and activation of circulating neutrophils into the interstitium (28) where these cells may augment the sepsis-induced intracardial inflammation, and contribute to an increased vascular leakage, which has been described to also impair cardiac function and compliance secondary to myocardial edema (29,30). Yet, studies have failed to confirm cellular hypoxia in a murine sepsis model (31). Cardiosuppressing Circulating Proinflammatory MediatorsAnother hypothesis suggested circulating myocardium-depressing factors as the cause of septic cardiomyopathy (32). Parrillo et al. (33) confirmed the existence of a cardiodepressant substance by incubating isolated rat cardiomyocytes with serum obtained from septic shock patients, leading to decreased amplitude and velocity of cardiomyocyte shortening. Levels of cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and the complement anaphylatoxin, C5a, are known to be elevated in the circulation during sepsis an...

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Sustained Elevation in Circulating Catecholamine Levels During Polymicrobial Sepsis

Cited by 97 publications

References 0 publications

Alcohol and hepatocyte-Kupffer cell interaction (Review)

Alcohol and hepatocyte-Kupffer cell interaction (Review)

Mechanism of the inhibitory effect of ghrelin in sepsis

Molecular Events in the Cardiomyopathy of Sepsis

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