Left ventricular systolic and diastolic dysfunction after infusion of tumor necrosis factor-alpha in conscious dogs.

Pagani, Francis D.; Baker, Lauren S.; Hsi, Charles; Knox, Mark A.; Fink, Mitchell P.; Visner, Marc S.

doi:10.1172/jci115873

Cited by 258 publications

(105 citation statements)

References 57 publications

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“…These observations are at odds with the suggestion that progression of circulatory dysfunction leads in advanced stages to a decrease in CO due to so-called cirrhotic cardiomyopathy. 30,31 In our study, despite the marked differences in TNF-a and other proinflammatory mediators, we could not demonstrate any decrease in CO in bactDNA(þ) patients. These findings suggest that a much greater increase in proinflammatory cytokines would be required to cause the impaired cardiac contractility reported in patients developing hepatorenal syndrome.…”

Section: Discussioncontrasting

confidence: 80%

Bacterial DNA translocation is associated with systemic circulatory abnormalities and intrahepatic endothelial dysfunction in patients with cirrhosis

et al. 2010

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Presence of bacterial DNA in noninfected patients with cirrhosis and ascites is associated with a marked inflammatory response including activation of the inducible form of nitric oxide synthase and release of nitric oxide, similar to that observed in patients with spontaneous bacterial peritonitis. Although presence of bacterial DNA is associated with an impaired prognosis, no information is available regarding its hemodynamic consequences. Systemic and hepatic hemodynamics before and after a liquid test meal were assessed in a series of 75 noninfected patients with cirrhosis (55 with ascites). Bacterial DNA was measured by polymerase chain reaction. Bacterial DNA was detected only in patients with ascites. Clinical data and liver function were similar in ascitic patients with presence (n 5 21) or absence of bacterial DNA (n 5 34). Bacterial-DNA(1) patients had significantly lower mean arterial pressure (P 5 0.002) and systemic vascular resistance (P 5 0.03) than bacterial-DNA(2) patients. Cardiac output, cardiopulmonary pressures, hepatic venous pressure gradient (HVPG), and hepatic blood flow were similar in both groups. Thirty minutes after the test meal, in response to increased blood flow caused by postprandial hyperemia, there was a significantly greater increase in HVPG and impaired hepatic vasorelaxation in bacterial-DNA(1) as compared with bacterial-DNA(2) patients, which indicates hepatic endothelial dysfunction. Indeed, the increase in HVPG after the test meal significantly correlated with serum bacterial DNA concentration. Conclusion: Presence of bacterial DNA, a marker of bacterial translocation, is associated with aggravation of peripheral vasodilation and with worsening of intrahepatic endothelial dysfunction. (HEPATOLOGY 2010;52:2044-2052 P ortal hypertension is a serious consequence of cirrhosis that can result in life-threatening complications with increased mortality and morbidity.1 The primary factor in the pathophysiology of portal hypertension is increased intrahepatic resistance to portal-collateral blood flow. Portal hypertension is further aggravated by increased portal venous inflow, caused by splanchnic vasodilation. Moreover, insufficient nitric oxide (NO) availability in the hepatic microcirculation is considered an important factor that contributes to increase the hepatic vascular resistance. Because of this, the cirrhotic liver, unlike the normal liver, cannot vasodilate in response to a volume flow load such as that caused by meals, which results in abrupt postprandial increases in portal pressure, a concept known as intrahepatic endothelial dysfunction. [2][3][4][5]

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Section: Discussioncontrasting

confidence: 80%

Bacterial DNA translocation is associated with systemic circulatory abnormalities and intrahepatic endothelial dysfunction in patients with cirrhosis

et al. 2010

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“…PA103, a strain of Pseudomonas aeruginosa; MAP, mean arterial pressure; %CO, % change of cardiac output from the beginning of the experiment; BE, base excess. diastolic function (49). Our findings are consistent with these previous studies because higher plasma concentrations of TNF-␣ were associated with hemodynamic instability in the macrophage-depleted rabbits.…”

Section: Discussionsupporting

confidence: 93%

Depletion of phagocytes in the reticuloendothelial system causes increased inflammation and mortality in rabbits withPseudomonas aeruginosapneumonia

Kurahashi¹,

Sawa²,

Ota³

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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TR, Wiener-Kronish JP. Depletion of phagocytes in the reticuloendothelial system causes increased inflammation and mortality in rabbits with Pseudomonas aeruginosa pneumonia. Am J Physiol Lung Cell Mol Physiol 296: L198 -L209, 2009. First published November 21, 2008 doi:10.1152/ajplung.90472.2008.-Phagocytes of the reticuloendothelial system are important in clearing systemic infection; however, the role of the reticuloendothelial system in the response to localized infection is not well-documented. The major goals of this study were to investigate the roles of phagocytes in the reticuloendothelial system in terms of bacterial clearance and inflammatory modulation in sepsis caused by Pseudomonas pneumonia. Macrophages in liver and spleen were depleted by administering liposome encapsulated dichloromethylene diphosphonate (clodronate) intravenously 36 h before the instillation of Pseudomonas aeruginosa into the lungs of anesthetized rabbits. Blood samples were analyzed for bacteria and cytokine concentrations. Lung injury was assessed by the bidirectional flux of albumin and by wet-to-dry weight ratios. Blood pressure and cardiac outputs decreased more rapidly and bacteremia occurred earlier in the clodronate-treated rabbits compared with the nondepleted rabbits. Plasma TNF-␣ (1.08 Ϯ 0.54 vs. 0.08 Ϯ 0.02 ng/ml) and IL-8 (6.8 Ϯ 1.5 vs. 0.0 Ϯ 0.0 ng/ml) were higher in the depleted rabbits. The concentration of IL-10 in liver of the macrophage-depleted rabbits was significantly lower than in normal rabbits at 5 h. Treatment of macrophage-depleted rabbits with intravenous IL-10 reduced plasma proinflammatory cytokine concentrations and reduced the decline in blood pressure and cardiac output. These results show that macrophages in the reticuloendothelial system have critical roles in controlling systemic bacteremia and reducing systemic inflammation, thereby limiting the systemic effects of a severe pulmonary bacterial infection. counterregulatory response; bacterial clearance; macrophages NOSOCOMIAL PNEUMONIA OCCURS in ϳ25% of mechanically ventilated patients (13,39). Pseudomonas aeruginosa is now one of the most common (18, 33) and most lethal (6,15,19) pathogens causing nosocomial pneumonia. One possible reason for the high mortality associated with P. aeruginosa pneumonia is the fact that pneumonia due to P. aeruginosa often leads to bacteremia (12,14,21). Clinical isolates of P. aeruginosa that are positive for type III secretion system cause more cytotoxicity to macrophage cell lines than those strains that are negative for type III secretion system (3). The intrapulmonary instillation of P. aeruginosa strains that produce ExoU, a toxin secreted via the type III secretion system, promotes entry of bacteria into the circulation as well as the transport of inflammatory mediators from the infected air spaces into the circulation, leading to lethal hypotension and acidosis (37). Local as well as systemic defense mechanisms are therefore important in the responses to intrapulmonary P. aeruginosa.The reticuloendothe...

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“…These effects include pulmonary edema, left ventricular dysfunction, left ventricular remodeling, cardiomyopathy and abnormalities in myocardial metabolism [3][4][5][6][7][8]. It is the particular balance of pro-inflammatory and anti-inflammatory cytokines that influence cardiac homeostasis.…”

Section: Introductionmentioning

confidence: 99%

The Immunoregulatory Role of Cytokines in Congestive Heart Failure

Chen¹,

Patel²,

Mohamed³

2014

Interdiscip J Microinflammation

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Background: Cytokines have been shown to be associated with heart failure and to have multiple biological effects that can lead to left ventricular dysfunction, pulmonaryedema, and left ventricular remodeling. However, the effects of different cytokines, separately and in combination have not been fully determined. We aim to evaluate the levels of both pro-inflammatory and anti-inflammatory cytokines in patients with congestive heart failure (CHF), as well as in patients with coronary artery disease (CAD) and compare them to levels in normal controls (individuals without CHF or CAD) as to suggest their possible etiologic role.

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Left ventricular systolic and diastolic dysfunction after infusion of tumor necrosis factor-alpha in conscious dogs.

Cited by 258 publications

References 57 publications

Bacterial DNA translocation is associated with systemic circulatory abnormalities and intrahepatic endothelial dysfunction in patients with cirrhosis

Bacterial DNA translocation is associated with systemic circulatory abnormalities and intrahepatic endothelial dysfunction in patients with cirrhosis

Depletion of phagocytes in the reticuloendothelial system causes increased inflammation and mortality in rabbits withPseudomonas aeruginosapneumonia

The Immunoregulatory Role of Cytokines in Congestive Heart Failure

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