Cellular Basis for the Acute Inhibitory Effects of IL-6 and TNF-   on Excitation-contraction Coupling

Sugishita, Kazuro; Kinugawa, Koh‐ichiro; Shimizu, Tatsuya; Harada, Kazumasa; Matsui, Hiroshi; Takahashi, Toshiyuki; Serizawa, Takashi; Kohmoto, Osami

doi:10.1006/jmcc.1999.0989

Cited by 93 publications

(112 citation statements)

References 36 publications

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“…Finally, another consideration is that the effects may be unique to different cytokines. In line with this hypothesis, it has been reported using the same model system that L-NMMA reversed effects on cell shortening and Ca 2+ that are induced by IL-6 but not by TNF-α [107].…”

Section: Effects Of No and Cytokines On Contraction In Isolated Cardisupporting

confidence: 60%

The complex role of iNOS in acutely rejecting cardiac transplants

Pieper

Roza

2008

Free Radical Biology and Medicine

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This review summarizes the evidence for a detrimental role of nitric oxide (NO) derived from inducible NO synthase (iNOS) and/or reactive nitrogen species such as peroxynitrite in acutelyrejecting cardiac transplants. In chronic cardiac transplant rejection, iNOS may have an opposing beneficial component. The purpose of this review is primarily to address issues related to acute rejection which is a recognized risk factor for chronic rejection. The evidence for a detrimental role is based upon strategies involving non-selective NOS inhibitors, NO neutralizers, selective iNOS inhibitors and iNOS gene deletion in rodent models of cardiac rejection. The review is discussed in the context of the impact on various components including graft survival, histological rejection and cardiac function which may contribute in toto to the process of graft rejection. Possible limitations of each strategy are discussed in order to understand better the variance in published findings including issues related to the potential importance of cell localization of iNOS expression. Finally, the concept of a dual role of NO and its down-stream product, peroxynitrite, in rejection vs. immune regulation is discussed.

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Section: Effects Of No and Cytokines On Contraction In Isolated Cardisupporting

confidence: 60%

The complex role of iNOS in acutely rejecting cardiac transplants

Pieper

Roza

2008

Free Radical Biology and Medicine

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“…Bick et al (3) have also shown that short-term neonatal rat cardiac myocyte exposure to TNF-␣ results in blunted contractility and cAMP response to isoproterenol but that responses to forskolin are preserved. Similarly, Sugishita et al (35) have shown that TNF-␣ acutely suppresses ␤-adrenergic-induced increases in contractility and I Ca transients.…”

Section: Discussionmentioning

confidence: 81%

“…Early depressant effects (Ͻ1 h) of TNF-␣ on isolated myocyte contractility have been ascribed to various mechanisms. These include sequential NO and cGMP generation (via calcium-dependent NOS activation rather than calcium-independent NOS induction consistent with the short time frame to onset of myocardial depression) (5,8,17) and sphingomyelinase-dependent signaling (5,23,35). There is some suggestion that these mechanisms do not necessarily operate exclusively of each other (5,19,30).…”

Section: Discussionmentioning

confidence: 96%

Nitric oxide-dependent and -independent mechanisms are involved in TNF-α-induced depression of cardiac myocyte contractility

Kumar

Paladugu²,

Mensing³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Nitric oxide-dependent and -independent mechanisms are involved in TNF-␣-induced depression of cardiac myocyte contractility. Am J Physiol Regul Integr Comp Physiol 292: R1900-R1906, 2007. First published January 18, 2007; doi:10.1152/ajpregu.00146.2006.-Previous studies have demonstrated the presence of myocardial depression in clinical and experimental septic shock. This response is mediated, in part, through circulating TNF-␣-induced, nitric oxide-dependent, depression of basal myocyte contractility. Other mechanisms of early myocardial dysfunction involving decreased response to adrenergic stimulation may exist. This study evaluated the presence and nitric oxide dependence of impaired adrenergic response to TNF-␣ in in vitro cardiac myocytes. The contraction of electrically paced neonatal rat cardiac myocytes in tissue culture was quantified using a closedloop video tracking system. TNF-␣ induced depression of baseline contractility over the first 20 min of cardiac myocyte exposure. This effect was blocked by N-methyl-arginine (NMA), a nitric oxide synthase inhibitor, in all studies. Contractile and cAMP response to increasing concentrations of isoproterenol was deficient in cardiac myocytes exposed to TNF-␣ regardless of the presence of NMA. In contrast, increasing concentrations of forskolin (a direct stimulant of adenylate cyclase) and dibutyryl cAMP (a metabolically active membrane-soluble analog of cAMP) completely reversed TNF-␣-mediated depression, though only in the presence of NMA. Forskolin-stimulated cAMP generation remained intact regardless of NMA. Increasing concentrations of exogenous calcium chloride, unlike other inotropic agents, corrected TNF-␣-mediated defects of contractility independent of the presence of NMA. These data suggest that TNF-␣ exposure is associated with a second nitric oxide-independent but calcium-dependent early depressant mechanism that is manifested by reduced contractile and cAMP response to ␤-adrenergic stimulation. sepsis; septic shock; adrenoreceptor; myocardial depression; myocyte; heart; myocardial depressant substance; cytokine THE NORMAL CARDIAC RESPONSE to septic shock involves biventricular dilatation and decreased ejection fractions (14,24,25). Clinically, septic myocardial depression is also reflected by a suboptimal stroke volume response to fluid resuscitation (22) and infusion of exogenous catecholamines (15,20,32).The causal role of circulating factors in myocardial depression in human septic shock is now well established (21,(27)(28)(29)31). Measurements of isolated cardiac myocyte contraction in the presence of serum from patients with acute septic shock demonstrate a depression of maximum extent and peak velocity of myocyte shortening that correlates quantitatively and temporally with depression of the patient's left ventricular ejection fraction as measured by radionuclide ventriculography (27,31). We have demonstrated that this depressant activity represents a synergistic combination of low-circulating concentrations of the proinflammatory cytokin...

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“…8 Furthermore, proinflammatory cytokines affect electrophysiological function and have an acute negative inotropic effect on cardiomyocytes. 27 Therefore, these inflammatory reactions could be responsible for left ventricular dilatation and decreased left ventricular contractile function in patients exposed to repetitive hypoxia. A previous study showed that CPAP therapy for patients with p=0.008 p=0.9…”

Section: Discussionmentioning

confidence: 99%

Beneficial Effects of Adaptive Servo Ventilation in Patients With Chronic Heart Failure

Koyama

Watanabe

Kobukai

et al. 2010

Circ J

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Background: Sleep-disordered breathing (SDB) is thought to be a state of inflammation caused by hypoxic stress. Whether adaptive servo ventilation (ASV) attenuates the inflammatory response and improves the cardiac function of patients with congestive heart failure (CHF) accompanied by SDB was not been investigated. Methods and Results:Seventeen inpatients with New York Heart Association (NYHA) II or III underwent polysomnography. There was a positive correlation between the apnea hypopnea index and high-sensitivity C-reactive protein (hs-CRP) level (r=0.753, P=0.016). The patients were divided into ASV (n=10) and non-ASV groups (n=7), and CHF-parameters were measured before and after ASV treatment. Improvement was noted for the NYHA class in the ASV group but not in the non-ASV group. In contrast to the non-ASV group, the level of brain natriuretic peptide (BNP), ejection fraction, and hs-CRP levels in the ASV group significantly improved (BNP, Conclusions: Anti-inflammatory effects of ASV are important contributors for improving cardiac function in patients with CHF accompanied by SDB. (Circ J 2010; 74: 2118 - 2124

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Cellular Basis for the Acute Inhibitory Effects of IL-6 and TNF- on Excitation-contraction Coupling

Cited by 93 publications

References 36 publications

The complex role of iNOS in acutely rejecting cardiac transplants

The complex role of iNOS in acutely rejecting cardiac transplants

Nitric oxide-dependent and -independent mechanisms are involved in TNF-α-induced depression of cardiac myocyte contractility

Beneficial Effects of Adaptive Servo Ventilation in Patients With Chronic Heart Failure

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