Effects of McI-154, a Calcium Sensitizer, on Cardiac Dysfunction in Endotoxic Shock in Rabbits

Ming, Mei; Hu, De-yao; Chen, Hui Sun; Liu, Liang Ming; Nan, Xuemei; Lu, Ru Quan

doi:10.1097/00024382-200006000-00007

Cited by 10 publications

(3 citation statements)

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“…The higher cardiac index in levosimendan-treated animals during sepsis could be caused by decreased left ventricular afterload (because of the abolition of the sepsis-induced acute increase in SVRI) or to a calcium-sensitizing effect. A role for calcium desensitization in the sepsis-induced myocardial depression has been previously suggested (14,15), and increased myocardial contractility after the administration of MCI-154, another calcium sensitizer, has been reported in endotoxemic rabbits (16). In accordance with its known vasodilatory properties, treatment with levosimendan was also associated with other beneficial effects in septic animals such …”

Section: Discussionmentioning

confidence: 76%

Levosimendan Increases Portal Blood Flow and Attenuates Intestinal Intramucosal Acidosis in Experimental Septic Shock

García-Septien¹,

Lorente²,

Delgado³

et al. 2010

Shock

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It has been proposed that vasodilatory therapy may increase microcirculatory blood flow and improve tissue oxygenation in septic shock. The authors aimed to evaluate the effects of levosimendan in systemic and splanchnic hemodynamics in a porcine model of septic shock in a randomized animal controlled study. This study was performed in an animal research facility in a university hospital. Anesthetized pigs were monitored with a pulmonary artery catheter and an ultrasonic blood flow probe in the portal vein for measurement of systemic and portal blood flows and with a tonometer placed in the small intestine for measurement of the intramucosal-arterial PCO2 gap. Three groups of pigs were studied: nonseptic (n = 7), septic (n = 7), and septic treated with levosimendan (n = 7). Levosimendan was administered i.v. at t = -10 min (200 microg/kg in i.v. bolus followed by 200 microg/kg per h). Sepsis was induced at t = 0 min by the administration of live Escherichia coli. Vascular reactivity was tested by the hemodynamic response to noradrenaline. Levosimendan markedly attenuated the sepsis-induced increase in pulmonary vascular resistance, decrease in portal/systemic blood flow, oliguria, impairment in oxygenation, hyperkalemia, and the widened intramucosal-arterial PCO2 gap. Systemic blood pressure and vascular resistance did not differ as compared with the septic untreated group. Responses to noradrenaline significantly improved in animals treated with levosimendan. Treatment with levosimendan in this animal model of sepsis attenuated pulmonary vasoconstriction and improved portal blood flow, intestinal mucosal oxygenation, pulmonary function, and vascular reactivity.

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Section: Discussionmentioning

confidence: 76%

Levosimendan Increases Portal Blood Flow and Attenuates Intestinal Intramucosal Acidosis in Experimental Septic Shock

García-Septien¹,

Lorente²,

Delgado³

et al. 2010

Shock

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“…Another mechanism by which ICAM-1 may mediate LPS-induced myocardial dysfunction is via alteration in intracellular calcium concentrations. Decreases in cardiomyocyte calcium sensitivity have been implicated in the depression of cardiac contractility by LPS (36,56). Antibody cross-linking of ICAM-1 has been reported to alter intracellular calcium concentrations in endothelial cells (4) and astrocytes (8); thus alteration of calcium flux via activation of ICAM-1 may contribute to LPS-induced contractile dysfunction.…”

Section: Discussionmentioning

confidence: 99%

ICAM-1 and VCAM-1 mediate endotoxemic myocardial dysfunction independent of neutrophil accumulation

Raeburn

Calkins

Zimmerman

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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Both intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) have been implicated in neutrophil-mediated lung and liver injury during sepsis. However, the role of these adhesion molecules as well as the contribution of neutrophils in myocardial dysfunction during sepsis remains to be determined. The purpose of this study was to examine the role of ICAM-1, VCAM-1, and neutrophils in lipopolysaccharide (LPS)-induced myocardial dysfunction. Mice were subjected to LPS (0.5 mg/kg ip) or vehicle (normal saline), and left ventricular developed pressure (LVDP) was determined by the Langendorff technique. LVDP was depressed by nearly 40% at 6 h after LPS. Immunofluorescent staining revealed a temporal increase in myocardial ICAM-1/VCAM-1 expression and neutrophils after LPS. Antibody blockade of VCAM-1 reduced myocardial neutrophil accumulation and abrogated LPS-induced cardiac dysfunction. Antibody blockade or absence of ICAM-1 (gene knockout) also abrogated LPS-induced cardiac dysfunction but did not reduce neutrophil accumulation. Neutrophil depletion (vinblastine or antibody) did not protect from LPS-induced myocardial dysfunction. Our results suggest that although endotoxemic myocardial dysfunction requires both ICAM-1 and VCAM-1, it occurs independent of neutrophil accumulation.

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“…The majority of sepsis patients have the myocardial injury (Zang et al, 2014). The myocardial injury caused by sepsis is a pathological process involving many factors, including inflammatory response, oxidative stress, microcirculation disturbance, mitochondrial dysfunction, calcium overload and so on (Ming et al, 2000;Horton et al, 2003;Tyagi et al, 2009;Piquereau et al, 2013). Therefore, it is necessary to study the pathogenesis of myocardial injury in sepsis and explore the effective and safe drugs.…”

Section: Introductionmentioning

confidence: 99%

Extraction of ginsenoside Rg2 from stems-leaves of Panax ginseng and its protective effect on myocardial injury in rats with sepsis

XU,

WANG,

FANG

et al. 2022

Food Sci. Technol

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Materials and methods Extraction of GRg2 from stems-leaves of Panax ginsengStems-leaves of Panax ginseng were taken, and soaked in water for 1 h, followed by decocting twice, 2 h each time. After filtering for each time, the filtrates were obtained, and combined, followed by concentrating under reduced pressure. The concentrated solution was purified with macroporous resin. The target eluent was collected. After concentrating under reduced

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Effects of McI-154, a Calcium Sensitizer, on Cardiac Dysfunction in Endotoxic Shock in Rabbits

Cited by 10 publications

References 0 publications

Levosimendan Increases Portal Blood Flow and Attenuates Intestinal Intramucosal Acidosis in Experimental Septic Shock

Levosimendan Increases Portal Blood Flow and Attenuates Intestinal Intramucosal Acidosis in Experimental Septic Shock

ICAM-1 and VCAM-1 mediate endotoxemic myocardial dysfunction independent of neutrophil accumulation

Extraction of ginsenoside Rg2 from stems-leaves of Panax ginseng and its protective effect on myocardial injury in rats with sepsis

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