Levosimendan as a new force in the treatment of sepsis-induced cardiomyopathy: mechanism and clinical application

Yang, Fei; Zhao, Li; Sun, Yi; Chen, Zhuang

doi:10.1177/0300060519837103

Cited by 27 publications

(17 citation statements)

References 42 publications

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“…Sepsis-induced myocardial injury triggers apoptosis in myocardiocytes via the mitochondrial pathway [17]. Apoptotic markers such as bax, bcl-2 and caspase-3 are central to mitochondrial function and any alteration in their expression levels will always result in apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Trigonoside II mitigates sepsis-induced myocardial injury via reduction in oxidative stress and regulation of TLR- 4/NF-kB inflammatory pathway

Wang¹,

Wu²,

Liang³

2020

Trop. J. Pharm Res

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Purpose: To investigate the protective effect of trigonoside II against sepsis-induced myocardial injury in rats, and the mechanism involved. Methods: Adult male Sprague Dawley rats (n = 30) weighing 200 - 230 g (mean weight = 215 ± 15 g) were used for this study. The rats were randomly assigned to 3 groups (10 rats/group): sham, cecal ligation puncture (CLP), and trigonoside II. Rats in the treatment group received trigonoside II at a dose of 2 mg/kg intraperitoneally (i.p.) at 3, 12 and 24 h post-surgery. Sepsis was induced using CLP method. Lactate dehydrogenase (LDH) and creatine kinase (CK-MB) activities, and hemodynamic functions were determined in the rats. The levels of interleukin (IL)-1β and IL-6, and tumor necrosis factor α (TNF-α) were assayed in rat serum. Oxidative stress and myocardial cell apoptosis were determined by measuring malondialdehyde (MDA) levels, while activities of glutathione peroxidase (GPx), superoxide dismutase (SOD) and myeloperoxidase (MPO), as well as levels of expression of bax, bcl-2 and caspase-3 were also assessed. Results: Treatment of myocardial injury rats with trigonoside II led to significant reductions in the activities of LDH, CK-MB and MPO, and decreases in levels of IL-1β, IL-6 and TNF-α (p < 0.05). It also significantly reversed the effects of sepsis on rat hemodynamic functions (p < 0.05). Trigonoside IItreatment significantly reduced MDA levels in rat myocardial tissues, but significantly increased SOD and GPx activities (p < 0.05). It significantly down-regulated protein expressions of NF-kB and TLR-4 in myocardial tissues (p < 0.05). The number of apoptotic cells and activity of caspase-3 were significant increased in myocardial tissues of rats in CLP group, when compared with sham group, but were reduced significantly in myocardial tissues of trigonoside II-treated rats (p < 0.05). Similarly, trigonoside II treatment down-regulated the protein expressions of caspase-3 and bax, but upregulated bcl-2 protein expression in the rat myocardial tissues (p < 0.05). Conclusion: The results of this study indicate that trigonoside II confers protection on sepsis-induced myocardial injury via reduction in oxidative stress and regulation of TLR-4/NF-kB inflammatory pathway. Keywords: Cecal ligation puncture, Myocardial injury, Oxidative stress, Sepsis, Trigonoside II

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Section: Discussionmentioning

confidence: 99%

Trigonoside II mitigates sepsis-induced myocardial injury via reduction in oxidative stress and regulation of TLR- 4/NF-kB inflammatory pathway

Wang¹,

Wu²,

Liang³

2020

Trop. J. Pharm Res

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“…Підвищення тропоніну зустрічається у 43-85 % хворих з септичним шоком та асоційоване з вищою летальністю [16]. З експериментальних робіт відомо, що порушення функції міокарда при сепсисі розвивається, незважаючи на достатню міо кардіальну перфузію та адекватне постачання кисню [11,21]. Основними механізмами ушкодження міокарда вважають вплив запальних цитокінів та ендотоксинів і дисфункцію мітохондрій [16].…”

Section: неішемічне ушкодження міокардаunclassified

Повреждение Миокарда

Yakovleva¹,

Yakovleva²

2021

ЕМ

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Останнім часом багато уваги в літературі приділяється ушкодженню міокарда. Підвищення рівня тропоніну, орган-специфічного структурного протеїну, наявного тільки в серцевому м'язі понад 99-й перцентиль верхньої межі норми,-чутливий лабораторний маркер ушкодження кардіоміоцитів, який, на жаль, не надає інформації щодо причини загибелі клітин. Серед серцевих причин ушкодження кардіоміо цитів найбільш очевидною є інфаркт міокарда (ІМ), а також серцева недостатність, перикардит/міокардит, кардіоміопатії, в тому числі кардіоміопатія такоцубо, порушення ритму, серцеві оперативні втручання та інвазивні процедури, забій серця, дисекція аорти, по-вторні дефібриляції, інфільтрація міокарда [8, 17]. Несерцеві причини включають тромбоемболію легеневої артерії, термінальні стадії хронічної хвороби нирок, сепсис і критичні стани, рабдоміоліз, фізичне навантаження, опіки, токсичну дію деяких ліків, інсульт та інші стани [9]. Термін «гострий інфаркт міокарда» правильно застосовувати за наявності гострого ушкодження міокарда і клінічних даних на користь гострої ішемії міокарда (хоча б одне з наступного: симптоми ішемії міокарда; нові ішемічні зміни на електрокардіограмі (ЕКГ); поява патологічних зубців Q; втрата міокарда за даними методів візуалізації, що відповідає ішемічному ураженню; виявлення внутрішньокоронарного тромбу-за

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“…In 2006, Rabuel and Mebazaa [ 44 ] concluded that approximately 15% of patients needed cardiotonic therapy to improve systemic circulation perfusion. As cardiotonic drugs, milrinone and levosimendan [ 45 – 47 ] are preferred. Catecholamines for sympathetic nerve excitation are not an option, which may have some connection with the stress explanation of LVSD in sepsis patients up to a point.…”

Section: Left Ventricular Systolic Dysfunction Vs mentioning

confidence: 99%

Induction and deduction in sepsis-induced cardiomyopathy: five typical categories

Wang¹,

Wang²,

Liu³

et al. 2020

Chinese Medical Journal

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Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. The heart is one of the most important oxygen delivery organs, and dysfunction significantly increases the mortality of the body. Hence, the heart has been studied in sepsis for over half a century. However, the definition of sepsis-induced cardiomyopathy is not unified yet, and the conventional conception seems outdated: left ventricular systolic dysfunction (LVSD) along with enlargement of the left ventricle, recovering in 7 to 10 days. With the application of echocardiography in intensive care units, not only LVSD but also left ventricular diastolic dysfunction, right ventricular dysfunction, and even diffuse ventricular dysfunction have been seen. The recognition of sepsis-induced cardiomyopathy is gradually becoming complete, although our understanding of it is not deep, which has made the diagnosis and treatment stagnate. In this review, we summarize the research on sepsis-induced cardiomyopathy. Women and young people with septic cardiomyopathy are more likely to have LVSD, which may have the same mechanism as stress cardiomyopathy. Elderly people with ischemic cardiomyopathy and hypertension tend to have left ventricular diastolic dysfunction. Patients with mechanical ventilation, acute respiratory distress syndrome or other complications of increased right ventricular afterload mostly have right ventricular dysfunction. Diffuse cardiac dysfunction has also been shown in some studies; patients with mixed or co-existing cardiac dysfunction are more common, theoretically. Thus, understanding the pathophysiology of sepsis-induced cardiomyopathy from the perspective of critical care echocardiography is essential.

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Levosimendan as a new force in the treatment of sepsis-induced cardiomyopathy: mechanism and clinical application

Cited by 27 publications

References 42 publications

Trigonoside II mitigates sepsis-induced myocardial injury via reduction in oxidative stress and regulation of TLR- 4/NF-kB inflammatory pathway

Trigonoside II mitigates sepsis-induced myocardial injury via reduction in oxidative stress and regulation of TLR- 4/NF-kB inflammatory pathway

Повреждение Миокарда

Induction and deduction in sepsis-induced cardiomyopathy: five typical categories

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