Myocardial Depression in Sepsis and Septic Shock

Wong, Johnson; Kumar, Anand

doi:10.1007/0-387-34574-4_6

Cited by 4 publications

(9 citation statements)

References 85 publications

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“…Sel-sel yang bersirkulasi seperti makrofag, neutrofil dan platelet diikutsertakan pada daerah cedera atau terinfeksi serta sel-sel tersebut berhubungan dengan endotel dan memengaruhinya. 8,11 Perubahan struktur, fungsi dan metabolisme sel endotel akan memengaruhi permeabilitas kapiler melalui produksi dan pelepasan mediator endogen yang berlebihan. 11,12 Banyaknya sudut pandang mengenai mediator, patogenesis abnormalitas kardiovaskular, dan terapi sepsis membuat hal ini sulit dijelaskan dengan singkat.…”

Section: Patogenesis Sepsis Dan Syok Septikunclassified

“…8,11 Perubahan struktur, fungsi dan metabolisme sel endotel akan memengaruhi permeabilitas kapiler melalui produksi dan pelepasan mediator endogen yang berlebihan. 11,12 Banyaknya sudut pandang mengenai mediator, patogenesis abnormalitas kardiovaskular, dan terapi sepsis membuat hal ini sulit dijelaskan dengan singkat. 2,12 Sepsis dimulai dengan infeksi (nidus) yang harus ada walau sulit dibuktikan secara klinis bahkan tidak dapat ditemukan.…”

Section: Patogenesis Sepsis Dan Syok Septikunclassified

“…Aktivitas yang terjadi secara berlebihan akan merugikan. 11,17 Secara umum syok septik merupakan ekspresi klinis respons pejamu yang berlebihan. 18 Sistem kinin yang teraktivasi endoktosin atau kompleks antigen-antibodi menyebabkan peningkatan permeabilitas kapiler, vasodilatasi, peningkatan aktivitas fagosit, dan serangan langsung komplemen terhadap patogen tersebut.…”

Section: Patogenesis Sepsis Dan Syok Septikunclassified

“…2,10 Gambaran hemodinamik klasik syok septik pada manusia ialah hipotensi karena vasodilatasi arteri sehingga tahanan vaskular sistemik sangat rendah dengan curah jantung yang tinggi. [1][2][3]7,11,23 Setelah pemberian cairan yang agresif untuk mendapatkan beban awal yang optimal, didapatkan curah jantung awal yang normal atau tinggi pada 80% kasus. 9,21,23…”

Section: Karakteristik Fungsi Jan-tung Dalam Syok Septikunclassified

“…Walaupun ujiklinik fase III yang lebih besar telah memperlihatkan tidak ada manfaat harapan hidup secara keseluruhan jika antibodi monoklonal anti-TNF-α diberikan pada pasien syok septik, namun fungsi ventrikel kiri membaik pada grup pasien ini. 7,11,27 Interleukin-1β menginduksi respons patofisiologik yang sama dengan TNF-α. Interleukin-1β meningkat pada modelmodel sepsis dan syok septik manusia dan hewan.…”

Section: Lipopolisakarida Dan Sitokinunclassified

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Disfungsi Miokard Pada Sepsis Dan Syok Septik

Rampengan

2015

JBM

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Sepsis and septic shock are serious clinical problems causing increased morbidity and mortality, which are highly associated with the event of myocardium dysfunction. Compared to previous data of four decades ago, there is an increase of mortality rate due to sepsis which is recorded based on the age from 0.5 to 7 per 100,000 sepsis episodes. The most common cause of sepsis is bacteria, which currently has shifted from negative to positive Gram bacteria. The most common organs affected by infection are lung (40%), followed by abdomen (30%) and urinary tract (10%). Sepsis begins with an infection (nidus), which has to be present although finding the clinical evidence may be difficult or the evidence may not be found. Shock is a condition of inadequate blood flow to the tissues to maintain high-energy phosphates at the necessary level to keep normal cellular function. Patients with septic shock who did not survive were found to have progressive hypotension or being unresponsive and had multi-organ dysfunction. The most common effect of septic shock on cardiovascular system is defined by the characteristics of hemodynamic profiles including increased cardiac index and reduced systemic vascular resistance. Myocardium dysfunction is an important variable for sepsis and septic shock. Keywords: myocardium dysfunction, sepsis, shock. Abstrak: Sepsis dan syok septik merupakan masalah klinik serius yang banyak menyebabkan peningkatan morbiditas maupun mortalitas, yang erat kaitannya dengan kejadian disfungsi miokard. Dibandingkan dengan empat dekade yang lalu, tercatat angka mortalitas berdasarkan usia akibat sepsis meningkat dari 0,5 menjadi 7 per 100.000 episode sepsis. Sepsis paling sering disebabkan oleh bakteri yang saat ini penyebabnya telah bergeser dari bakteri Gram negatif ke bakteri Gram positif. Organ yang paling sering terjadi infeksi ialah paru (40%) diikuti abdomen (30%) dan traktus urinarius (10%). Sepsis dimulai dengan infeksi (nidus) yang harus ada walau sulit dibuktikan secara klinis bahkan mungkin tidak dapat ditemukan. Syok adalah tidak cukupnya aliran darah jaringan dalam mempertahankan fosfat energi tinggi pada tingkat yang dibutuhkan untuk mempertahankan fungsi sel. Pasien syok septik yang tidak selamat didapati mengalami hipotensi progresif atau tidak responsif serta disfungsi multi organ. Efek syok septik yang tersering pada sistem kardiovaskular ialah karakteristik pada profil hemodinamik berupa peningkatan indeks jantung dan penurunan resistensi vaskular sistemik. Disfungsi miokard merupakan variabel penting pada sepsis dan syok septik. Kata kunci: disfungsi miokard, sepsis, syok.

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Section: Patogenesis Sepsis Dan Syok Septikunclassified

Section: Karakteristik Fungsi Jan-tung Dalam Syok Septikunclassified

Section: Lipopolisakarida Dan Sitokinunclassified

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Disfungsi Miokard Pada Sepsis Dan Syok Septik

Rampengan

2015

JBM

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ECAIS study: Inadvertent cardiovascular adverse events in sepsis

Duque

Olivera

Torres

et al. 2012

Medicina Intensiva (English Edition)

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To Explore the Protective Mechanism of PTEN-Induced Kinase 1 (PINK1)/Parkin Mitophagy-Mediated Extract of Periplaneta Americana on Lipopolysaccharide-Induced Cardiomyocyte Injury

Shi

Zhang

et al. 2019

Med Sci Monit

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Background Sepsis is defined as a systemic inflammatory response syndrome caused by an infection (suspicious or confirmed). Its essence is inflammatory mediators and cytokines mediated by host immune response. The present study aimed to investigate the role of Periplaneta americana extracts (XML) on PTEN-induced kinase 1 (PINK1)/Parkin mediated mitophagy in cardiomyocyte injury by sepsis. Material/Methods H9C2 cells were cultured and transfected with Mdivi-1 and Atg7 siRNA. The cell viability and drug toxicity were detected using Cell Counting Kit-8 assay. ELISA (enzyme-linked immunosorbent assay) was used to assess cardiac injury factors and inflammatory factors. Fluorescence levels of LC3 were detected using immunofluorescence assay. Then, the protein and mRNA expression levels were analyzed using western blot and qRT-PCR. Intracellular adenosine triphosphate (ATP) levels were measured using an ATP kit. Finally, flow cytometry was used to detected apoptosis. Results The result showed that XML significantly increase cell viability in H9C2 cells. Compared with XML+LPS (lipopolysaccharide) group, the level of cTNI, CK-MB, interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α was significantly upregulation in LPS+XML+Mdivi-1 or LPS+XML+Atg7 siRNA group. In addition, the release of LC3 was significant decreased. The protein and mRNA expression of PINK1, Parkin, Nix, Beclin-1 was significantly increased, but decreased expression of Mitofusin1, Mitofusin2, Opa1, Drp1, and P62 in LPS+XML+Mdivi-1 or LPS+XML+Atg7 siRNA groups. More importantly, we found that cell apoptosis was induced by Mdivi-1 and Atg7 siRNA. Conclusions The study provided evidence that XML regulated the process of LPS-induced cardiomyocyte injury through mitophagy by the PINK1/Parkin pathway.

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Myocardial Depression in Sepsis and Septic Shock

Cited by 4 publications

References 85 publications

Disfungsi Miokard Pada Sepsis Dan Syok Septik

Disfungsi Miokard Pada Sepsis Dan Syok Septik

ECAIS study: Inadvertent cardiovascular adverse events in sepsis

To Explore the Protective Mechanism of PTEN-Induced Kinase 1 (PINK1)/Parkin Mitophagy-Mediated Extract of Periplaneta Americana on Lipopolysaccharide-Induced Cardiomyocyte Injury

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