Dobutamine Pretreatment Improves Survival, Liver Function, and Hepatic Microcirculation After Polymicrobial Sepsis in Rat

Fink, Tobias; Heymann, Paul; Taha-Melitz, Stefanie; Taha, Anas; Wolf, Beate; Rensing, Hauke; Volk, Thomas; Mathes, Alexander

doi:10.1097/shk.0b013e31829c361d

Cited by 23 publications

(14 citation statements)

References 38 publications

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“…Anyway, these results are surprising, as previous studies demonstrated decreased liver function and increased hepatocyte damage in rats after 5 h of CLI sepsis (Fink et al, 2013). However, melatonin treatment did influence the expression levels of the UPR mediators PERK and CHOP in the liver of septic mice.…”

Section: Discussioncontrasting

confidence: 54%

Melatonin modifies cellular stress in the liver of septic mice by reducing reactive oxygen species and increasing the unfolded protein response

Kleber

Kubulus

Rössler

et al. 2014

Experimental and Molecular Pathology

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Section: Discussioncontrasting

confidence: 54%

Melatonin modifies cellular stress in the liver of septic mice by reducing reactive oxygen species and increasing the unfolded protein response

Kleber

Kubulus

Rössler

et al. 2014

Experimental and Molecular Pathology

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“…Furthermore, we found that intravenous dobutamine at a dose up to 10 µg/kg signi cantly improved the survival in septic rats with myocardial dysfunction. This nding dovetails well with other studies which demonstrated that DOB had improved the survival in patients with septic shock and animal models of sepsis [34,35]. We also found intravenous dobutamine at a dose of 10 µg/kg markedly increased serum IL-10 level in CLP rats.…”

Section: Discussionsupporting

confidence: 91%

Effect of dobutamine on intrinsic myocardial function and myocardial apoptosis in septic rats with myocardial dysfunction

Tang¹,

Xu²,

Dai³

et al. 2020

Preprint

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Background Dobutamine (DOB) has been recommended as the first-line inotrope for septic patients with low cardiac output, but its long-term impact on intrinsic myocardial dysfunction during sepsis remains unclear. This study investigated the long-term effect of DOB on intrinsic myocardial function and cardiomyocyte apoptosis in sepsis. Methods Male Sprague-Dawley rats were randomly divided into sham and cecal ligation and puncture (CLP) groups. The intrinsic myocardial function and other organ functions were measured at different time points, the inflammatory response and serum biomarkers of myocardial injury were also determined. In separate experiments, the effect of DOB (5 or 10 µg/kg) treatment on survival, intrinsic myocardial function, serum and myocardial cytokines and myocardial apoptosis were measured in septic rats. Results The mortality rate of septic rats was 70% on day 10 after CLP. At 6 h after CLP, the left ventricular ± dP/dt were significantly depressed, serum tumor necrosis factor (TNF) –α level, cardiac TNF-α, intercellular adhesion molecule and vascular cell adhesion molecule-1 (VCAM-1) mRNA, and VCAM-1 protein levels were increased, but not serum cTnI, N-terminal pro-brain natriuretic peptide (NT-proBNP), heart-type fatty acid-binding protein (H-FABP), creatinine and urea nitrogen concentrations as well as lung wet-dry weight ratios in CLP group compared with those in sham group. At 9 h after CLP, serum alanine aminotransferase and aspartate aminotransferase activities were higher in CLP rats than controls. At 6 h after CLP, treatment with DOB did not affect the left ventricular ± dP/dt, the levels of TNF-α, interleukin (IL) − 1β and IL-6 in the serum and myocardium as well as cardiomyocyte apoptosis at 20 h after CLP. However, administration of 10.0 µg/kg DOB at 6 h after CLP significantly increased serum IL-10 level and improved survival in septic rats. Conclusions The intrinsic myocardial depression occurs earlier than hepatic and renal dysfunction in severe sepsis and serum cTnI, NT-proBNP and H-FABP are not suitable as an early biomarker for this kind of cardiac dysfunction. For septic rats, DOB treatment in the presence of intrinsic myocardial dysfunction neither improves myocardial function nor attenuates myocardial inflammation and cardiomyocyte apoptosis at the later stage of sepsis.

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“…Pretreatment with dobutamine improves survival rate, liver function and hepatic microcirculation in septic rats via β1-adrenoceptor activation, in addition to its circulatory mechanism. [59] Dexmedetomidine, a novel lipophilic imidazole derivative with a high affinity for α2-adrenoceptors, has a protective effect on liver injury during experimental sepsis. It attenuates central venous congestion, hepatic sinusoids congestion and dilation, and portal tract inflammation.…”

Section: Therapeutic Considerations For Sepsis-associated Liver Dysfumentioning

confidence: 99%

Advances in sepsis-associated liver dysfunction

2014

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Recent studies have revealed liver dysfunction as an early event in sepsis. Sepsis-associated liver dysfunction is mainly resulted from systemic or microcirculatory disturbances, spillovers of bacteria and endotoxin (lipopolysaccharide, LPS), and subsequent activation of inflammatory cytokines as well as mediators. Three main cell types of the liver which contribute to the hepatic response in sepsis are Kupffer cells (KCs), hepatocytes and liver sinusoidal endothelial cells (LSECs). In addition, activated neutrophils, which are also recruited to the liver and produce potentially destructive enzymes and oxygen-free radicals, may further enhance acute liver injury. The clinical manifestations of sepsis-associated liver dysfunction can roughly be divided into two categories: Hypoxic hepatitis and jaundice. The latter is much more frequent in the context of sepsis. Hepatic failure is traditionally considered as a late manifestation of sepsis-induced multiple organ dysfunction syndrome. To date, no specific therapeutics for sepsis-associated liver dysfunction are available. Treatment measure is mainly focused on eradication of the underlying infection and management for severe sepsis. A better understanding of the pathophysiology of liver response in sepsis may lead to further increase in survival rates.

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Dobutamine Pretreatment Improves Survival, Liver Function, and Hepatic Microcirculation After Polymicrobial Sepsis in Rat

Cited by 23 publications

References 38 publications

Melatonin modifies cellular stress in the liver of septic mice by reducing reactive oxygen species and increasing the unfolded protein response

Melatonin modifies cellular stress in the liver of septic mice by reducing reactive oxygen species and increasing the unfolded protein response

Effect of dobutamine on intrinsic myocardial function and myocardial apoptosis in septic rats with myocardial dysfunction

Advances in sepsis-associated liver dysfunction

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