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

2020 ◽  
Author(s):  
Xiang-Xu Tang ◽  
Ya-Qian Xu ◽  
Xiao-Meng Dai ◽  
Yun Xing ◽  
Duo-Meng Yang ◽  
...  
Keyword(s):  
Adhesion Molecule ◽  
Myocardial Function ◽  
Myocardial Dysfunction ◽  
Cecal Ligation ◽  
Left Ventricular ◽  
Cardiomyocyte Apoptosis ◽  
Fatty Acid Binding ◽  
Myocardial Apoptosis ◽  
Tnf Α

Abstract 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.

Neutralization of IL-18 attenuates lipopolysaccharide-induced myocardial dysfunction

2002 ◽  
Vol 283 (2) ◽  
pp. H650-H657 ◽  
Author(s):  
Christopher D. Raeburn ◽  
Charles A. Dinarello ◽  
Michael A. Zimmerman ◽  
Casey M. Calkins ◽  
Benjamin J. Pomerantz ◽  
...  
Keyword(s):  
Adhesion Molecule ◽  
Cardiac Dysfunction ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Tnf Α ◽  
Developed Pressure ◽  
Factor Α ◽  
Cell Adhesion Molecule 1

Tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) have been implicated in cardiac dysfunction during endotoxemia. Because IL-18 is a proinflammatory cytokine known to mediate the production of TNF-α and IL-1β and to induce the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), we hypothesized that neutralization of IL-18 would attenuate lipopolysaccharide (LPS)-induced cardiac dysfunction. Mice (C57BL/6) were injected with 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 38% at 6 h after LPS. LPS-induced myocardial dysfunction was associated with increased myocardial levels of TNF-α and IL-1β as well as increased expression of ICAM-1/VCAM-1. Pretreatment with neutralizing anti-mouse IL-18 antibody attenuated LPS-induced myocardial dysfunction (by 92%) and was associated with reduced myocardial IL-1β production (65% reduction) and ICAM-1/VCAM-1 expression (50% and 35% reduction, respectively). However, myocardial TNF-α levels were not influenced by neutralization of IL-18. In conclusion, neutralization of IL-18 protects against LPS-induced myocardial dysfunction. IL-18 may mediate endotoxemic myocardial dysfunction through induction of and/or synergy with IL-1β, ICAM-1, and VCAM-1.

Improvement by isosorbide dinitrate of exercise-induced regional myocardial dysfunction

1980 ◽  
Vol 239 (3) ◽  
pp. H399-H405
Author(s):  
T. Kumada ◽  
K. P. Gallagher ◽  
M. Miller ◽  
M. McKown ◽  
F. White ◽  
...  
Keyword(s):  
Isosorbide Dinitrate ◽  
Myocardial Function ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Segment Length ◽  
Wall Thickening ◽  
Regional Myocardial Function ◽  
Exercise Induced ◽  
Coronary Obstruction ◽  
Control Exercise

Sonomicrometry was used in 10 conscious dogs to measure regional segment length and dynamic wall thickness by telemetry in a zone supplied by the left circumflex coronary artery after implantation of an ameroid constrictor. When coronary obstruction was nearly complete and collaterals had developed (24-42 days), control exercise and exercise runs after oral isosorbide dinitrate were carried out. During control runs, significant increases occurred in hemodynamic parameters, and percent shortening in normal segments increased (P < 0.01). During the repeat runs after isosorbide dinitrate, there were smaller increases in left ventricular systolic and end-diastolic pressures and significantly reduced end-diastolic dimensions. In addition, percent wall thickening and percent segment shortening in the ischemic zone did not deteriorate significantly during exercise. In this animal model, which appears to mimic chronic single-vessel coronary heart disease, isosorbide dinitrate can prevent exercise-induced deterioration of regional myocardial function.

Myocardial protection from ischemic arrest: potassium and verapamil cardioplegia

1981 ◽  
Vol 240 (3) ◽  
pp. H326-H335 ◽  
Author(s):  
W. W. Pinsky ◽  
R. M. Lewis ◽  
J. B. McMillin-Wood ◽  
H. Hara ◽  
C. J. Hartley ◽  
...  
Keyword(s):  
Calcium Transport ◽  
Myocardial Protection ◽  
Myocardial Function ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
The Other ◽  
Myocardial Segment ◽  
Intracoronary Infusion ◽  
Hemodynamic Function ◽  
And Function

Prolonged normothermic myocardial ischemic arrest results in myocardial dysfunction. This study has investigated the technique of preserving myocardial function by a single bolus intracoronary infusion of combination potassium and verapamil at the onset of ischemic arrest. Sixty-one dogs underwent cardiopulmonary bypass with 60 min of ischemic arrest: 25 received no myocardial protection, 12 received a single intracoronary bolus of KCl, 12 received combination verapamil and KCl, and 12 received verapamil alone. Following the ischemic arrest, hearts protected by combination of potassium and verapamil demonstrated better survival evidenced by the ability of all 12 dogs to resume normal hemodynamic function. The hemodynamic function in the combination potassium and verapamil group also demonstrated better cardiac output, left ventricular dF/dt, and myocardial segment shortening than survivors in the other groups. Subsarcolemmal (SSL) and intermyofibrillar IMF) mitochondria were isolated from these hearts and function evaluated. NADH-linked oxygen consumption was impaired as was calcium transport in the SSL from unprotected ischemic hearts. Intermyofibrillar mitochondria were not different from control or sham. The hearts protected by verapamil and potassium demonstrated normal mitochondrial function.

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

2002 ◽  
Vol 283 (2) ◽  
pp. R477-R486 ◽  
Author(s):  
Christopher D. Raeburn ◽  
Casey M. Calkins ◽  
Michael A. Zimmerman ◽  
Yong Song ◽  
Lihua Ao ◽  
...  
Keyword(s):  
Adhesion Molecule ◽  
Cardiac Dysfunction ◽  
Gene Knockout ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Immunofluorescent Staining ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Neutrophil Accumulation

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.

scholarly journals MicroRNA-495 serves as a diagnostic biomarker in patients with sepsis and regulates sepsis-induced inflammation and cardiac dysfunction

2019 ◽  
Vol 24 (1) ◽  
Author(s):  
Hailei Guo ◽  
Liying Tang ◽  
Jianjun Xu ◽  
Cai Lin ◽  
Xiangwei Ling ◽  
...  
Keyword(s):  
Sofa Score ◽  
Cardiac Dysfunction ◽  
Troponin I ◽  
Cecal Ligation ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Apache Ii Score ◽  
Diagnostic Biomarker ◽  
Blood Cytokines ◽  
Tnf Α

Abstract Background Sepsis leads to severe inflammatory and cardiac dysfunction. This study aimed to explore the clinical value of miR-495 in sepsis, as well as its role in sepsis-induced inflammation and cardiac dysfunction. Methods 105 sepsis patients were recruited; receiver operating characteristic (ROC) curve was plotted to assess the diagnostic value of miR-495 in sepsis. A model of sepsis in rats was created via performing cecal ligation and puncture (CLP). After modeling, the cardiac function, including left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP) and maximum rate of rise/fall of left ventricle pressure (± dp/dtmax), and serum cardiac troponin I (CTn-I), creative kinase isoenzyme MB (CK-MB) were detected. The blood cytokines levels including TNF-α, IL-6, IL-1β were also measured. Quantitative real-time PCR (qRT-PCR) was used for the measurement of the expression level of miR-495. Results MiR-495 was significantly downregulated in sepsis patients, especially patients who suffered from septic shock (SS). MiR-495 expression was negatively associated with Scr, WBC, CRP, PCT, APACHE II score and SOFA score. MiR-495 could distinguish patients with SS from non-SS patients. MiR-495 and SOFA score were better indictors for the occurrence of cardiac dysfunction in sepsis patients. In CLP-induced sepsis model. CLP rats experienced deterioration of LVSP, LVEDP, ± dp/dtmax, and had a rise in serum CTn-I, CK-MB, TNF-α, IL-6 and IL-1β, which were improved by miR-495 agomir injection. Conclusions MiR-495 might be a potential diagnostic biomarker for sepsis patients, and overexpression of miR-495 alleviated sepsis-induced inflammation and cardiac dysfunction.

scholarly journals Left Ventricular Remodeling and Myocardial Work: Results From the Population-Based STAAB Cohort Study

2021 ◽  
Vol 8 ◽  
Author(s):  
Floran Sahiti ◽  
Caroline Morbach ◽  
Vladimir Cejka ◽  
Judith Albert ◽  
Felizitas A. Eichner ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cohort Study ◽  
General Population ◽  
Myocardial Function ◽  
Myocardial Dysfunction ◽  
Blood Pressure Level ◽  
Hypertensive Heart Disease ◽  
Left Ventricular ◽  
Work Efficiency ◽  
Lv Mass

Introduction: Left ventricular (LV) dilatation and LV hypertrophy are acknowledged precursors of myocardial dysfunction and ultimately of heart failure, but the implications of abnormal LV geometry on myocardial function are not well-understood. Non-invasive LV myocardial work (MyW) assessment based on echocardiography-derived pressure-strain loops offers the opportunity to study detailed myocardial function in larger cohorts. We aimed to assess the relationship of LV geometry with MyW indices in general population free from heart failure.Methods and Results: We report cross-sectional baseline data from the Characteristics and Course of Heart Failure Stages A-B and Determinants of Progression (STAAB) cohort study investigating a representative sample of the general population of Würzburg, Germany, aged 30–79 years. MyW analysis was performed in 1,926 individuals who were in sinus rhythm and free from valvular disease (49.3% female, 54 ± 12 years). In multivariable regression, higher LV volume was associated with higher global wasted work (GWW) (+0.5 mmHg% per mL/m2, p &lt; 0.001) and lower global work efficiency (GWE) (−0.02% per mL/m2, p &lt; 0.01), while higher LV mass was associated with higher GWW (+0.45 mmHg% per g/m2, p &lt; 0.001) and global constructive work (GCW) (+2.05 mmHg% per g/m2, p &lt; 0.01) and lower GWE (−0.015% per g/m2, p &lt; 0.001). This was dominated by the blood pressure level and also observed in participants with normal LV geometry and concomitant hypertension.Conclusion: Abnormal LV geometric profiles were associated with a higher amount of wasted work, which translated into reduced work efficiency. The pattern of a disproportionate increase in GWW with higher LV mass might be an early sign of hypertensive heart disease.

scholarly journals Role of Two-Dimensional Speckle-Tracking Echocardiography in Early Detection of Left Ventricular Dysfunction in Dogs

Animals ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 2361
Author(s):  
Lina Hamabe ◽  
Ahmed S. Mandour ◽  
Kazumi Shimada ◽  
Akiko Uemura ◽  
Zeki Yilmaz ◽  
...  
Keyword(s):  
Early Detection ◽  
Clinical Application ◽  
Speckle Tracking ◽  
Myocardial Function ◽  
Speckle Tracking Echocardiography ◽  
Comprehensive Evaluation ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Deformation Analysis ◽  
Two Dimensional

Two-dimensional speckle-tracking echocardiography (2D–STE) is an advanced echocardiographic technique based on deformation imaging that allows comprehensive evaluation of the myocardial function. Clinical application of 2D–STE holds great potential for its ability to provide valuable information on both global and regional myocardial function and to quantify cardiac rotation and synchronicity, which are not readily possible with the conventional echocardiography. It has gained growing importance over the past decade, especially in human medicine, and its application includes assessment of myocardial function, detection of subclinical myocardial dysfunction and serving as a prognostic indicator. This review illustrates the fundamental concepts of deformation analysis and gives an overview of the current understanding and its clinical application of this technique in veterinary medicine, with a focus on early detection of left ventricular (LV) dysfunction in dogs.

P952Choosing an effective methods for assessing the results of percutaneous coronary interventions in post-myocardial infarction patients

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
Y Rustamova ◽  
V Azizov ◽  
T Dzhahangirov ◽  
G Imanov ◽  
D A Maximkin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Stress Echocardiography ◽  
Myocardial Function ◽  
Left Ventricular ◽  
Functional Class ◽  
Long Term Results ◽  
Percutaneous Coronary Interventions ◽  
Average Difference ◽  
Percutaneous Coronary

Abstract Aim To evaluate the effectiveness of cardiac magnetic resonance (CMR) and stress-echocardiography in the assessment of long-term results of percutaneous coronary interventions (PCI) in post-MI patients with dysfunctional myocardium. Methods 112 patients were participated in the study. Inclusion criteria: myocardial infarction in previously; angina II-III functional class (CCS); multivessel coronary disease (SYNTAXscore I <32); the presence of segments with abnormality left ventricular local contractility; chronic heart failure I-III functional class (NYHA); left ventricular ejection fraction (LVEF) is less than 45%. All patients underwent stenting of the coronary arteries in the zone of viable myocardium. Only drug-eluting stents were implanted in coronary arteries. Long-term results were followed up 18 months after PCI in all patients. All patients underwent stress-echocardiography and CMR for visualization of myocardium after PCI. Results On average, initially accounted for 2.12±0.74 segments with abnormality kinetic per patient according CMR, whereas, according to stress echocardiography, the average number of segments was 1.96±0.42. The average difference was 0.16 segment [0.11–0.18; 95% CI, p=0.003]. In the postoperative period, after 18 months, there was a significant decrease a segments with abnormality kinetics in the zone of hibernated myocardium, from 2.12 to 1.08, according to CMR (the average difference was 1.04 segment) [0.98–1.1; 95% CI, p<0.01], and from 1.96 to 0.98 according to stress-echocardiography (the average difference was 0.98 segments) [0.94–0.99; 95% CI, p=0.023]. There is a significant discrepancy between the number of identified segments with abnormality kinetics using CMR and stress- echocardiography. There was a significant decrease in the transmurality index from 0.42 to 0.31 (according to CMR). The difference was 0.11 [0.09–0.14; 95% CI, p<0.05]. At the same time, recovery of myocardial function was clearly manifested in patients with a trasmurality index of 0.3–0.5, whereas with a transmurality index of more than 0.5, reliable recovery of myocardial function was not observed. Conclusion CMR allows a more objective analysis of the results of PCI in patients with dysfunctional myocardium, as compared with the stress-echocardiography method. Acknowledgement/Funding Russian Academic Excellence Project 5-100

scholarly journals Potential role of a disintegrin and metalloproteinase-17 (ADAM17) in age-associated ventricular remodeling of rats

RSC Advances ◽  
2019 ◽  
Vol 9 (25) ◽  
pp. 14321-14330 ◽  
Author(s):  
Hainiang Liu ◽  
Haoren Wang ◽  
Dong Cheng ◽  
Qinfu Wang ◽  
Zuowei Pei ◽  
...  
Keyword(s):  
Potential Role ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Tnf Α ◽  
A Disintegrin And Metalloproteinase ◽  
Factor Α ◽  
Necrosis Factor

Excessive tumor necrosis factor-α (TNF-α) could enhance cell death and aggravate left ventricular remodeling and myocardial dysfunction.

KATP channel activation reduces the severity of postresuscitation myocardial dysfunction

2000 ◽  
Vol 279 (4) ◽  
pp. H1609-H1615 ◽  
Author(s):  
Wanchun Tang ◽  
Max Harry Weil ◽  
Shijie Sun ◽  
Andrej Pernat ◽  
Earl Mason
Keyword(s):  
Ischemic Preconditioning ◽  
Channel Blocker ◽  
Myocardial Function ◽  
Myocardial Dysfunction ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Channel Activation ◽  
Channel Opener

Postresuscitation myocardial dysfunction has been recognized as a leading cause of the high postresuscitation mortality rate. We investigated the effects of ischemic preconditioning and activation of ATP-sensitive K+(KATP) channels on postresuscitation myocardial function. Ventricular fibrillation (VF) was induced in 25 Sprague-Dawley rats. Cardiopulmonary resuscitation (CPR), including mechanical ventilation and precordial compression, was initiated after 4 min of untreated VF. Defibrillation was attempted after 6 min of CPR. The animals were randomized to five groups treated with 1) ischemic preconditioning, 2) KATP channel opener, 3) ischemic preconditioning with KATP channel blocker administered 1 min after VF, 4) KATPchannel blocker administered 45 min before induction of ischemic preconditioning, and 5) placebo. Postresuscitation myocardial function, as measured by the rate of left ventricular pressure increase at 40 mmHg, the rate of left ventricular decline, cardiac index, and duration of survival, was significantly improved in both preconditioned and KATP channel opener-treated animals. KATP channel blocker administered 45 min before induction of ischemic preconditioning completely abolished the myocardial protective effects of preconditioning. We conclude that ischemic preconditioning significantly improved post-CPR myocardial function and survival. These results also provide evidence that the myocardial protective effects of ischemic preconditioning are mediated by KATP channel activation.

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