Improved myocardial performance induced by dofibrate during reperfusion after acute myocardial infarction

1988 ◽  
Vol 66 (12) ◽  
pp. 1518-1523 ◽  
Author(s):  
M. Renuka Prasad ◽  
Ronald Clement ◽  
Hajime Otani ◽  
Randall Jones ◽  
Dipak K. Das ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Myocardial Injury ◽  
Left Ventricular ◽  
Ischemia And Reperfusion ◽  
Cardioplegic Arrest ◽  
Beneficial Effects ◽  
Hypolipidemic Drug ◽  
And Control ◽  
Experimental Pigs

The increase of cellular fatty acids appears to be one of the causes of the myocardial injury during ischemia and reperfusion. This study was designed to examine whether a hypolipidemic drug such as clofibrate can reduce the myocardial injury during ischemia and reperfusion. Clofibrate was fed to experimental pigs for 9 days. Isolated in situ hearts from both experimental and control pigs were subjected to 60 min of regional ischemia induced by occluding the left anterior descending coronary artery, followed by 60 min of global ischemia by hypothermic cardioplegic arrest and 60 min of reperfusion. The clofibrate feeding resulted in the better cardiac performance as judged by increased coronary blood flow, improved left ventricular function, and reduced myocardial injury as judged by creatine kinase release. Although the clofibrate-fed animals contained higher levels of thiobarbituric reactive materials, the free fatty acid levels of plasma and myocardium were much lower compared with control animals. The clofibrate feeding was also associated with increased peroxisomal catalase and (β-oxidation of fatty acids. These results suggest that decreased levels of free fatty acids in the plasma and the myocardium and increased catalase activity induced by antilipolytic therapy appear to provide beneficial effects to the myocardium during ischemia and reperfusion.

Abstract 1712: The P2Y 12 Antagonist Cangrelor and the GP IIb/IIIa Blocker Abciximab Reduce Platelet-Mediated Myocardial Injury After Ischemia and Reperfusion

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jose A Barrabes ◽  
Javier Inserte ◽  
Maribel Mirabet ◽  
Adoracion Quiroga ◽  
Victor Hernando ◽  
...  
Keyword(s):  
Myocardial Injury ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Myocardial Salvage ◽  
Ischemia And Reperfusion ◽  
Activated Platelets ◽  
Rat Hearts ◽  
Developed Pressure ◽  
Enddiastolic Pressure ◽  
Isolated Rat

Objective: Platelets activated during experimental acute myocardial infarction (AMI) contribute to myocardial injury. We aimed to investigate whether platelets from patients with AMI increase myocardial damage after transient ischemia in isolated rat hearts and the modification of this effect by the P2Y 12 receptor antagonist cangrelor and the GPIIb/IIIa receptor blocker abciximab. Methods: Platelets were obtained from 9 AMI patients (7 thrombolyzed, all on aspirin) within 24 h after symptom onset. Incubation with 100 μM cangrelor or 50 μg/ml abciximab resulted, respectively, in 78 ± 4 and 90 ± 2% inhibition of aggregation (optical aggregometry). Isolated rat hearts (four simultaneous experiments per patient) were subjected to 40 min of global ischemia and 60 min of reperfusion. Hearts received no additional intervention (Control) or were infused during the 5 min prior to ischemia with platelets (22.5x10 6 /min), either untreated or treated with cangrelor or abciximab. Results: P-selectin expression (flow cytometry) in isolated platelets before infusion was 31 ± 3% (P = NS between groups). Platelets augmented myocardial injury, as demonstrated by worse left ventricular developed pressure (LVDevP), higher left ventricular enddiastolic pressure (LVEDP) and coronary resistance, and greater LDH release and infarct size (TTC staining), and both cangrelor and abciximab greatly attenuated these effects (Table ). Conclusions: Activated platelets from patients with AMI increase myocardial injury after ischemia and reperfusion, and cangrelor and abciximab attenuate this effect. The results support the notion that very early antiplatelet treatment may increase myocardial salvage by direct effects on the microcirculation in these patients.

scholarly journals Relationship between myocardial edema and left ventricular wall thickness in acute myocardial ischemia: A Magnetic Resonance Imaging study

2014 ◽  
Vol 1 (2) ◽  
pp. 23
Author(s):  
Yoko Mikami ◽  
Andreas Kumar ◽  
Hassan Abdel-Aty ◽  
Matthias G. Friedrich
Keyword(s):  
Magnetic Resonance ◽  
Myocardial Ischemia ◽  
Wall Thickness ◽  
Myocardial Injury ◽  
Myocardial Edema ◽  
Left Ventricular ◽  
Acute Myocardial Ischemia ◽  
Ischemia And Reperfusion ◽  
Significant Difference ◽  
T2 Weighted Images

Purpose: We sought to assess the relationship between left ventricular regional end-diastolic myocardial wall thickness (EDWT) and myocardial edema defined using T2-weighted Cardiovascular Magnetic Resonance (CMR) after acute myocardial ischemia and reperfusion. Methods: T2-weighted and cine CMR images for 7 dogs at baseline, during coronary occlusion (mean 33 ± 4 minutes) and after reperfusion were studied. The EDWT was measured in segments with high signal intensity (SI) on T2-weighted images, adjacent segments and remote segments according to a 16-segment model. Results: The EDWT after reperfusion in segments with high SI on T2-weighted images was significantly increased compared to baseline (6.28 ± 1.06 mm and 5.51 ± 1.40 mm, p < 0.05), whereas EDWT after the reperfusion in adjacent and remote segments did not show significant difference compared to baseline (adjacent: 6.48 ± 1.55 mm and 6.38 ± 1.26 mm, p = N.S., remote: 6.41 ± 1.11mm and 6.42 ± 1.27mm, p = N.S.). The % increase in EDWT after reperfusion from baseline in segments with high SI on T2-weighted images was higher than those in adjacent and remote segments (19 ± 30%, 1.3 ± 15% and 1.5 ± 16%, respectively, p < 0.05). Conclusions: After a brief period of ischemia and reperfusion, edema as defined by high SI on T2-weighted CMR is related to an increase in EDWT. This increase however is too small to be clinically relevant to be used for the detection of acute myocardial injury. Edema imaging is more sensitive and is an essential part of the reliable assessment of acute ischemic myocardial injury.

Abstract 1553: Comparative Gene Expression Analysis of Blood and Heart Identifies Genomic Predictors of Myocardial Injury Following Cardiopulmonary Bypass and Cardioplegic Arrest in the Rat

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Mihai V Podgoreanu ◽  
Kenji Yoshitani ◽  
Adrian Dobra ◽  
Qing Ma ◽  
Bin Zhu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cardiac Surgery ◽  
Cardiopulmonary Bypass ◽  
Myocardial Injury ◽  
Expression Profiles ◽  
Left Ventricular ◽  
Male Rats ◽  
Cardioplegic Arrest ◽  
Fatty Acid Binding ◽  
Tissue Specific

Background: Perioperative myocardial injury (PMI) complicating cardiac surgery remains poorly predicted by clinical risk factors. In a novel rat model of cardiopulmonary bypass (CPB) and cardioplegic arrest (CA) we tested the hypothesis that microarray expression profiles in peripheral blood leukocytes (PBL) can accurately predict degree of PMI, and compared genomic signatures in left ventricular myocardium (LVM) and PBL to identify PMI-associated genes that generalize across tissues. Methods: Male rats subjected to CPB only (75 min), CPB with CA (30 min), and sham surgery (n=5 each) had plasma heart fatty acid binding protein (HFABP) and cardiac troponin I (cTnI) measured 1 hour post CPB and microarray profiling of total RNA from LVM and PBL. PMI genomic classification models were constructed using shotgun stochastic search approach and Bayesian model averaging and their accuracy tested by five-fold cross validation. Results: A spectrum of PMI was observed in the experimental groups as well as robust deregulation of gene expression in a stimulus and tissue-specific manner (Figure ). Estimates of PMI classification accuracy from PBL and LVM are presented in Table . Conclusions: Cardiac surgery induces changes in leukocyte gene expression that predict the spectrum of PMI, with potential applications in perioperative risk stratification and selection of cardioprotective strategies. Predictive accuracy of tissue-specific myocardial injury genomic classifiers

Limiting sarcolemmal Na+entry during resuscitation from ventricular fibrillation prevents excess mitochondrial Ca2+accumulation and attenuates myocardial injury

2007 ◽  
Vol 103 (1) ◽  
pp. 55-65 ◽  
Author(s):  
Sufen Wang ◽  
Jeejabai Radhakrishnan ◽  
Iyad M. Ayoub ◽  
Julieta D. Kolarova ◽  
Domenico M. Taglieri ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Chest Compression ◽  
Myocardial Injury ◽  
Troponin I ◽  
Myocardial Dysfunction ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Ischemia And Reperfusion ◽  
Reverse Mode ◽  
Ventricular Compliance

Background: intracellular Na+accumulation during ischemia and reperfusion leads to cytosolic Ca2+overload through reverse-mode operation of the sarcolemmal Na+-Ca2+exchanger. Cytosolic Ca2+accumulation promotes mitochondrial Ca2+(Ca2+m) overload, leading to mitochondrial injury. We investigated whether limiting sarcolemmal Na+entry during resuscitation from ventricular fibrillation (VF) attenuates Ca2+moverload and lessens myocardial dysfunction in a rat model of VF and closed-chest resuscitation. Methods: hearts were harvested from 10 groups of 6 rats each representing baseline, 15 min of untreated VF, 15 min of VF with chest compression given for the last 5 min (VF/CC), and 60 min postresuscitation (PR). VF/CC and PR included four groups each randomized to receive before starting chest compression the new NHE-1 inhibitor AVE4454B (1.0 mg/kg), the Na+channel blocker lidocaine (5.0 mg/kg), their combination, or vehicle control. The left ventricle was processed for intracellular Na+and Ca2+mmeasurements. Results: limiting sarcolemmal Na+entry attenuated cytosolic Na+increase during VF/CC and the PR phase and prevented Ca2+moverload yielding levels that corresponded to 77% and 71% of control hearts at VF/CC and PR, without differences among specific Na+-limiting interventions. Limiting sarcolemmal Na+entry attenuated reductions in left ventricular compliance during VF and prompted higher mean aortic pressure (110 ± 7 vs. 95 ± 11 mmHg, P < 0.001) and higher cardiac work index (159 ± 34 vs. 126 ± 29 g·m·min−1·kg−1, P < 0.05) with lesser increases in circulating cardiac troponin I at 60 min PR. Conclusions: Na+-limiting interventions prevented excess Ca2+maccumulation induced by ischemia and reperfusion and ameliorated myocardial injury and dysfunction.

scholarly journals Improved cardiac protection with Sabax cardioplegia in Langendorff isolated rat hearts

2014 ◽  
Vol 60 (6) ◽  
pp. 254-259
Author(s):  
M. Perian ◽  
M. Mărginean ◽  
D. Dobreanu ◽  
Alina Scridon
Keyword(s):  
Myocardial Protection ◽  
Myocardial Injury ◽  
Left Ventricular ◽  
Mechanical Activity ◽  
Cardioplegic Arrest ◽  
Rat Hearts ◽  
Langendorff Perfusion ◽  
Perfusion Apparatus ◽  
Solution Methods ◽  
Male Wistar Rats

Abstract Objective: Cardioplegia is an important step to facilitate cardiac surgery while limiting intraoperative myocardial injury. Although recent advances in cardioplegic arrest methods have significantly contributed to better postoperative outcomes, there is still controversy regarding the optimal composition and temperature of the cardioplegic solution. Accordingly, we aimed to assess whether cold or lukewarm Sabax cardioplegia offer improved myocardial protection compared with the classical Krebs-Henseleit solution. Methods: The hearts of 40 male Wistar rats were isolated and submitted to constant-flow retrograde perfusion using a Langendorff perfusion apparatus. The hearts were randomly assigned to cold Krebs-Henseleit (K-H), cold Sabax, or lukewarm Sabax cardioplegia. The ECG, heart rates, and left ventricular systolic pressures (LVSP) were recorded pre- and post-cardioplegia. The time needed for cardioplegia induction and post-cardioplegia recovery were also noted. Results: Both cold and lukewarm Sabax cardioplegia insured faster induction and faster recovery following isothermic reperfusion compared to the standard K-H solution (both p< 0.01). With K-H cardioplegia, the hearts presented a 21.7% force loss after reperfusion (p< 0.001), whilst Sabax cardioplegia was associated with a slight increase in ventricular mechanical activity (3% LVSP increase with lukewarm Sabax cardioplegia, p< 0.001 and 2% LVSP increase with cold Sabax cardioplegia, p = 0.02). With Sabax cardioplegia the hearts displayed considerably less major arrhythmic events and presented less significant bradycardia. Conclusions: The present data suggest that Sabax cardioplegia may be superior to the classical cold crystalloid K-H solution in preserving mechanical activity of the heart and may provide superior protection against major arrhythmias.

scholarly journals Interactions of ethanol drinking with n-3 fatty acids in rats: potential consequences for the cardiovascular system

2008 ◽  
Vol 100 (6) ◽  
pp. 1237-1244 ◽  
Author(s):  
Annabelle Guiraud ◽  
Michel de Lorgeril ◽  
Sabrina Zeghichi ◽  
François Laporte ◽  
Patricia Salen ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Cell Membranes ◽  
Harmful Effect ◽  
Left Ventricular ◽  
Experimental Myocardial Infarction ◽  
Cardiac Mitochondria ◽  
Ethanol Drinking ◽  
Ischaemia And Reperfusion ◽  
Few Data ◽  
And Control

Moderate ethanol drinking (ED) and n-3 fatty acids have both been associated with low cardiac mortality. However, there are few data evaluating the interactions of ED with n-3. We recently reported that moderate ED results in increased n-3 in cardiac patients. The main aim of the present study was, through a well-controlled experimental model, to confirm that chronic ED actually results in increased n-3. Secondary aims were to examine the effects of chronic ED on cardiac mitochondria, cardiac function and experimental myocardial infarction. We studied the fatty acid profiles of plasma, cell membranes and cardiac mitochondria phospholipids in a rat model of chronic ED. In plasma and cell membranes, ED actually resulted in higher n-3 (P = 0·005). In mitochondria phospholipids of ED rats, n-3 were also increased (P < 0·05) but quite modestly. Cardiac mitochondrial function and left ventricular function were not significantly different in ED and control rats, while infarct size after 30 min ischaemia and reperfusion was smaller (P < 0·0001) in ED rats. This is the first animal study confirming interaction of alcohol drinking with n-3. We found no harmful effect of chronic ED on the heart in that model but a significant cardioprotection. Further studies are warranted to investigate the mechanisms by which moderate ED alters the metabolism of n-3 and whether n-3 are the mediators of the ED-induced cardioprotection.

Reduction of asymmetric dimethylarginine involved in the cardioprotective effect of losartan in spontaneously hypertensive rats

2007 ◽  
Vol 85 (8) ◽  
pp. 783-789 ◽  
Author(s):  
Dai Li ◽  
Ke Xia ◽  
Nian-Sheng Li ◽  
Dan Luo ◽  
Shan Wang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Creatine Kinase ◽  
Cardiac Function ◽  
Spontaneously Hypertensive Rats ◽  
Myocardial Injury ◽  
Asymmetric Dimethylarginine ◽  
Left Ventricular ◽  
Ischemia And Reperfusion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Previous studies have indicated that nitric oxide synthase (NOS) inhibitors can induce an increase of blood pressure and exacerbate myocardial injury induced by ischemia and reperfusion, whereas angiotensin II receptor antagonists protect the myocardium against injury induced by ischemia and reperfusion. Isolated hearts from male spontaneously hypertensive rats (SHR) or male Wistar-Kyoto rats (WKY) were subjected to 20 min global ischemia and 30 min reperfusion. Heart rate, coronary flow, left ventricular pressure, and its first derivatives (±dP/dtmax) were recorded, and serum concentrations of asymmetric dimethylarginine (ADMA) and NO and the release of creatine kinase in coronary effluent were measured. The level of ADMA was significantly increased and the concentration of NO was decreased in SHR. Ischemia and reperfusion significantly inhibited the recovery of cardiac function and increased the release of creatine kinase, and ischemia and reperfusion-induced myocardial injury in SHR was aggravated compared with WKY. Vasodilation responses to acetylcholine of aortic rings were decreased in SHR. Treatment with losartan (30 mg/kg) for 14 days significantly lowered blood pressure, elevated the plasma level of NO, and decreased the plasma concentration of ADMA in SHR. Treatment with losartan significantly improved endothelium-dependent relaxation and cardiac function during ischemia and reperfusion in SHR. Exogenous ADMA also aggravated myocardial injury induced by ischemia and reperfusion in isolated perfused heart of WKY, as shown by increasing creatine kinase release and decreasing cardiac function. The present results suggest that the protective effect of losartan on myocardial injury induced by ischemia and reperfusion is related to the reduction of ADMA levels.

scholarly journals Left ventricular mural thrombi with multisystem thrombosis in patients with COVID-19 and myocardial injury: a case series

2021 ◽  
Vol 5 (6) ◽  
Author(s):  
Aakash Garg ◽  
Hisham Hakeem ◽  
Gouthami Chennu ◽  
Qaisra Saeed ◽  
Esad Vucic ◽  
...  
Keyword(s):  
Myocardial Injury ◽  
Coronary Thrombosis ◽  
Case Series ◽  
Right Ventricular Dysfunction ◽  
Regional Wall Motion ◽  
Left Ventricular ◽  
Coagulation Cascade ◽  
Lv Function ◽  
Severe Respiratory Distress

Abstract Background Cardiovascular and thromboembolic complications have been reported in patients with Coronavirus disease-2019 (COVID-19)-related severe respiratory distress syndrome. Although myocarditis associated with COVID-19 pneumonia has been described, evidence of left ventricular (LV) mural thrombi with other multisystem events has not been reported. Case summary We report two cases with severe COVID-19 pneumonia and myocardial injury with large LV thrombi and other multisystem thrombotic events. The first patient represents an unusual case of large LV apical thrombus without concordant regional wall motion abnormality and mildly reduced LV function. A subsequent inferior ST-elevation myocardial infarction (STEMI) was likely related to either an embolic event or in situ coronary thrombosis. We could not ascertain whether the acute right ventricular dysfunction was due to in situ pulmonary thrombosis or inferior STEMI. The catastrophic cerebrovascular accident was likely an embolic phenomenon. Similarly, the second patient demonstrated multiple large pedunculated thrombi occupying one-third of the LV cavity with moderately reduced LV function. A segmental pulmonary embolism was diagnosed on computed tomography chest, confirming multiple territories of in situ thrombosis. Discussion COVID-19-related inflammatory cytokine release has been linked to activation of coagulation pathways. Marked elevation of ferritin and C-reactive protein levels in both patients were consistent with evidence of a hyperinflammatory state with ‘cytokine storm’. Furthermore, the finding of elevated D-dimer levels lends support to the altered coagulation cascade that plausibly explains the multisystem thrombosis observed in our patients. The direct viral endothelial involvement and subsequent endothelial dysfunction may play an important role in the development of thrombosis in different vascular beds, as seen in our patients.

Preischemic glycogen reduction or glycolytic inhibition improves postischemic recovery of hypertrophied rat hearts

1994 ◽  
Vol 267 (1) ◽  
pp. H66-H74 ◽  
Author(s):  
M. F. Allard ◽  
P. G. Emanuel ◽  
J. A. Russell ◽  
S. P. Bishop ◽  
S. B. Digerness ◽  
...  
Keyword(s):  
Myocardial Injury ◽  
Left Ventricular ◽  
Lv Function ◽  
Ischemia And Reperfusion ◽  
Rat Hearts ◽  
Glycolytic Inhibitor ◽  
Lactate Levels ◽  
Developed Pressure ◽  
Postischemic Recovery ◽  
Krebs Buffer

The purpose of this study was to determine whether metabolites produced by glycolysis during ischemia significantly contribute to myocardial injury of hypertrophied hearts. The accumulation of glycolytic metabolites during ischemia was reduced by means of glycogen reduction or by treatment with the glycolytic inhibitor, 2-deoxy-D-glucose (2-DG) before ischemia. Hearts from aortic-banded (Band) and sham-operated (Sham) rats (8 wk postop) were isolated, perfused with Krebs buffer, and had a left ventricular (LV) balloon to measure developed pressure. A 15-min perfusion with hypoxic buffer (glycogen reduction, GR) or a 10-min perfusion with 10 mM 2-DG (glycolytic inhibition) was followed by 25 min global, normothermic, no-flow ischemia and 30 min normoxic reperfusion. Heart weights were greater in Band than Sham [2.76 +/- 0.06 vs. 1.5 +/- 0.04 (mean +/- SE) g; P < 0.001]. GR and 2-DG each resulted in reduced ATP levels measured at the beginning of ischemia in both Band and Sham groups compared with untreated groups, but there were no differences among groups after 25 min of ischemia. Myocardial lactate levels at the end of ischemia were significantly reduced in both Band and Sham hearts with GR or 2-DG compared with untreated controls. Recovery of LV function after ischemia and reperfusion was significantly improved in Band after GR (206% increase) and after 2-DG treatment (126% increase) compared with their respective untreated controls. Diastolic dysfunction during reperfusion was ameliorated in Band by preischemic GR but not by 2-DG treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

The rumen solubility of a calcium soap of palm fatty acids

1989 ◽  
Vol 1989 ◽  
pp. 151-151
Author(s):  
D I Givens ◽  
Jeannie M Everington ◽  
N Shepperson
Keyword(s):  
Fatty Acids ◽  
Cell Walls ◽  
Dry Matter ◽  
Calcium Soap ◽  
Beneficial Effects ◽  
Ruminant Diets ◽  
Soya Oil ◽  
In Situ Formation

Several experiments have shown (see Armstrong and Ross, 1968) that the addition of fats to ruminant diets can lead to a reduction in the digestibilities of forage cell walls due to adverse effects on the rumen microflora. Jenkins and Palmquist (1982) showed in vitro that the in situ formation of calcium soaps in the rumen could prevent this problem. Subsequently Jenkins and Palmquist (1984) have provided evidence that the feeding of preformed calcium soaps of tallow and soya oil fatty acids to dairy cows allowed normal rumen digestion of cell walls whereas non-saponified tallow fatty acids caused cell wall digestibility to be reduced.Givens et al (1988) reported that a calcium soap of palm fatty acids (Protector, UFAC-UK Ltd) did not cause any reduction in the digestibility of neutral detergent fibre (NDF) when fed to sheep at up to 152.4 gkg-1 of total diet dry matter (DM). Since it is believed that these beneficial effects of calcium soaps are due to their reduced rumen solubility, the present experiment has examined this aspect in further detail.

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