Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the effects of different pH HEPES-KH reperfusate solution on immature myocardial protection, isolated perfused Langendorff model from immature rabbit hearts were developed formed. Control group (C) was perfused only with pH 7.4 HEPES-KH solution for 90 min. Ischemia/reperfusion group (group I/R) was perfused with pH 7.4 HEPES-KH solution before ischemia or after ischemia. Experimental group (group E), after ischemia, was perfused with pH 6.8, pH 7.1 and pH 7.4 HEPES-KH solutions for 5 min, 5 min, and 20 min, respectively. The left ventricular function recovery, MWC, LDH and CK leakage, MDA, ATP content, and SOD activity were determined. Our results showed that the left ventricular function recovery, ATP content and SOD activity in group E were higher than those of group I/R (P < 0.05). MWC, MDA content, LDH and CK leakage in group E were lower than those of group I/R (P < 0.05). These findings suggested that pH paradox might be one of important mechanisms for immature myocardial ischemia-reperfusion injury, and acidic perfusate, at the beginning of reperfusion, might attenuate pH paradox and ameliorate functional recovery in isolated perfused immature rabbit hearts.
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PMID:Acidic HEPES-KH reperfusion enhances myocardial protection in immature rabbits. 1265 46

Opioids have been shown to confer late preconditioning against ischemia/reperfusion injury in several species. However, it is unknown whether gender or aging affects opioid-induced cardioprotection. Isolated perfused hearts from Fischer 344 rats were subjected to 20 min of global ischemia followed by 20 min of reperfusion. BW373U86, a delta-opioid receptor agonist, was administered s.c. at varying doses (0.1, 0.33, 1.0 mg/kg) 24 h before (BW0.1, BW0.33 and BW1.0, respectively). In 12-week-old male (YM) rats, the recovery of LV developed pressure (LVDP) after ischemia/reperfusion improved significantly in BW0.33 and BW1.0, compared with the control (C). In 78-week-old male (OM) rats, the recovery of LV function after ischemia/reperfusion improved and the total release of CK and LDH during reperfusion was attenuated in BW1.0. In 12-week-old female (YF) rats, the recovery of LV function improved only in BW0.33 but not in BW0.1 and BW1.0. The cardioprotective effect afforded by BW373U86 was completely abolished by NS-398, a COX-2 selective inhibitor, in YM, YF, and OM, although NS-398 in itself did not affect myocardial ischemia/reperfusion injury. The levels of 6-keto-PGF(1alpha) (a stable metabolite of PGI(2)) in coronary effluent during reperfusion were higher in the BW373U86-pretreated group that showed cardioprotection than in C and this increase in PGI(2) production was also inhibited by NS-398 in YM, YF, and OM. In conclusion, BW373U86-induced late preconditioning can be observed in aged and female hearts. A COX-2-dependent increase in PGI(2) production is essential for BW373U86-induced late PC in both sexes and in both young and old rats.
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PMID:Gender and aging do not impair opioid-induced late preconditioning in rats. 1468 5

The dysfunction of muscles, especially that of the cardiac muscle, is one of the most dangerous for the life pathological states. The determination of biochemical indexes such as AST, ALT, CK, LDH, mioglobin, etc., which has been used so far in animals is not a sufficient diagnostic method. Therefore, new markers, levels of which could reflect the state of a patient more precisely, have been sought. Troponin, a protein found in skeletal and cardiac muscles only, has been considered a reliable index of myocardial ischemia in animals, especially in dogs. Its diagnostic properties have appeared to be a valuable complementation of the other diagnostic methods and thus could have gained a lot of veterinary practitioners interest.
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PMID:Troponin--a new marker in the diagnostics of muscle diseases in animals. 1470 75

This study investigated the effects of cariporide, an inhibitor of sodium-proton exchanger (NHE), during myocardial ischemia and reperfusion in senescence. Isolated Langendorff perfused hearts from 4 (adult) and 24 (senescent) month old male Wistar rats were submitted to prolonged low-flow ischemia (LFI) at 15% of initial coronary flow (180 min) or to 45 min of LFI (15% of initial coronary flow) followed by 30 min of reperfusion, without or with cariporide (10(-6)M). In senescent hearts, but not in adults, treatment with cariporide during prolonged LFI attenuated the elevation of coronary resistances (578 +/- 84 vs 1020 +/- 129% of baseline value after 180 min, P < 0.05) and delayed the decrease in active tension (35.6 +/- 5.1 vs 22.2 +/- 3.4% of baseline value after 60 min; P < 0.05). During reperfusion following LFI, the coronary flow impairment was more pronounced in senescents than in adults (48.4 +/- 9.4 and 75.3 +/- 4.9% of baseline value, respectively; P < 0.05) but was fully prevented in senescent hearts by cariporide treatment (95.6 +/- 17.0% of baseline value; P < 0.05 vs untreated group). This beneficial effect of cariporide on coronary tone was associated with an improvement of active and resting tensions and lower LDH release. Such functional protective effects of cariporide suggest an operative NHE during LFI at both coronary and myocardial levels in senescent heart. In addition, cariporide-associated improvement of post-ischemic recovery of coronary and contractile function as well as the limitation of cellular injury suggests a major role of calcium overload via NHE activation during reperfusion of senescent ischemic heart.
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PMID:Cardioprotection with cariporide, a sodium-proton exchanger inhibitor, after prolonged ischemia and reperfusion in senescent rats. 1548 53

Recent evidence indicates that peroxynitrite represents a major cytotoxic effector in heart diseases, but its mechanisms of action are still not known exactly. Notably, the ability of peroxynitrite to trigger cardiomyocyte apoptosis, a crucial mode of cell death in many cardiac conditions, remains poorly defined. We evaluated apoptotic and necrotic cell death in cultured H9C2 cardiomyocytes, following a brief (20 min) exposure to peroxynitrite (50-500 microM). Peroxynitrite-dependent myocardial toxicity was then investigated in a rat model of myocardial ischemia-reperfusion (MIR), where the effects of peroxynitrite were blocked by the superoxide dismutase mimetics and peroxynitrite scavenger Mn(III)-tetrakis(4-benzoic acid) porphyrin (MnTBAP). In vitro, peroxynitrite killed cardiomyocytes mostly through apoptosis (DNA fragmentation, apoptotic nuclear alterations, caspase-3 activation, and PARP cleavage), but not necrosis (propidium iodide staining and LDH release). In vivo, MIR triggered myocardial oxidative stress (malondialdehyde generation), nitrotyrosine formation, neutrophil accumulation, and the cleavage of caspase-3 and PARP, indicating ongoing myocardial apoptosis. MnTBAP suppressed these alterations, allowing a considerable reduction of myocardial injury. Thus, peroxynitrite triggers apoptosis in cardiomyocytes in vitro and in the myocardium in vivo, through a pathway involving caspase-3 activation and the cleavage of PARP. These results provide important novel information on the mechanisms of myocardial toxicity of peroxynitrite.
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PMID:Peroxynitrite is a major trigger of cardiomyocyte apoptosis in vitro and in vivo. 1693 67

Nitric oxide (NO) plays a protective role in myocardial ischemia-reperfusion (I/R) injury. However, the concomitant production of superoxide and other reactive oxygen species (ROS) during I/R may diminish the bioavailability of NO and hence compromise the beneficial effects. The objective of this study was to investigate the protective effect of the coadministration of NCX-4016 [2-(acetyloxy)benzoic acid 3-(nitrooxymethyl)phenyl ester] (an NO donor) with antioxidants Tempol, superoxide dismutase (SOD), or urate on I/R injury. Isolated rat hearts, perfused with Krebs-Henseleit buffer, were subjected to 30 minutes of global ischemia, followed by 45 minutes of reperfusion. Before the induction of ischemia, the hearts were infused for 1 minute with NCX-4016 (100 microM) either alone or in combination with Tempol (100 microM), SOD (200 U/mL), or urate (100 microM). Hearts pretreated with NCX-4016 showed a significantly enhanced recovery of function and decreased infarct size and LDH/CK release compared with the controls. However, treatment of hearts with NCX-4016 + Tempol, SOD, or urate showed a significantly enhanced recovery of heart function compared with NCX-4016 alone. The treatment of hearts with NCX-4016 + Tempol showed significantly enhanced NO generation and decreased ROS and dityrosine (a marker of peroxynitrite) formation. In conclusion, NCX-4016 in combination with Tempol demonstrated significant cardioprotection and, thus, may offer a novel therapeutic strategy to prevent I/R-mediated myocardial injury.
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PMID:Prevention of postischemic myocardial reperfusion injury by the combined treatment of NCX-4016 and Tempol. 1703 Dec 60

This study is to investigate if madecassoside can protect against myocardial reperfusion injury in rabbit heart in vivo. The ischemia reperfusion model was established. Left ventricular function and ECG were monitored at the ischemia and reperfusion period. The infarct areas were expressed as percentage. The levels of LDH, CK, MDA and SOD were measured and C-reactive protein (CRP) in serum was measured by ELISA kit. Cardiomyocyte apoptosis were measured by TUNEL staining. A monoclonal rabbit anti-goat Bcl-2 proteins as primary antibody was used for Bcl-2 immunohistochemical staining. Treatment with madecassoside (3.2, 1.6 and 0.8 mg x kg(-1)) i.v. during ischemia reperfusion injury attenuated myocardial damage, that is, characteristic of decreasing infarct size, decreasing LDH and CK release. Activities of SOD were diminished and MDA level increased obviously in control group whereas pretreatment with madecassoside significantly blunted the decrease of SOD activity, markedly reduced the levels of MDA, CRP and cardiomyocyte apoptosis, and upregulated the expression of Bcl-2. Madecassoside has the protective effect against myocardial ischemia reperfusion injury, and effects of anti-lipid peroxidation, enhancement of SOD activity, anti-inflammation and anti-apoptosis.
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PMID:[Protective effect of madecassoside against reperfusion injury after regional ischemia in rabbit heart in vivo]. 1770 67

Reactive oxygen species (ROS) are critical in tissue responses to ischemia-reperfusion. The enzyme methionine sulfoxide reductase-A (MsrA) is capable of protecting cells against oxidative damage by reversing damage to proteins caused by methionine oxidation or by decreasing ROS through a scavenger mechanism. The current study employed adenovirus mediated over-expression of MsrA in primary neonatal rat cardiac myocytes to determine the effect of this enzyme in protecting against hypoxia/reoxygenation in this tissue. Cells were transduced with MsrA encoding adenovirus and subjected to hypoxia/reoxygenation. Apoptotic cell death was decreased by greater than 45% in cells over-expressing MsrA relative to cells transduced with a control virus. Likewise total cell death as determined by levels of LDH release was dramatically decreased by MsrA over-expression. These observations indicate that MsrA is protective against hypoxia/reoxygenation stress in cardiac myocytes and point to MsrA as an important therapeutic target for ischemic heart disease.
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PMID:MsrA protects cardiac myocytes against hypoxia/reoxygenation induced cell death. 1808 15

We evaluated the cardioprotection against myocardial ischemia-reperfusion injury induced by sevoflurane postconditioning (SpostC) in chronically-infarcted rat hearts, and investigated the roles of phosphoinositide 3-kinase (PI3K)-protein kinase B/Akt (PKB/Akt), mitogen-activated extracellular regulated kinase 1/2 (MEK 1/2)-extracellular regulated kinase 1/2 (ERK 1/2), and mitochondrial permeability transition pore (mPTP). Left anterior descending (LAD) coronary artery was ligated to induce myocardial infarction in rats. Six weeks later, chronically-infarcted hearts were isolated and subjected to 30 min of global ischemia, followed by 1 h of reperfusion with Krebs-Henseleit (K-H) buffer. SpostC was administered by perfusing the hearts with K-H buffer saturated with 3% sevoflurane during the first 15 min of reperfusion. To evaluate the role of PI3K-PKB/Akt and MEK 1/2-ERK 1/2 in SpostC, PI3K inhibitor LY294002 (15 microM) and MEK 1/2 inhibitor PD98059 (20 microM) were administered alone or together with sevoflurane during the first 15 min of reperfusion. We found that exposure of 3% sevoflurane during early reperfusion significantly improved functional recovery (improved left ventricular developed pressure (LVDP), +/-dp/dt, CF, HR and reduced left ventricular end-diastolic pressure (LVEDP)), decreased myocardial infarct size and reduced LDH and CK-MB release, when compared with unprotected hearts. However, these protective effects were abolished in the presence of either LY294002 or PD98059, which was accompanied by the prevention of PKB/Akt and ERK 1/2 phosphorylation, and reduction of myocardial nicotinamide adenine dinucleotide (NAD+) content. These findings suggest that sevoflurane postconditioning protects chronically-infarcted rat hearts against ischemia-reperfusion injury by inhibiting mPTP opening via recruitment of PKB/Akt and ERK 1/2.
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PMID:Sevoflurane postconditioning protects chronically-infarcted rat hearts against ischemia-reperfusion injury by activation of pro-survival kinases and inhibition of mitochondrial permeability transition pore opening upon reperfusion. 1988 Dec 97

Recently, a potential link between infectious agents and athero-sclerosis has been suggested. H. pylori strains bearing the cytotoxin associated gene A (Cag-A) provoked a heightened inflammatory response in vivo and showed stronger relation to gastric complication of this infection. The association between Cag-A positive strain and vascular diseases producing conflicting results. So, the present study aimed to estimate the seroprevalence of H. pylori Cag-A positive strains as a risk factor among different groups of ischemic heart disease and to study its interaction with high sensitivity CRP (hs-CRP) and IL6 as inflammatory host responses. The present study was conducted on anti H. pylori IgG positive 60 ischemic heart disease (IHD) patients and 20 apparently healthy individuals as a control group. IHD patients were classified into 3 groups: (group I) with acute myocardial infarction, unstable angina pectoris patients (group II), chronic stable angina pectoris patients (group III). For all patients and control groups serum anti Cag-A IgG, IL6, hs-CRP, CK, CKMB, LDH, AST and Lipid profile were estimated. IL6 and hs-CRP levels were increased in groups I, II and III as compared with group IV (P < 0.001) with positive correlation between IL6 and hs-CRP in groups I, II and III (P < 0.05). The percentage of anti Cag-A positive cases was similar among the patient groups, but significantly higher than in the control group. Thus, infection with Cag-A positive H. pylori strain may play a role as a risk factor in development of ischemic heart diseases through provocation of high inflammatory response or through other mechanism. Therefore eradication of this infection is important as it is much less expensive than long term treatment of the other risk factors.
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PMID:Relation of Cag-A-positive Helicobacter pylori strain and some inflammatory markers in patients with ischemic heart diseases. 2072 21


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