Myocardial Infarction In Wistar Rats Research Articles

Protective Effect of Prunetin on Isoproterenol-Induced Myocardial Infarction in Wistar Rats via Biochemical Characterization.

The development of MI following ischemia damage is influenced by oxidative stress. Myocardial Infarction (MI) generates myocardial ischemia injury, which damages the cardiomyocytes. Ischemia builds up to a critical level over time in MI, causing permanent myocardial cell damage or death. The current study sought to determine whether Prunetin (PRU) could protect against Isoproterenol (ISO)-induced cardiac heart failure in rats by examining cardiac diagnostic markers, lipid peroxidation products, enzymatic and non-enzymatic antioxidant levels, and histological changes. PRU (20 mg/kg bwt) was orally administered for 19 days to rats, and after the treatment, ISO (85 mg/kg bwt) was subcutaneously administered with an intermission of 24 h for a couple of days to induce myocardial infarction on 20th and 21st days. ISO-treated rats exhibited considerable alterations in cardiac-sensitive markers in the serum. The levels of lipid peroxidation markers augmented drastically in the plasma and myocardium. Enzymatic antioxidant levels in erythrocytes and myocardium and the states of non-enzymatic antioxidants were diminished in the plasma and heart tissue of ISO-treated rats. The histopathological examination of heart tissue exhibited cardiac damage in ISO-induced rats. The oral administration of PRU significantly lowered the levels of lipid peroxidation and biochemical indicators, while significantly improving the antioxidant system function of ISO-interposed rats. In PRU-treated ISO-injected rats, histological examinations revealed suppressed myocardial destruction. Our research shows that oral pretreatment of PRU prevented ISO-induced oxidative stress in MI.

Cardioprotective effects of Musanga cecropioides Welw. Ex Benth extracts on isoproterenol-induced acute myocardial infarction in Wistar rats.

Background of the study: Acute myocardial infarction (AMI) is a prominent etiology of heart failure-related death worldwide. Musanga cecropioides Welw. Ex Benth bark water extract is used by the Yoruba tribe in Nigeria for the treatment of several metabolic diseases, inflammatory diseases, wounds, coughs, and toothaches. Aim: This work evaluates the cardioprotective effects of M. cecropioides water extract on isoproterenol (ISO)-induced AMI in Wistar rats. Methodology: ISO (100 mg/kg, subcutaneous (s.c.)) was used to induce AMI in rats. Thirty rats (n = 5) were pretreated orally for seven days with normal saline (1.0 ml/kg/day, no-AMI control), normal saline + ISO (1.0 ml/kg/day + 100 mg/kg AMI, control), normal saline + M. cecropioides water extract (1.0 ml/kg/day + 500 mg/kg/day, non-AMI group), M. cecropioides water extract 500 and 1000 mg/kg/day, and captopril (5 mg/kg/po/day) before induction of AMI on the eighth and ninth days. Electrocardiographic changes, lipid peroxidation, biochemical enzyme profile, hematological, and histopathological changes were determined. Results: ISO significantly increased AST, ALT, lipid 15 profile, and oxidative stress marker (MDA). In addition, it caused ST segment elevation, increased heart rate, R-R interval, and degenerative changes in cardiac tissues. Pretreatment with M. cecropioides water extract (500 and 1000 mg/kg) significantly suppressed the biochemical enzyme profile and lipid peroxidation. It also significantly improved changes in histopathological and electrocardiographic imaging of the myocardium. Conclusion: The outcome of this work shows evidence that M. cecropioides water extract may have cardioprotective effects on AMI in rats.

Effects of <i>Lactobacillus delbrueckii</i> TS1-06 probiotic strain on the size of myocardial infarction in Wistar rats with systemic inflammatory response syndrome

Experimental medicine provides the scientific community with a plethora of information on therapeutic efficacy of probiotic strains. However, from the point of view of evidence-based medicine, the list of disorders controlled by probiotics is limited to antibiotic-associated diarrhea in adults and children, Clostridium difficile-associated diarrhea, acute infectious diarrhea in children and adults, eradication therapy, ulcerative colitis and irritable bowel syndrome. Recently, these indications are also amended by well-validated clinical guidelines for the usage of probiotic preparations, in order to modulate immunity. Given the permeability of gastrointestinal and immune system barriers for pathogenic and opportunistic microbiota, it seems logical to assume the effectiveness of probiotics as potential symbiotic regulators of nervous and cardiovascular systems. It should also be taken into account that metabolic disorders, e.g., obesity, with a low-intensity inflammatory response and characteristic cytokine pattern, are acquired as a gain of human civilization. In this regard, we propose a scientific hypothesis about the effectiveness of probiotic microbial strains in increasing myocardial resistance to ischemic-reperfusion injury, due to their ability to block individual links of the cytokine cascade during the development of inflammatory response, for its subsequent translation into clinical practice.The development and validation of a new experimental model of systemic inflammatory response syndrome (SIRS) in male Wistar rats, including obesity, acute inflammatory process of the colon, and antibiotic-induced dysbiosis, became basic to the study of efficacy of probiotic drugs in terms of myocardial resistance to ischemicreperfusion injury (IRI). Rats with SIRS showed a significantly increased size of the infarction area (+28%) upon experiments with isolated perfused heart under global ischemia-reperfusion conditions. Significant changes in the leukocyte formula and immunological parameters associated with SIRS were corrected by introduction of a mixture of probiotic strains L. acidophilus (LA-5) and B. animalis subsp. lactis (BB-12), and the isolated strain L. delbrueckii TS1-06. In both groups with probiotic correction, there was a decrease in the infarction area compared to the SIRS group. General and specific changes in IL-2, transforming growth factor-b (TGF-b) and tumor necrosis factor-a (TNFa) were noted. The reduction of myocardial infarction by probiotics may be related to the blocking of first-order cytokines, which leads to a «break» of proinflammatory cascade. A need for in-depth study of cardioprotective mechanisms mediated by probiotics was confirmed due to their potential usage as a symbiotic alternative to biological drugs which block the main pro-inflammatory cytokines.

Myocardial infarction impaired wall mechanics and hemodynamics in peripheral arteries.

Myocardial infarction (MI) impaired both cardiac functions and peripheral arteries. The changes in normal and shear stresses in the peripheral artery wall are of importance for understanding the progression of MI-induced heart failure (HF). The aim of the study is to investigate the corresponding changes of normal and shear stresses. The coronary artery ligation was used to induce the MI in Wistar rats. The analysis of wall mechanics and hemodynamics was performed based on in vivo and in vitro measurements. Myocardial infarction increased wall stiffness in elastic carotid and muscular femoral arteries significantly albeit different changes occurred between the two vessels from 3 to 6weeks postoperatively. Moreover, the hemodynamic analysis showed the gradually deteriorated wall shear stress, oscillatory shear index and relative residence time in the two arteries. This study probably shed light on understanding the interaction between abnormal systemic circulation and peripheral mechanics and hemodynamics during the development of MI-induced HF.

Cardioprotective potential of the antioxidant-rich bioactive fraction of Garcinia pedunculata Roxb. ex Buch.-Ham. against isoproterenol-induced myocardial infarction in Wistar rats.

This Study aimed to characterise the phenolic compounds in Garcinia pedunculata extract and assess their potential antioxidant activity as well as its cardioprotective potential in isoproterenol-induced cardiac hypertrophy in an experimental animal model. In vitro antioxidant properties were determined using DPPH, ABTS, FRAP, PMD assays. In vitro lipid peroxidation experiment was also performed with heart tissues. Cardioprotective and cardiotoxicity effects were determined using the cell line studies. The cardioprotective effect of GP was assessed in a rat model of isoproterenol-(ISO-) induced cardiac hypertrophy by subcutaneous administration. Heart weight/tail length ratio and cardiac hypertrophy indicators were reduced after oral administration of GP. Additionally, GP reduced oxidative stress and heart inflammation brought on by ISO. In H9c2 cells, the antihypertrophic and anti-inflammatory effects of the extract of GP were seen in the presence of ISO, which were further supported by the in vivo observations. This study makes a compelling case for the possibility that supplementing with dried GP fruit can prevent heart hypertrophy by reducing oxidative stress and inflammation.

Long-Term Inhalation of Ultrafine Zinc Particles Deteriorated Cardiac and Cardiovascular Functions in Rats of Myocardial Infarction.

Substantial ultrafine zinc particles exist in air pollutions. The level of Zn concentrations in serum and tissue could affect patients with myocardial infarction (MI). The aim of the study is to investigate the change of cardiac functions and peripheral hemodynamics in MI rats after long-term inhalation of ultrafine Zn particles. Coronary artery ligation surgery was performed to induce MI in Wistar rats. The inhalation of ultrafine Zn particles was carried out for 6 weeks after the operation. Physiological and hemodynamic measurements and computational biomechanics analysis were demonstrated in eight groups of rats at postoperative 4 and 6 weeks. There was no statistical significance between shams and shams with inhalation of ultrafine Zn particles. There were significant impairments of cardiac and hemodynamic functions in MI rats. In comparison with MI rats, the inhalation of ultrafine Zn particles for 4 weeks slowed down the progression from MI to heart failure, but the inhalation for 6 weeks accelerated the process. The long-term inhalation of ultrafine zinc particles induced excessive accumulation of zinc in serum and tissue, which deteriorated cardiac and hemodynamic dysfunctions in MI rats. The findings suggested the importance for regulating Zn intake of MI patients as well as looking at ways to lower zinc concentrations in air pollutions.

Bergapten mediated inflammatory and apoptosis through AMPK/eNOS/AKT signaling pathway of isoproterenol-induced myocardial infarction in Wistar rats.

Bergapten (BeG) is explored for its anti-inflammatory and antioxidant properties. Myocardial infarction (MI) is reported to be one of the leading cardiovascular diseases characterized by mitochondrial dysfunction and apoptosis. The main purpose of this study is to assess the cardiopreventive effects of BeG (50 mg/kg) in isoproterenol (ISO)-induced MI in Wistar rats. The increased infarct size after ISO induction was reduced simultaneously on treatment with BeG. Similarly, augmented levels of cardiac biomarkers, namely cardiac troponin T, creatine kinase (CK), cardiac troponin I, and CK-MB were also suppressed by BeG. The increased rate of lipid hydroperoxidesand thiobarbituric acid reactive substances owingto the oxidative stress caused by free radical generation in ISO-inducedrats were also inhibited by BeG. Antioxidants reduce oxidative stress by scavenging free radicals. ISO induction reduces these antioxidant enzymes glutathione peroxidase, catalase, superoxide dismutase, and glutathione, andlevels causing oxidative cardiac damage to the heart tissue. BeG supplementation improved these enzymes synthesis preventing potential damage to the myocardium. Inflammation caused by ISO pretreatment increased the secretion of proinflammatory cytokines in ISO-inducedrats. Pretreatment with BeG suppressed these inflammatory cytokines to a normal level in ISO + BeG-treated rats. The histopathological examination of the morphological characteristics showed that the intensity of cardiac damage caused by ISO induction was less in BeG pretreated rats with less inflammatory cells and no necrosis. BeG also showed promising results in the molecular alteration of AMP-activated protein kinase/endothelialnitric oxide synthase/protein kinase B signaling molecules. These observations emphasize the cardioprotective effects of BeG and its potential use as a drug in the near future.

Responses of some matrix metalloproteinases activities to an acute session of endurance exercise and electrical stimulation in induced myocardial infarction in Wistar rats.

Myocardial infarction is the irreversible cell death of cardiac muscle that takes place after the blood flow is cut off to a specific region of the heart muscle. The molecular angiogenesis process that may follow after the incidence, due to any activity or its intensity, is unknown. The purpose of this research was to examine some of the matrix metalloproteinase (MMP) responses to an acute course of endurance exercise and electrical stimulation in induced myocardial infarcted Wistar rats. In this experimental case-control study, 40 induced myocardial infarcted Wistar rats (8-week-old, mean weight 130±30 g) were randomly assigned into 4 conditions: endurance exercise, exercise + electrical stimulation, only electrical stimulation, and control group. The infarction was induced 24 hours after the subcutaneous injection of 150 mg/kg of Isoproterenol. The exercise and exercise plus electrical stimulation groups performed a session of endurance exercise on an animal treadmill, at 20 m/min for one hour. The electrical stimulation was delivered by foot shock, set with the intensities of 0.5 mA for 20 minutes. Immediately after the cessation of the treatment protocol, MMP1, MMP2, and MMP9 were measured by the ELISA method. Data analysis was performed by using Two-way ANOVA and significance was set at α = 0.05. One session of endurance exercise or electric stimulation, or their combination, had no significant effect on the level of MMPs. One session of acute endurance exercise, stimulation, or their combination, elicited no significant effect on the level of MMPs of artificially induced myocardial infarcted Wistar rats.

Mechanisms of Regenerative Potential Activation in Cardiac Mesenchymal Cells.

Recovery of the contractile function of the heart and the regeneration of the myocardium after ischemic injury are contemporary issues in regenerative medicine and cell biology. This study aimed to analyze early transcriptional events in cardiac tissue after infarction and to explore the cell population that can be isolated from myocardial tissue. We induced myocardial infarction in Wistar rats by permanent ligation of the left coronary artery and showed a change in the expression pattern of Notch-associated genes and Bmp2/Runx2 in post-MI tissues using RNA sequencing and RT-PCR. We obtained primary cardiac mesenchymal cell (CMC) cultures from postinfarction myocardium by enzymatic dissociation of tissues, which retained part of the activation stimulus and had a pronounced proliferative potential, assessed using a “xCELLigence” real-time system. Hypoxia in vitro also causes healthy CMCs to overexpress Notch-associated genes and Bmp2/Runx2. Exogenous activation of the Notch signaling pathway by lentiviral transduction of healthy CMCs resulted in a dose-dependent activation of the Runx2 transcription factor but did not affect the activity of the Bmp2 factor. Thus, the results of this study showed that acute hypoxic stress could cause short-term activation of the embryonic signaling pathways Notch and Bmp in CMCs, and this interaction is closely related to the processes of early myocardial remodeling after a heart attack. The ability to correctly modulate and control the corresponding signals in the heart can help increase the regenerative capacity of the myocardium before the formation of fibrotic conditions.

Protective effect of ginsenoside Rd against isoproterenolinduced myocardial infarction in Wistar rats

Purpose: To investigate the protective effect of ginsenoside Rd (GRd) against isoproterenol (ISO)- induced myocardial infarction in a rat model.Methods: Forty healthy male rats were equally divided into four groups (10/group). Rats in the control group received only saline, whereas rats in GRd group were intraperitoneally (i.p.) injected GRd at a dose of 50 mg/kg body weight (b.wt.) for 14 days. The other two groups were ISO-treated rats. One group (MI model) received ISO at a dose of 80 mg/kg b.wt i.p. for 2 days, while the other group (GRd + ISO group) was pretreated with GRd at a dose of 50 mg/kg for 14 days prior i.p. administration of the same dose of ISO.Results: Treatment with GRd (for 14 days) prior to ISO exposure resulted in significant increase in the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) as well as significant decreases in heart-to-body weight ratio, infarct size, inflammatory markers {tumour nectosis factor alpha (TNF-α), nuclear factor kappa B (NF-κB), interleukin 1 beta (IL-1β) and interleukin 6 (IL-6)}, relative to ISO-treated rats (p > 0.05). In addition, prior exposure to ISO led to significant elevation in malondialdehyde (MDA), cardiac troponin T (cTnT), creatine kinase (CPK), lactate dehydrogenase (LDH) and apoptotic markers (caspase-3 and caspase-9). However, pre-treatment with GRd reversed the ISO-induced histopathological changes (necrosis/oedema and altered cardiac fibres) in cardiac tissue.Conclusion: These results demonstrate that GRd ameliorates ISO-induced cardiotoxicity in rats via upregulation of the activities of antioxidants, and suppression of inflammatory and apoptotic biomarkers. Thus, GRd has cardio-protective properties.Keywords: Ginsenoside Rd, Myocardial infarction, Apoptosis, Inflammation, Antioxidants

Protective effect of omeprazole and lansoprazole on β-receptor stimulated myocardial infarction in Wistar rats.

We investigated the effect of omeprazole (OPZ) and lansoprazole (LPZ) on the pathophysiology of myocardial necrosis in rats by inspecting a series of indicators like hemodynamic parameters, biochemical estimations and histopathological changes in the myocardial tissue. Rats received either OPZ, LPZ (50mg/kg/day, p.o.) individually for 7days with concurrent administration of isoproterenol (ISO) (150mg/kg, s.c.) on 6th and 7th day of study period to induce myocardial infarction. On the 8th day after measuring hemodynamic parameters, rats were killed and parameters were evaluated. ECG waves were found to be normal in the treatment group. ISO control rats revealed escalation in the oxidative stress as evidenced by depletion in the content of SOD, GSH, catalase and increase in the level of MDA and NO as compared with the normal rats. Treatment with OPZ and LPZ significantly reduced the ROS, indicated by an increase in the endogenous antioxidants and a decrease in NO and MDA levels. ISO control rats showed a significant elevation in the levels of pro-inflammatory cytokine TNF-α as compared to the normal and treatment group of rats. Administration of OPZ and LPZ does not exhibit any significant toxicity. Our findings reveal that multiple doses of OPZ and LPZ may have distinctly minimized the ISO-induced myocardial necrosis by declining the hmodynamic parameters, oxidative stress and pro-inflammatory cytokine TNF-α in myocardial infarcted rats.

Changes in kidney tissue and effects of erythropoietin after acute heart failure

Impairment of cardiac function causes renal damage. Renal failure after heart failure is attributed to hemodynamic derangement including reduced renal perfusion and increased venous pressure. One mechanism involves apoptosis and is defined as cardiorenal syndrome type 1. Erythropoietin (EPO) is a cytokine that induces erythropoiesis under hypoxic conditions. Hypoxia inducible factor 1 alpha (HIF-1α) plays a regulatory role in cellular response to hypoxia. Protective effects of EPO on heart, kidney and nervous system are unrelated to red blood cell production. We investigated early changes in and effects of EPO on renal tissues of rats with myocardial infarction by morphology and immunohistochemistry. Coronary artery ligation was used to induce myocardial infarction in Wistar rats. Group 1 comprised sham operated rats; groups 2, 3 and 4 included rats after coronary artery ligation that were sacrificed 6 h after ligation and that were treated with saline, 5,000 U/kg EPO or 10,000 U/kg EPO, respectively; group 5 included rats sacrificed 1 h after ligation. Group 2 showed increased renal tubule damage. Significantly less tubule damage was observed in EPO treated groups. EPO and EPO receptor (EPO-R) immunostaining intensities increased slightly for group 5 and became more intense for group 2. EPO and EPO-R immunostaining was observed in the interstitial area, glomerular cells and tubule epithelial cells of EPO treated groups. HIF-1α immunostaining was observed in collecting tubules in the medulla only in group 2. Caspase-3 immunostaining is an indicator of apoptosis. Caspase-3 staining intensity decreased in renal medulla of EPO treated groups. EPO treatment may exert a protective effect on the renal tissues of patients with cardiorenal syndrome.

Butanol extract of Morinda Lucida (BEML) protects against Isoproterenol‐induced myocardial infarction in Wistar rats

With the rising rates of cardiovascular diseases, increase cost of modern therapeutic drugs, as well as the adverse effects of the modern medicine on the users; there is a surge in the need to search for herbs with excellent antioxidant properties for use in preventive medicine. Morinda Lucida, commonly found in the Tropics, precisely in the rain forest of West Africa; it is an important medicinal plant known for its antioxidant and therapeutic uses. The aim of this study was to investigate the cardioprotective effects of the Butanol extract of Morinda Lucida (BEML) against Isoproterenol‐induced myocardial infarction in Wistar rats. Male albino Wistar rats (n=60) were pre‐treated with BEML for a period of 10 days. Group A (control) received food and water ad‐libitum. Group B was challenged with 70 mg/kg Isoproterenol (ISO) alone. Group C: Isoproterenol + 100 mg/kg BEML. Group D: Isoproterenol + 200 mg/kg BEML Group E: 100 mg/kg BEML alone and Group F: 200 mg/kg BEML alone. Groups B, C and D were challenged with ISO on the 11th day. This study found out that ISO induced severe myocardial injuries associated with significant increase in markers of oxidative stress, as confirmed by elevated Malondialdehyde (MDA), as well as decreased reduced Glutathione (GSH), Glutathione peroxidase (GPx), Glutathione, Glutathione‐S‐transferase (GST), Catalase (CAT), Superoxide dismutase (SOD) relative to ISO alone. Pre‐treatment with BEML prior to administration of ISO significantly reduced serum Creatinine kinase myocardial band (CK‐MB) and Lactate dehydrogenase (LDH and also suppressed the expressions of Cardiac troponin I (CTnI), and nuclear factor kappa beta (NF‐κB), respectively. Pre‐treatment with BEML reduced infarct size and restored cardiac ultrastructural integrity. Gas Chromatography Mass Spectrometry (GCMS) analysis revealed the presence of Phytol, 11‐Eicosenoic acid, Palmitoleic acid, Nonacosylic acid, Methyl Palmitoleate, Stearic acid, Vitamin E (alpha‐Tocopherol), Tocopheryl acetate, 17α‐Hydroxyprogesterone, β‐Amyrin acetate, Alpha‐Amyrin acetate, lupenone, and Sclareol in BEML. Together, we conclude that BEML act as potential protective agent against myocardial infarction and other cardiac conditions through its antioxidant, anti‐inflammatory and free radical scavenging activity. The observed cardio‐protective effect might be due to the presence of arrays of phytonutrients.Support or Funding InformationNoneThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Molecular and biochemical evidence on the protective effects of quercetin in isoproterenol-induced acute myocardial injury in rats.

Cardioprotection represents one of the most important and realistic aspects of preventive therapy today. Quercetin, a naturally occurring dietary flavone, has been studied extensively for its antioxidant properties. The objective of present study is to find out the cardioprotective activity and to explore the underlying mechanisms of quercetin pretreatment (50 mg/kg body weight, orally) for 14 days against isoproterenol (ISO; 100 mg/kg body weight, subcutaneously) induced myocardial infarction in Wistar rats. Cardiac diagnostic markers, oxidative stress, inflammatory cytokines, histopathology along with gene expression analysis of calpain 1 and 2 were carried out in experimental rats. Quercetin pretreatment showed protective effects on heart by significantly attenuating the ISO-induced oxidative stress, inflammation, protecting heart architecture, and by downregulation of the expression of calpain. Overall, these findings revealed the cardio-protective potential of quercetin and its mechanism of action against ISO-induced MI in rats.

Abstract 268: Advanced Glycation End Products Effect on the Polarization of Macrophages Cardiac After Acute Myocardial Infarction in Wistar Rats

Macrophage phenotypes play an important role in post-MI cardiac remodeling. M1 macrophages have a proinflammatory phenotype and are found in the heart early after MI whereas M2 macrophages arise after and replace M1 macrophages in order to mediate the resolution of inflammation and angiogenesis. Advanced glycation end products (AGE) may modulate macrophage polarization but its functional role in the context of post-MI remains incompletely understood. Our goal is to assess whether AGE can polarize macrophages in post-MI and interfere in cardiac remodeling. We have collected experimental data from 68 male Wistar rats (2-3 month-old) divided in 4 groups: sham, MI + 0.9% NaCl (i.p.), MI + methylglyoxal (AGE inducer, 17 mg/kg/day; i.p.); and MI + aminoguanidine (anti-AGE agent, 0.5 g/L in drinking water). Subgroups were euthanized on days 2, 6, and 10 days post-MI. The echocardiographic analysis did not show differences in ejection fraction or akinetic/hypokinetic area among the MI groups. Cytokine levels were assessed by multiplex analysis in cardiac tissue homogenate. There was an increase of proinflammatory cytokine IL-6 on 10th day after surgery in MI group at the remote area, while IL-1β and IL-12 showed reduction compared with the sham group. Anti-inflammatory cytokine IL-10 did not show any difference among the groups. Until now, it is not possible to conclude whether AGE can induce macrophage polarization in vivo. More analyses are necessary to respond our objective.

Histamine H3 Receptor Agonist Imetit Attenuated Isoproterenol Induced Renin Angiotensin System and Sympathetic Nervous System Overactivity in Myocardial Infarction of Rats.

Myocardial infarction is an alarming health issue, needs great attention. The present study investigated the role of histamine-H3 receptor (H3R) agonist imetit in relationship to sympathetic and renin angiotensin system in Wistar rats. Subcutaneous injection of isoproterenol (85 mg/kg) on last 2 consecutive days in per se group and 7 days treatment of different groups at 24 h interval induced myocardial infarction in Wistar rats. H3R agonist imetit (10 mg/kg), H3R antagonist thioperamide (5 mg/kg), losartan (10 mg/kg) were administered orally to evaluate imetit's cardioprotective potential effect by measuring plasma cardiac antioxidant markers, angiotensin II, norepinephrine levels and histopathological analysis. Isoproterenol significantly elevated the angiotensin II and norepinephrine levels in rat plasma. This study revealed that pre-treatment with imetit similar to losartan attenuated norepinephrine and angiotensin II levels whereas thioperamide showed its antagonistic effect by diminishing imetit's effects. Furthermore, its protective effect was confirmed by restoration of cardiac antioxidant markers and histopathological improvement of myocardium integrity. This study confirm imetit's cardioprotective potential and also reveals renin angiotensin system, sympathetic system and H3R correlation in isoproterenol induced toxicity in rats. However, molecular studies must be warranted to prove the role of H3R in myocardial infarction.

Cardioprotective activity of fruit of <i>Garcinia pedunculata</i> on isoprenaline-induced myocardial infarction in rat

<p>The present study reveals the protective effect of<em> Garcinia pedunculata</em> aqueous fruit extract in isoprenaline-induced myocardial infarction in Wistar rats. Isoprenaline (200 mg/kg) administration subcutaneous once daily for two consecutive days significantly (p<0.01) increased the CK-MB, AST, ALT, ALP activity and CRP (p<0.05) levels. Pretreatment with extract (400 mg/kg) orally for 14 consecutive days significantly ameliorated the effect of isoprenaline by reducing the activity of CK-MB and the levels of ALP, SGPT respectively. No significant changes were seen in the case of SGOT activity and CRP levels. Severe necrotic lesions in the myocardial tissue were observed in isoprenaline-treated group. In extract-treated group, mild degenerative changes of myo-cardial tissues to nearly normal cytoarchitecture were seen. The results indicate the cardioprotective effect of <em>G. pedunculata</em> against isoprenaline- induced myocardial infarction rat model.</p><p> </p>

Sundarban Honey Confers Protection against Isoproterenol-Induced Myocardial Infarction in Wistar Rats.

The present study was designed to investigate the cardioprotective effects of Sundarban honey (SH) in rats with isoproterenol- (ISO-) induced myocardial infarction. Adult male Wistar Albino rats were pretreated with Sundarban honey (5 g/kg) daily for a period of 6 weeks. After the treatment period, ISO (85 mg/kg) was subcutaneously injected into the rats at 24 h intervals for 2 days. ISO-induced myocardial damage was indicated by increased serum cardiac specific troponin I levels and cardiac marker enzyme activities including creatine kinase-MB, lactate dehydrogenase, aspartate transaminase, and alanine transaminase. Significant increases in serum total cholesterol, triglycerides, and low-density lipoprotein-cholesterol levels were also observed, along with a reduction in the serum high-density lipoprotein-cholesterol level. In addition to these diagnostic markers, the levels of lipid peroxide products were significantly increased. The activities of antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, and glutathione reductase were significantly decreased in the hearts after ISO-induced myocardial infarction. However, pretreatment of ischemic rats with Sundarban honey brought the biochemical parameters to near normalcy, indicating the protective effect of Sundarban honey against ISO-induced ischemia in rats. Histopathological findings of the heart tissues further confirmed the biochemical findings, indicating that Sundarban honey confers protection against ISO-induced oxidative stress in the myocardium.

Exploration of the preventive effect of S. lessoniana liver oil on cardiac markers, hematological patterns and lysosomal hydrolases in isoproterenol-induced myocardial infarction in wistar rats: a novel report

The purpose of this study was to explore thein vivocardioprotective potency of liver (digestive gland) oil fromS. lessonianaon isoproterenol induced myocardial infracted wistar rats.

Cardioprotective effect of linseed oil against isoproterenol-induced myocardial infarction in Wistar rats: a biochemical and electrocardiographic study.

The present study was designed to evaluate the cardioprotective effect of Tunisian flaxseed oil (Linum usitatissimum) against isoproterenol-induced myocardial infarction in rats by studying hypertensive and cardiac damage markers especially electrocardiographic changes and troponin T serum level. In vitro, the extracted oil showed an important inhibition of angiotensin converting enzyme (ACE) with an IC50 = 85.96μg/ml. According to chemical analysis, this extract is composed essentially of alpha linolenic acid (ALA), an n-3 polyunsaturated fatty acid (58.59%). Male rats were randomly divided into three groups, namely control (C), isoproterenol (ISO), and isoproterenol-treated group with flaxseed oil (FO + ISO). Isoproterenol injection showed changes in ECG pattern, including ST-segment elevation (diagnostic of myocardial infarction), increase in the serum levels of Troponin T and cardiac injury markers (creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), aspartate transaminase (AST), and alanine transaminase (ALT)). However, Linum oil pre-co-treatment prevented almost all the parameters isoproterenol-induced myocardial infarction in rats. Results of the present study proved that flaxseed oil has a significant effect by heart protection against isoproterenol-induced myocardial infarction through beneficial effect of the important fraction of ALA.