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Biomedical subjects

G Keren

Publications and source records attributed to G Keren.

At least 19 recordsLinked to original sources
PubMed2006

Circulating adiponectin concentrations in patients with congestive heart failure.

OBJECTIVES: To determine concentrations of adiponectin and its predictive value on outcome in a cohort of patients with congestive heart failure (CHF). METHODS: Serum and clinical data were obtained for outpatients with clinically controlled CHF (n = 175). Serum concentrations of adiponectin, C reactive protein, N-terminal pro-brain natriuretic peptide (NT-proBNP), interleukin (IL) -1beta, IL-6, IL-8, IL-10, IL-12, tumour necrosis factor alpha and CD-40 ligand were determined. The association of adiponectin with the clinical severity of CHF was sought as well as the predictive value of this adipokine on mortality, CHF hospitalisations or the occurrence of each of these end points. RESULTS: Concentrations of adiponectin were significantly increased in patients with CHF. Patients with higher New York Heart Association class had significantly higher serum concentrations of adiponectin. Adiponectin serum concentrations were lower in patients with diabetes and CHF as well as in patients with ischaemic cardiomyopathy. Serum adiponectin concentration was positively associated with age and NT-proBNP but was negatively correlated with C reactive protein concentrations. Serum adiponectin above the 75th centile was found to be an independent predictor of total mortality, CHF hospitalisations or a composite of these end points over a two-year prospective follow up. CONCLUSION: Adiponectin is increased in CHF patients and predicts mortality and morbidity.

Adiponectin↗
PubMed2004

Correction of anemia in patients with congestive heart failure increases resting energy expenditure.

BACKGROUND & AIM: Congestive heart failure (CHF) and anemia were reported to affect resting energy expenditure (REE). The aim of this study was to evaluate the effect of the correction of anemia on REE in subjects with CHF. PATIENTS AND METHODS: Nine anemic patients with compensated CHF and CRF were studied before and after correction of anemia. REE was studied by an open circuit indirect calorimeter, body composition by dual-energy-X-ray absorption and total body and extracellular water by multi-frequency bioelectrical impedence. Four anemic and 5 non-anemic CHF patients who did not receive any new treatment served as controls. RESULTS: After the correction of their anemia patients tended to increase weight (P<0.06), but no significant changes were observed in body composition. Daily caloric intake increased significantly (P<0.02). Ejection fraction increased (P<0.05) and pulse rate decreased significantly (P<0.001). REE and REEPP were in the normal range before correction but increased significantly afterwards (1402+/-256 vs. 1496+/-206 kcal/d, and 101+/-9 vs. 109+/-8, P<0.023 and P<0.006, respectively). CONCLUSION: Correction of anemia in patients with CHF increases their REE. This can be related either to improved tissue oxygenation and/or to increased caloric intake.

Aged↗
PubMed2004

Overexpression of 15-lipoxygenase in the vascular endothelium is associated with increased thymic apoptosis in LDL receptor-deficient mice.

BACKGROUND: 15-Lipoxygenase (15-LO) is a nonheme iron-containing enzyme that catalyzes the peroxidation of fatty acids. Herein, we studied the effect of 15-LO overexpression in the vascular endothelium on thymocyte apoptosis by evaluating thymuses from low-density lipoprotein receptor-deficient (LDL-RD) mice and LDL-RD/15-LO mice. Thymuses were evaluated by immunohistochemistry and by TUNEL whereas in vitro studies were carried out by employing freshly isolated thymocytes from the respective mice and evaluation of apoptosis by propidium iodide and annexin V cytometry. METHODS AND RESULTS: The apoptotic index in LDL-RD/15-LO mice was significantly higher than in the LDL-RD mice. In the thymic medulla the difference was smaller, although still significant. Freshly isolated thymus cells from LDL-RD/15-LO mice exhibited a higher rate of spontaneous cell death than controls. Incubation of thymus cells in the presence of the cell-permeable caspase-3 inhibitor DEVD-CMK resulted in a decrease in the frequency of apoptotic cells in LDL-RD/15-LO thymocytes, whereas no effect was evident in control thymocytes. The antioxidant N-acetylcysteine causes the increase in apoptosis in both groups. CONCLUSION: LDL-RD/15-LO mice exhibit increased thymocyte apoptosis both in vivo and in vitro. These findings may suggest a role for 15-LO in the natural selection of thymocytes.

Acetylcysteine↗
PubMed2004

[The effect of spouse participation in cardiac rehabilitation program on patients' compliance and exercise level].

BACKGROUND: Exercise-based cardiac rehabilitation programs have proven to be associated with decreased morbidity and mortality after cardiac events. Unfortunately, attendance is often poor, and long term compliance is low. This study examined the effect of the active participation of spouses in the exercise program on the compliance and physical fitness level of their partners. METHODS: During the years 1998-2001, 24 couples joined our cardiac rehabilitation program. The couples were divided into 2 groups on the basis of their medical status. In Group 1--Rehabilitation program (n = 14); one of the couple had suffered a myocardial infraction or underwent a coronary bypass surgery at least 3 weeks before starting the program. In Group 2--secondary prevention (n = 10); one of the couple had a medical history of cardiac disease. The third Group included the spouse. Each group was compared with a matched control group based on their medical condition. The parameters that were measured were: the number of sessions attended, basic and final physical training level. RESULTS: In the rehabilitation groups, the participants attended a larger number of sessions (87.3 + 17) compared to control (47.7 + 6) (p < 0.05). There was no difference in the basic training level between the groups (3.5 + 0.2 METS; compared with 3.4 + 0.2 METS) (P = 0.5) and both groups had similarly improved their training level by 0.79 + 0.1 METS compared with 0.6 + 0.1 METS in the control group (p = 0.2). In the secondary preventive groups, the control group attended a larger number of sessions (51 + 13 compared with 31.2 + 6 sessions) (p < 0.02). There was no difference in the basic training level between groups 3.7 + 0.3 METS compared with 4.2 + 0.2 in the control group (p = 0.2). However, at the end of the training period, the control group showed greater improvement in their training level by 0.7 + 0.2 METS compared to 0.3 + 0.1 METS (p < 0.05). The spouses themselves had attended a greater number of sessions (45 + 10 compared with 37 + 6 in the control group) (p = 0.2). There was no difference between those groups in the training level at baseline and at the end of training period. CONCLUSION: Active support during the rehabilitation program may improve the rates of participation but in the secondary prevention program active spouse support may encourage early dropout.

Aged↗
PubMed2002

The correction of anemia in severe resistant heart failure with erythropoietin and intravenous iron prevents the progression of both the heart and the renal failure and markedly reduces hospitalization.

Both Congestive Heart Failure (CHF) and Chronic Renal Failure (CRF) are increasing steadily in the community. We propose that there is a vicious circle established whereby CHF and CRF both cause anemia and the anemia then worsens both the CHF and CRF causing more anemia and so on. We call this the Cardio Renal Anemia (CRA) syndrome. By the combination of active treatment of the CHF and control of the anemia with subcutaneous erythropoietin and intravenous iron, the progression of both the CHF and the CRF can be slowed or stopped in most cases, the quality of life improved and the need for recurrent hospitalization reduced. This will involve cooperation between internists, cardiologists, and nephrologists to allow early and maximal therapy of both the CHF and the anemia.

Aged↗
PubMed2001

Accelerated intimal thickening in carotid arteries of balloon-injured rats after immunization against heat shock protein 70.

OBJECTIVES: The goal of this study was to test the hypothesis that induction of an immune response to heat shock protein (Hsp) 70 would increase intimal thickening in a rat carotid-injury model. BACKGROUND: Restenosis resulting from intimal thickening poses a major limitation to the long-term success of coronary angioplasty. Several studies have proposed that infectious agents increase restenosis. Heat shock proteins are highly conserved structures, produced by all cells in response to nonspecific forms of stress. Infectious agents are known to contain Hsp70, which is markedly immunogenic and can elicit a strong immune response. METHODS: To investigate whether Hsp70 immunity can affect neointimal thickening, we immunized rats with either Hsp70 (n = 11), bovine serum albumin ([BSA] n = 9) or with a control adjuvant (n = 10). Three weeks later, rats were boosted using the same regimen to achieve a sustained immune response to Hsp70 after which carotid injury was applied to all animals. RESULTS: Arterial injury was associated with upregulation of Hsp70, 3, 7 and 14 days after induction of the injury as evidenced by Western blotting and immunohistochemistry. Intimal area and intimal/medial ratio was significantly increased in Hsp70-immunized rats in comparison with BSA or control-injected rats. CONCLUSIONS: Our results imply that upregulation of Hsp70 in balloon-injured arteries can serve as a target for anti-Hsp70 immune response, thereby facilitating enhanced intimal thickening. These observations may provide a possible mechanism that explains the accelerated intimal thickening that has been associated with the occurrence of infectious pathogens.

Angioplasty, Balloon, Coronary↗
PubMed2001

The effect of correction of mild anemia in severe, resistant congestive heart failure using subcutaneous erythropoietin and intravenous iron: a randomized controlled study.

OBJECTIVES: This is a randomized controlled study of anemic patients with severe congestive heart failure (CHF) to assess the effect of correction of the anemia on cardiac and renal function and hospitalization. BACKGROUND: Although mild anemia occurs frequently in patients with CHF, there is very little information about the effect of correcting it with erythropoietin (EPO) and intravenous iron. METHODS: Thirty-two patients with moderate to severe CHF (New York Heart Association [NYHA] class III to IV) who had a left ventricular ejection fraction (LVEF) of < or =40% despite maximally tolerated doses of CHF medications and whose hemoglobin (Hb) levels were persistently between 10.0 and 11.5 g% were randomized into two groups. Group A (16 patients) received subcutaneous EPO and IV iron to increase the level of Hb to at least 12.5 g%. In Group B (16 patients) the anemia was not treated. The doses of all the CHF medications were maintained at the maximally tolerated levels except for oral and intravenous (IV) furosemide, whose doses were increased or decreased according to the clinical need. RESULTS: Over a mean of 8.2+/-2.6 months, four patients in Group B and none in Group A died of CHF-related illnesses. The mean NYHA class improved by 42.1% in A and worsened by 11.4% in B. The LVEF increased by 5.5% in A and decreased by 5.4% in B. The serum creatinine did not change in A and increased by 28.6% in B. The need for oral and IV furosemide decreased by 51.3% and 91.3% respectively in A and increased by 28.5% and 28.0% respectively in B. The number of days spent in hospital compared with the same period of time before entering the study decreased by 79.0% in A and increased by 57.6% in B. CONCLUSIONS: When anemia in CHF is treated with EPO and IV iron, a marked improvement in cardiac and patient function is seen, associated with less hospitalization and renal impairment and less need for diuretics.

Aged↗
PubMed2001

Whole body hyperthermia accelerates atherogenesis in low-density lipoprotein receptor deficient mice.

The application of brief periods of heat stress prior to induction of various forms of tissue injury (ischemia-reperfusion, myocardial infarction, endothelial denudation) has been shown to result in preconditioning and attenuation of subsequent damage. Atherosclerosis represents a state of heightened response to injury at the level of the vessel wall, involving endothelial cells, smooth muscle cells, and macrophages. In the current study, we studied the effects of whole body hyperthermia (WBH) on diet-induced atherosclerosis in a murine model. Low-density lipoprotein receptor deficient mice were either exposed to a 30-min WBH (n = 10) or nontreated (n = 7). Animals were given a high-fat ("Paigen"-type) diet to speed the progression of atherosclerosis immediately following WBH for 6 weeks. Aortic and plaque heat shock protein (HSP) 70, suggested to mediate thermotolerance, was assessed by immunohistochemisry and Western blot at different time points following induction of WBH. Aortic sinus plaque formation was significantly accelerated in WBH-treated mice (275,800 +/- 19,540 microm(2) ) in comparison with their control litters (152,100 +/- 18,200 microm(2); P = 0.0004). Plaque composition was also influenced by WBH as lesions were more mature and had an increased proportion of lipid core/fibrous cap accompanied by increased numbers of apoptotic cells. Total cholesterol and triglyceride levels were not affected significantly by WBH. HSP70 protein expression in the aortas was increased 30 min and 6 and 12 h following WBH induction. Thus, induction of WBH, which affords protection in models of arterial injury, appears to have a proatherogenic role in murine atherosclerosis, despite its upregulatory influence on the expression of HSP70.

Animals↗
PubMed2001

The effect of intravenous immunoglobulins on the progression of experimental autoimmune myocarditis in the rat.

The aim of this study was to evaluate the efficacy of two experimental regimes of human intravenous immunoglobulins (IVIG) on the progression of experimental autoimmune myocarditis (EAM). EAM is induced by immunization against myosin and represents a T-cell-dependent disorder that progresses toward dilated cardiomyopathy similar to the human equivalent. No effective treatment is currently at hand for management of the disorder, as immunosuppressant drugs are associated with multiple side effects. Three groups of Lewis rats were induced to develop EAM by immunization with porcine myosin and sacrificed 21 days later. Group A received a 5-day regimen of IVIG (800 mg/kg) following induction of the disorder; Group B received a daily dose of IVIG (800 mg/kg) and group C was treated with PBS. IVIG given daily but not during the first 5 days significantly suppressed myocarditis score (0.81 +/- 0.26 and 1.14 +/- 0.42, respectively) in comparison with controls (mean score of 1.78 +/- 0.36). The effect was accompanied by a reduction in the cellular and humoral immune response of the respective animals toward myosin. IVIG was deposited within the extracellular matrix surrounding the damaged myocytes. TNF-alpha expression was reduced in both groups treated with IVIG, whereas iNOS expression paralleled the extent of myocardial inflammation regardless of treatment. IVIG at doses twice those applied for human disease are effective in ameliorating the progression of EAM. The effect may be mediated by suppression of the cellular and humoral response to myosin. IVIG may be found clinically feasible in humans as an adjuvant or single therapy for autoimmune myocarditis.

Animals↗
PubMed2001

The state of leukocyte adhesiveness/aggregation in the peripheral blood of patients with type 2 diabetes and ischemic vascular disease.

White blood cells have a potential role in the pathogenesis of vasculopathy in diabetic patients. We studied the circulating peripheral blood in a cohort of patients with documented ischemic heart or brain disease with and without type 2 diabetes by means of image analysis and flow cytometry. Our study showed that the state of leukocyte adhesiveness/aggregation is slightly increased in those who had concomitant diabetes but that there was no difference regarding the expression of CD11b/CD18 and CD62L antigens on the surface of the peripheral blood white blood cells. The finding of a significantly increased number of white blood cells in the peripheral blood of patients with ischemic vascular diseases is important insofar as it is associated with a poorer prognosis.

Aged↗
PubMed2001

Non-obese diabetic (NOD) mice exhibit an increased cellular immune response to glycated-LDL but are resistant to high fat diet induced atherosclerosis.

Diabetes mellitus is one of the major risk factors for atherosclerosis. In recent years several murine models have been developed in an attempt to reproduce the accelerated atherosclerosis by combining induced hyperglycemia with hyperlipidemia. In the present study we wished to examine the effect of spontaneous hyperglycemia and hyperlipidemia induced by high fat diet on atherosclerosis development and on markers of the immune system in diabetes prone NOD mice. We tested two high fat dietary regimens (with or without cholate supplementation) in female NOD mice that either developed or did not develop diabetes. Plasma fasting glucose, lipid profile, antibodies to oxidized-LDL and glycated-LDL were assessed. The spleens from both groups were evaluated for their proliferative response. The extent of atherosclerosis was assessed at the aortic sinus. It was found that the two high fat dietary regimens were insufficient to elicit atherosclerosis in the diabetic and non-diabetic NOD mice. The diabetic hyperlipidemic NOD mice displayed an increased cellular immune response to glycated-LDL in comparison with their non-diabetic littermates. The immune response towards copper oxidized LDL was similar in both groups despite an increased susceptibility of LDL extracted from diabetic hyperlipidemic mice to undergo copper induced oxidation. We conclude that the NOD mouse is highly resistant to atherosclerosis even in the presence of hyperglycemia-hyperlipidemia and increased susceptibility to copper induced LDL oxidation.

Animals↗
PubMed2001

The effect of intravenous immunoglobulins on intimal thickening in a mouse model of arterial injury.

Inflammatory mechanisms appear to influence the progression of intimal thickening in experimental models of arterial injury. Intravenous immunoglobulin (IVIG) is a polyspecific preparation of human immunoglobulin (Ig)G employed for treatment of autoimmune disorders. In this study, we sought to investigate whether treatment with IVIG could influence intimal thickening in a model of murine arterial injury. Intimal thickening was induced by placement of a periadventitial cuff over the right femoral artery of male C57BL/6 mice. In the first experiment, IVIG or human serum albumin (HSA) (10 mg/mouse) were administered intraperitoneally for five consecutive days starting 1 day prior to cuff placement. In the second experiment, IVIG or HSA treatment were delivered similarly, but initiated 3 days following induction of arterial injury. Neointimal area and intimal/medial ratio were significantly reduced in mice treated with IVIG prior to cuff placement as compared with HSA treatment. No differences were noted with regard to neointimal area or intimal/medial ratio, between IVIG- and HSA-treated mice when the treatment was commenced 3 days following induction of injury. IVIG treatment reduced the proliferative capacity of splenocytes to the non-specific mitogen Con-A. Treatment with IVIG was associated with a significantly enhanced secretion of interleukin (IL)-10) by the respective splenocytes in comparison with HSA-treated mice. No effect of IVIG was evident on the secretion of IL-4 or IFN-gamma. Thus, IVIG has proven beneficial in ameliorating intimal thickening in a mouse model of arterial injury. The effect could be mediated by upregulation of T-cell secretion of the anti-inflammatory cytokine IL-10.

Animals↗
PubMed2001

Acute mastoiditis--the antibiotic era: a multicenter study.

OBJECTIVES: To evaluate the clinical course and identify the causative organisms of acute mastoiditis in a community where most of the patients who develop acute otitis media are treated with antibiotics. METHODS: A multicenter retrospective review of a series of 223 consecutive cases of acute mastoiditis. SETTING: Nine secondary or tertiary academic or non-academic referral centers. RESULTS: Prior to the diagnosis of acute mastoiditis, 121 of the patients (54.3%) had been receiving oral antibiotic treatment for acute otitis media for periods ranging from 1 to 21 days (mean 5.3 days). Samples for bacterial culture were obtained from 152 patients. Cultures were negative in 60 patients. The organisms isolated in the 92 positive cultures were: Streptococcus pneumoniae (15 patients), Streptococcus pyogenes (14 patients), Staphylococcus aureus (13 patients), Staphylococcus coagulase negative (three patients), Pseudomonas aeruginosa (eight patients), Haemophilus influenzae (four patients), Proteus mirabilis (two patients), Escherichia coli (two patients), Klebsiella pneumoniae (one patient), Enterobacter (one patient), Acinetobacter (one patient), anaerobic gram-negative bacilli (one patient), and fungi (two patients). Ten patients had mixed flora. Sixteen patients presented with complications (cerebellar abscess, perisinus empyema, subdural abscess or empyema, extradural abscess, cavernous sinus thrombosis, lateral sinus thrombosis, bacterial meningitis, labyrinthitis, petrositis, or facial nerve palsy). CONCLUSIONS: Antibiotic treatment cannot be considered an absolute safeguard against the development of acute mastoiditis. Early myringotomy for acute otitis media seems to decrease the incidence of complications. The distribution of causative organisms in acute mastoiditis differs from that in acute otitis media. Intracranial complications in acute mastoiditis are not rare. Because of the diversity of causative organisms in acute mastoiditis and the growing resistance of bacteria to the various antibiotics, all means to obtain a sample for culture prior to antibiotic treatment, including general anesthesia.

Acute Disease↗
PubMed2001

Combined leukocyte and erythrocyte aggregation in patients with acute myocardial infarction.

OBJECTIVES: To determine whether the increased aggregability of both white and red blood cells previously reported in acute myocardial infarction (aMI) correlates with each other. DESIGN: Cross-sectional study comparing two groups of patients and a group of healthy controls. SETTING: A tertiary university affiliated hospital (Intensive Cardiac Care Unit and Department of General Internal Medicine). PATIENTS: Consecutive patients with aMI, patients with chest pain and no infarction, and healthy controls. MEASUREMENTS AND RESULTS: We adapted a simple slide test and image analysis to reveal the state of both leukocyte and erythrocyte adhesiveness/aggregation in the peripheral blood of patients with aMI. A significant (P=0.0001) increment in the aggregation of both cellular populations was noted in 48 patients with aMI as opposed to the 141 patients with ischemic heart disease and no infarction and in 45 matched controls. In addition, a significant correlation was noted between the various variables of the leukocyte and erythrocyte adhesiveness/aggregation tests. CONCLUSIONS: The significant correlation between the aggregability of white and red blood cells in patients with aMI is suggestive of there being a commonly shared adhesive protein(s). The prompt identification of patients with increased aggregation might have clinical and therapeutic implications.

Analysis of Variance↗
PubMed2001

Parameters of red blood cell aggregation as correlates of the inflammatory state.

To identify clinically relevant parameters of red blood cell (RBC) aggregation, we examined correlations of aggregation parameters with C-reactive protein and fibrinogen in unstable angina (UA), acute myocardial infarction (AMI), and bacterial infection (BI). Aggregation parameters were derived from the distribution of RBC population into aggregate sizes (cells per aggregate) and changing of the distribution by flow-derived shear stress. Increased aggregation was observed in the following order: UA, AMI, and BI. The best correlation was obtained by integration of large aggregate fraction as a function of shear stress. To differentiate plasmatic from cellular factors in RBC aggregation, we determined the aggregation in the presence and absence of plasma and formulated a "plasma factor" (PF) ranging from 0 to 1. In AMI the enhanced aggregation was entirely due to PF (PF = 1), whereas in UA and BI it was due to both plasmatic and cellular factors (0 < or = PF < or = 1). It is proposed that clinically relevant parameters of RBC aggregation should express both RBC aggregate size distribution and aggregate resistance to disaggregation and distinguish between plasmatic and cellular factors.

Acute-Phase Reaction↗
PubMed2001

Imaging of aortic atherosclerotic lesions by (125)I-LDL, (125)I-oxidized-LDL, (125)I-HDL and (125)I-BSA.

OBJECTIVE: The aim of the present study was to compare the accumulation of (125)I-labeled low-density lipoproteins (LDL), oxidized LDL (oxLDL), HDL and BSA in advanced atherosclerotic lesions of apoE-deficient mice. METHODS: (125)I-lipoproteins or (125)I-BSA were injected into the tail vein of apoE-deficient mice. Blood clearance of (125)I-lipoproteins and (125)I-BSA and their accumulation in atherosclerotic lesions were assayed. RESULTS: Blood clearance of (125)I-LDL and (125)I-HDL was moderate, and approximately 30% of the injected lipoproteins were present in plasma 24 h following injection. oxLDL was removed much faster from plasma, and less than 10% of (125)I-oxLDL was present in the circulation 30 min after (125)I-oxLDL injection. The clearance of (125)I-BSA from the circulation was slower than the lipoprotein clearance. The highest accumulation of LDL, oxLDL, HDL and BSA was detected in atherosclerotic lesions in the aortic arch and abdominal aorta, while lower accumulation was detected in the less atherosclerotic descending thoracic aorta. CONCLUSION: Our findings demonstrate that both (125)I-HDL and (125)I-BSA as well as (125)I-LDL are accumulated in atherosclerotic plaques and that they can be used for the detection of atherosclerotic lesions.

Animals↗
PubMed2001

The effect of agmatine administration on ischemic-reperfused isolated rat heart.

BACKGROUND: The natural polyamine Agmatine (Ag) plays a significant role in protection of nerve cell ischemic injury. A previous report indicated that Ag given intraperitoneally to rats enhanced the recovery of the heart from ischemic injury. Based on this initial observation, a larger investigation was undertaken to explore a dose-response effect and possible mechanisms underlying the protective effects. METHODS: Using the modified Langendorff model, 36 isolated hearts were divided into five groups: group 1, hearts receiving 100 microM/L Ag pre-ischemia (n=7); group 2, hearts receiving 100 microM/L Ag pre- and post-ischemia, (n=7); group 3, hearts receiving 250 microM/L Ag pre-ischemia (n=7); group 4, hearts receiving 250 microM/L Ag pre- and postischemia (n=7); and group 5, hearts receiving Krebs-Hensleit solution served as control (n=8). The study design included 20 minutes of perfusion, 30 minutes of global ischemia, and 30 minutes of reperfusion. RESULTS: After ischemia, group 2 developed higher left ventricular pressure P(max) (P<0.01), improved first-derivative of the rise (dP/dt max; P<0.02), and fall (dP/dt min; P<0.04) in left ventricular pressure, and the area calculated under the left-ventricle developed pressure curve (pressure-time integral; P<0.015), but coronary flow was not significantly increased (P=0.06) compared to the control group. Group 1 had improved diastolic recovery: dP/dt min (P<0.05) and coronary flow (P<0.03), compared with the control group. Group 3 had improved P(max) (P<0.01), dP/dt min (P<0.01), and coronary flow (P<0.02); group 4 had no improvement in all hemodynamic parameters. CONCLUSION: Low doses of Ag given pre- and post-ischemia, and high doses given only pre-ischemia have favorable, protective effects on the hemodynamic recovery of isolated rat heart undergoing global ischemia and reperfusion.

Agmatine↗