1,720,973 research outputs found
Experimental view of arrhythmias in a model of isolated hearts during ischemia or hypoxia.
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Myocardial metabolism and function in acutely ischaemic and hypoxemic isolated rat hearts
No full textPostgenomic up-regulation of CCL3L1 expression in HTLV-2-infected persons curtails HIV-1 replication
No full textAtenolol depresses post-ischaemic recovery in the isolated rat heart
Full text linkMetabolic events during ischaemia are probably important in determining post-ischaemic myocardial recovery. The aim of this study was to assess the effects of the β-blocker atenolol and the high energy demand in an ischaemia-reperfusion model free of neurohormonal and vascular factors. We exposed Langendorff-perfused isolated rat hearts to low-flow ischaemia (30 min) and reflow (20 min). Three groups of hearts were used: control hearts (n = 11), hearts that were perfused with 2.5 μg l-1 atenolol (n = 9), and hearts electrically paced during ischaemia to distinguish the effect of heart rate from that of the drug (n = 9). The hearts were freeze-clamped at the end of reflow to determine high-energy phosphates and their metabolites. During ischaemia, the pressure-rate product was 2.3 ± 0.2, 5.2 ± 1.1, and 3.3 ± 0.3 mmHg 103 min in the control, atenolol and paced hearts, respectively. In addition, the ATP turnover rate, calculated from venous (lactate), oxygen uptake and flow, was higher in atenolol (11.2 ± 1.7 μmol min-1) and paced (8.1 ± 0.8 μmol min-1) hearts than in control (6.2 ± 0.8 μmol min-1). At the end of reflow, the pressure x rate product recovered 75.1 ± 6.4% of baseline in control vs 54.1 ± 9.1 and 48.8 ± 4.4% in atenolol and paced hearts (P < 0.05). In addition, the tissue content of ATP was higher in the control hearts (15.8 ± 1.0 μmol g(dw)-1) than in atenolol (10.5 ± 2.6 μmol g(dw)-1) and paced (10.9 ± 1.3 μmol g(dw)-1) hearts. Thus, by suppressing the protective effects of down-regulation both atenolol and pacing apparently depress myocardial recovery in this model
Effects of atenolol and pacing on performance and metabolism of the ischemic-reperfused rat heart
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Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Effects of trimetazidine on metabolic and functional recovery of postischemic rat hearts.
No full textThe objective of this study was to test the hypothesis that the beneficial effect of trimetazidine during reflow of ischemic hearts is mediated by energy sparing and ATP pool preservation during ischemia. Isolated rat hearts (controls and rats treated with 10(-6) M trimetazidine, n = 17 per group) underwent the following protocol: baseline perfusion at normal coronary flow (20 minutes), low-flow ischemia at 10% flow (60 minutes), and reflow (20 minutes). We measured contractile function, O2 uptake, lactate release, venous pH and PCO2, and the tissue content of high-energy phosphates and their metabolites. During baseline, trimetazidine induced higher venous pH and lower PCO2 without influencing performance and metabolism. During low-flow ischemia, trimetazidine reduced myocardial performance (P = 0.04) and ATP turnover (P = 0.02). During reflow, trimetazidine improved performance (91 +/- 6% versus. 55 +/- 6% of baseline), prevented the development of diastolic contracture and coronary resistance, and reduced myocardial depletion of adenine nucleotides and purines. ATP turnover during low-flow ischemia was inversely related to recovery of the rate-pressure product (P = 0.002), end-diastolic pressure (P = 0.007), and perfusion pressure (P = 0.05). We conclude that trimetazidine-induced protection of ischemic-reperfused hearts is also mediated by energy sparing during ischemia, which presumably preserves the ATP pool during reflow
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