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Ischemic Period (ischemic + period)
Selected AbstractsLevosimendan cardioprotection in acutely ,-1 adrenergic receptor blocked open chest pigsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 1 2010C. METZSCH Background: Levosimendan and volatile anesthetics have myocardial pre-conditioning effects. ,-1 adrenergic receptor antagonists may inhibit the protective effect of volatile anesthetics. No information exists as to whether this also applies to the pre-conditioning effect of levosimendan. We therefore investigated whether levosimendan added to metoprolol would demonstrate a cardioprotective effect. Methods: Three groups of anesthetized open chest pigs underwent 30 min of myocardial ischemia and 90 min of reperfusion by temporary occlusion of the largest side branch from the circumflex artery or the left anterior descending artery. One group (CTRL) served as a control, in another group (BETA), a metoprolol-loading dose was intravenously injected 30 min before ischemia, and in a third group (BETA+L), a levosimendan infusion was added to metoprolol. Myocardial tissue concentrations of glucose, glycerol, and lactate/pyruvate ratio as the primary end-points were investigated with microdialysis in ischemic and non-ischemic tissues. Results: At the end of the ischemic period, statistically significant differences were only found between CTRL and BETA+L in the ischemic myocardium, with a lower lactate/pyruvate ratio, lower glycerol, and higher glucose concentrations in BETA+L as compared with CTRL. There were no differences in non-ischemic myocardium. From 10 to 90 min of reperfusion, no more differences were found between groups. Conclusion: The cardioprotective effect of levosimendan on ischemic metabolism with a reduction in the myocardial lactate/pyruvate ratio, less glycerol accumulation, and better preserved glucose concentration does not seem to be prevented by ,-1 adrenergic receptor antagonism with metoprolol. [source] Studies on the effects of lactate transport inhibition, pyruvate, glucose and glutamine on amino acid, lactate and glucose release from the ischemic rat cerebral cortexJOURNAL OF NEUROCHEMISTRY, Issue 1 2001J. W. Phillis A rat four vessel occlusion model was utilized to examine the effects of ischemia/reperfusion on cortical window superfusate levels of amino acids, glucose, and lactate. Superfusate aspartate, glutamate, phosphoethanolamine, taurine, and GABA were significantly elevated by cerebral ischemia, then declined during reperfusion. Other amino acids were affected to a lesser degree. Superfusate lactate rose slightly during the initial ischemic period, declined during continued cerebral ischemia and then was greatly elevated during reperfusion. Superfusate glucose levels declined to near zero levels during ischemia and then rebounded beyond basal levels during the reperfusion period. Inhibition of neuronal lactate uptake with ,-cyano-4-hydroxycinnamate dramatically elevated superfusate lactate levels, enhanced the ischemia/reperfusion evoked release of aspartate but reduced glutamine levels. Topical application of an alternative metabolic fuel, glutamine, had a dose dependent effect. Glutamine (1 mm) elevated basal superfusate glucose levels, diminished the decline in glucose during ischemia, and accelerated its recovery during reperfusion. Lactate levels were elevated during ischemia and reperfusion. These effects were not evident at 5 mm glutamine. At both concentrations, glutamine significantly elevated the superfusate levels of glutamate. Topical application of sodium pyruvate (20 mm) significantly attenuated the decline in superfusate glucose during ischemia and enhanced the levels of both glucose and lactate during reperfusion. However, it had little effect on the ischemia-evoked accumulation of amino acids. Topical application of glucose (450 mg/dL) significantly elevated basal superfusate levels of lactate, which continued to be elevated during both ischemia and reperfusion. The ischemia-evoked accumulations of aspartate, glutamate, taurine and GABA were all significantly depressed by glucose, while phosphoethanolamine levels were elevated. These results support the role of lactate in neuronal metabolism during ischemia/reperfusion. Both glucose and glutamine were also used as energy substrates. In contrast, sodium pyruvate does not appear to be as effectively utilized by the ischemic/reperfused rat brain since it did not reduce ischemia-evoked amino acid efflux. [source] Inhibition of the initial wave of NF-,B activity in rat muscle reduces ischemia/reperfusion injuryMUSCLE AND NERVE, Issue 4 2001Sean T. Lille MD Abstract Nuclear factor kappaB (NF-,B) is thought to play an important role in the expression of genes expressed in response to ischemia/reperfusion (I/R) injury. In this report, the activation of NF-,B in rat skeletal muscle during reperfusion following a 4-h ischemic period was studied. NF-,B activation displayed a biphasic pattern, showing peak activities from 30 min to 3 h postperfusion and 6 h to 16 h postperfusion, with a decline to baseline binding activity levels between 3 h and 6 h. Inhibition of NF-,B activation was investigated using proline dithiocarbamate (Pro-DTC). NF-,B binding activity during reperfusion was significantly reduced by intravenous administration of Pro-DTC. Additionally, Pro-DTC resulted in decreased muscle edema and neutrophil activity, with an increased percentage of muscle survival compared with vehicle controls. These results demonstrate that NF-,B is activated during reperfusion in a biphasic manner and that the regulation of the initial phase of NF-,B activation affords physiological protection against a severe ischemic stress. Selective inhibition of NF-,B during early reperfusion may therefore be a therapeutic intervention for I/R injury. © 2001 John Wiley & Sons, Inc. Muscle Nerve 24: 534,541, 2001 [source] Significance of determining the point of reperfusion failure in experimental torsion of testisINTERNATIONAL JOURNAL OF UROLOGY, Issue 1 2005ELIJAH O KEHINDE Abstract Background:, Experimental studies of the use of free radical scavengers in ischemic/reperfusion (I/R) injury following detorsion of the torted testis have yielded conflicting results due to differences in the period of ischemia used. The authors studied I/R injury in the rabbit model, to define the point beyond which there is reperfusion failure. Methods:, Ischemia/reperfusion injury of the testis was created in 3,6-month-old male New Zealand white rabbits by cross-clamping the left spermatic cord for periods of ischemia lasting 0, 15, 30, 60, 90, 120 and 180 min. There were eight animals per experimental group. The right testis served as internal control. Both testes were harvested after 24 h of reperfusion in four animals and after 3 months in the remaining four animals for each group. Testicular malondialdehyde (MDA), a measure of free radical damage, was determined by using the thiobarbituric acid reaction on testicular homogenates. Johnsen score was used to assess morphological damage caused by the ischemia. Results:, After 24 h of reperfusion, the mean testicular MDA in the control right testes at 0, 15, 30, 60, 90, 120 and 180 min was 2.1, 2.5, 2.9, 2.4, 2.1 and 1.9 nmol/mg protein, respectively. The mean left testicular MDA at corresponding ischemic periods was 1.6, 2.0, 3.9, 10.0, 4.4, 6.1 and 1.0 nmol/mg protein, respectively. The maximum left testicular MDA was at 60 min (10.0 nmol/mg protein), following which the level dropped significantly to 1.0 nmol/mg protein at 180 min. At 3 months, the mean Johnsen scores for left testes subjected to 0, 60, 120 and 180 min ischemia were 9.4, 8.8, 2.3, 3.5, respectively. Conclusion:, The results suggest that following ischemia of up to 60 min in the rabbit testis, adequate reperfusion is possible, but ischemia lasting beyond 60 min results in inadequate reperfusion leading to irreversible damage. Thus, in experiments for assessing the effect of antioxidants on I/R injury of the testis in rabbits, periods up to 60 min of ischemia should be regarded as optimum to observe an effect. [source] Ischemic preconditioning and intermittent clamping improve murine hepatic microcirculation and Kupffer cell function after ischemic injuryLIVER TRANSPLANTATION, Issue 4 2004Katarína Vajdová The aim of this study was to evaluate whether the protective effect of intermittent clamping and ischemic preconditioning is related to an improved hepatic microcirculation after ischemia/reperfusion injury. Male C57BL/6 mice were subjected to 75 or 120 min of hepatic ischemia and 1 or 3 hours of reperfusion. The effects of continuous ischemia, intermittent clamping, and ischemic preconditioning before prolonged ischemia on sinusoidal perfusion, leukocyte-endothelial interactions, and Kupffer cell phagocytic activity were analyzed by intravital fluorescence microscopy. Kupffer cell activation was measured by tissue levels of tumor necrosis factor (TNF)-,, and the integrity of sinusoidal endothelial cells and Kupffer cells were evaluated by electron microscopy. Continuous ischemia resulted in decreased sinusoidal perfusion rate and phagocytic activity of Kupffer cell, increased leukocyte-endothelial interactions and TNF-, levels. Both protective strategies improved sinusoidal perfusion, leukocyte-endothelial interactions and phagocytic activity of Kupffer cells after 75-minutes of ischemia, and intermittent clamping also after 120 minutes ischemia. TNF-, release was significantly reduced and sinusoidal wall integrity was preserved by both protective procedures. In conclusion, both strategies are protective against ischemia/reperfusion injury by maintaining hepatic microcirculation and decreasing Kupffer cell activation for clinically relevant ischemic periods, and intermittent clamping appears superior for prolonged ischemia. (Liver Transpl 2004;10:520,528.) [source] | ||||||||||