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Reperfusion Experiments

Guinea pig hearts were perfused for 30 min before experiments were begun in order to allow the heart rate and the contractile amplitude to stabilize. Normothermic global ischemia was induced by a 10-min complete interruption of coronary perfusion (Imamura etal., 1994). This was followed [Pg.401]


Fig. 5. USB- and NBT-stained sections of infarcted myocardium show the cardioprotective effect of ATP-L after 30 min of coronary occiusion and foiiowing 3 h of reperfusion in rabbits with an acute experimentai myocardiai infarction, (a, b) Controi K-H buffer-treated animai (c, d) EL treated animai and (e, f) ATP-L treated animai. (a, b, e) area at risk (USB-unstained red tissue) deveioped as a resuit of occiusion (b, c, f) infarcted area at the end of occiusion/reperfusion experiment (NBT-unstained tissue) heart siices i to V represents base-to-apex. Beproduced with permission from (31)... Fig. 5. USB- and NBT-stained sections of infarcted myocardium show the cardioprotective effect of ATP-L after 30 min of coronary occiusion and foiiowing 3 h of reperfusion in rabbits with an acute experimentai myocardiai infarction, (a, b) Controi K-H buffer-treated animai (c, d) EL treated animai and (e, f) ATP-L treated animai. (a, b, e) area at risk (USB-unstained red tissue) deveioped as a resuit of occiusion (b, c, f) infarcted area at the end of occiusion/reperfusion experiment (NBT-unstained tissue) heart siices i to V represents base-to-apex. Beproduced with permission from (31)...
Although these data provided indirect evidence of iron involvement in ischaemia-reperfusion injury in kidneys and the combined administration of DFX and indomethacin had proved beneficial in actual survival experiments (Gower etal., 1989a), we still felt fhistrated by our inability to generate more direct evidence. At that time, information was just emerging that a small pool of intracellular iron was available in catalytic form as chelates... [Pg.88]

It was earlier thought that activated neutrophils do not play an important role in reoxygenation injury [1]. However, Duilio et al. [16] pointed out that this conclusion was drawn from the experiments with brief episodes of ischemia resulted in myocardial stunning, while neutrophil-mediated damage is expected after prolonged ischemia associated with myocardial infraction. These authors demonstrated that neutrophils were a major source of oxygen radicals in hearts reperfused under in vivo conditions after prolonged ischemia. [Pg.917]

Animal studies with the Impella pump have demonstrated a decrease in myocardial oxygen demand during ischemia and reperfusion, resulting in a smaller infarct size [23]. Initial experience in patients with cardiogenic shock treated with the Impella pump system showed improvements in cardiac output and mean blood pressure and a reduction in pulmonary capillary wedge pressure [24]. [Pg.88]

Kardanov VZ, Petrosian EA, Pasechnikov VD et al. (2005) The estimation of efficiency of use of the haemosorbents modified with glutathion in treatment of an ischaemic syndrome -reperfusion extremities in experiment. Efferent Therapy 2 23-26... [Pg.321]

Fig. 2. Transient retinal ischemia increases intravitreal glutamate in rat. Neurochemical data from microdialysis experiments carried out in anesthetized rats to demonstrate that ischemia/reperfusion insult increases intravitreal glutamate. The extracellular level of glutamate shows a moderate increase during the first 10 min of ischemia, more evident toward the end of the ischemic period, to reach statistical significance at 10 and 150 min of reperfusion. Baseline glutamate concentrations (basal values) are the mean concentrations obtained by averaging six samples collected consecutively at 10 min intervals immediately before the onset of ischemia (n — 6 rats). Glutamate values (pM) are expressed as mean S.E.M. Statistical significance was assessed by ANOVA followed by Dunnett s test for multiple comparisons. P < 0.05 and P < 0.001 versus basal values. Fig. 2. Transient retinal ischemia increases intravitreal glutamate in rat. Neurochemical data from microdialysis experiments carried out in anesthetized rats to demonstrate that ischemia/reperfusion insult increases intravitreal glutamate. The extracellular level of glutamate shows a moderate increase during the first 10 min of ischemia, more evident toward the end of the ischemic period, to reach statistical significance at 10 and 150 min of reperfusion. Baseline glutamate concentrations (basal values) are the mean concentrations obtained by averaging six samples collected consecutively at 10 min intervals immediately before the onset of ischemia (n — 6 rats). Glutamate values (pM) are expressed as mean S.E.M. Statistical significance was assessed by ANOVA followed by Dunnett s test for multiple comparisons. P < 0.05 and P < 0.001 versus basal values.
Since oxidative stress has been reported to produce subcellular redistribution and activation of NF-kB, we measured total NF-kB content in cytosolic and particulate fractions of the hearts subjected to ischemia/reperfusion. In another set of experiments, the activation of NF-kB protein was studied by measuring the total NF-kB and phospho-NF-KB in the heart homogenate. Elevated ratios of NF-kB in particulate versus cytosolic fraction and of phospho-NF-KB and total NF-kB in the hearts subjected to ischemia/reperfusion were reduced by selenium. As oxidative stress has been reported to produce subcellular redistribution and activation of NF-kB and antioxidants have been shown to prevent this alteration (Cargnoni et al. 2002), it is possible that our observation on selenium-induced NF-kB translocation might be due to its antioxidant action. It should be noted that since selenium treatment could reduce the tumor necrosis factor-cc (TNF-ct)-mediated activation of NF-kB (Kim and Stadtman 1997), it suggests a possible involvement of a reduction in the formation of TNF-tx in the hearts subjected to ischemia/reperfusion by selenium. [Pg.171]

Further natural history studies supported the mismatch model of the penumbra by demonstrating that if early reperfusion of the PI lesion occurs, growth of the acute DWI lesion is inhibited. Thus, there is salvage of the mismatch region and these patients may experience substantial clinical improvement (Barber et al. 1998b). [Pg.27]

In experiments with transient vessel obstruction, the lesion growth, as visualized on DWI, can be reversed if the brain is reperfused within 1 h post occlusion... [Pg.57]

A more complex time course of ADC changes is seen in the presence ofearly reperfusion (see Fig. 7.7). In animal experiments, ADC abnormalities resolve during the early reperfusion phase following ischemia of short duration (e.g., in the rat suture occlu-... [Pg.123]

We have shown that, with the exception of DMPO, all spin traps studied exerted a limited negative inotropic and chronotropic effect. This effect was only present at the highest concentrations studied [116]. Bolli et al. [104-108] have previously reported that intracoronary infusions of PBN at concentrations greater than 20 mmol/1 blood caused profound toxicity, as manifest by the rapid, complete and persistent loss of cardiac contractile function, in the absence of ischemia and reperfusion, in open-chest dogs. These authors subsequently used PBN at much lower concentrations ( 1.6 mmol/1) in all of their experiments, and questioned the validity of results obtained in previous studies where the... [Pg.342]

One of the classic experiments on anthocyanins was conducted on hamsters in Italy. Ischemia-reperfusion was created in the cheeks by a brief clamping, causing the white cells to clump onto the capillary wall and damage it. The administration of the bilberry supplementation for several weeks after the reperfusion could restore the normal blood supply through the capillaries, reducing the sticking of white blood cells to the vessel walls, and the permeability [15]. [Pg.17]

The left ventricular developed pressure, DP (DP=PSP-EDP), rates of contractility and relaxation (+dP/dt and -dP/dt, respectively), and end diastolic pressure (EDP) were continuously monitored during the phases of the experiment (preischemia, ischemia and reperfusion). [Pg.49]


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Reperfusion

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