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Ischaemic Insult (ischaemic + insult)
Selected AbstractsForce,frequency and force,length properties in skeletal muscle following unilateral focal ischaemic insult in a rat modelACTA PHYSIOLOGICA, Issue 3 2009G. N. Dormer Abstract Aim:, Our purpose was to quantify skeletal muscle properties following unilateral focal ischaemic insult (stroke) in a rat model. Methods:, Male rats were divided into two groups: stroke and 2 weeks recovery (n = 8) and control group (n = 7). Stroke was induced in the area of the motor neocortex containing hind limb corticospinal neurones. Contractile properties of the medial gastrocnemius muscle were measured in situ in both limbs. Force,length and force,frequency properties were measured before and 35 min after 5 min fatiguing stimulation. Results:, Stroke resulted in bilateral tetanic fade during 200 Hz stimulation. When normalized to 100 Hz contractions, force at 200 Hz was 95.4 ± 0.9% for the paretic muscles, 96.7 ± 1.7% for non-paretic muscles and 102.2 ± 1.0% for muscles of control rats (P = 0.006). Prior to fatiguing contractions, there was no difference in the length dependence of force. During repetitive contractions, active force fell significantly to 19 ± 4 and 25 ± 5% of initial force in paretic and non-paretic muscles of animals with a stroke respectively. In control animals active force fell to 37 ± 5%. During repetitive contractions, fusion index increased in muscles of stroke animals to 1.0 ± 0 but in control animals it was 0.95 ± 0.02. There was selective force depression at short lengths for fatigued paretic muscle (significant difference at muscle lengths less than reference length ,2 mm). Conclusion:, The tetanic fade at high stimulation frequencies indicates that there may be activation failure following focal ischaemic insult. The greater magnitude of fatigue and selective depression at short lengths following repetitive contractions should be investigated further. [source] Role of gap junctional coupling in astrocytic networks in the determination of global ischaemia-induced oxidative stress and hippocampal damageEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2006Jose L. Perez Velazquez Abstract While there is evidence that gap junctions play important roles in the determination of cell injuries, there is not much known about mechanisms by which gap junctional communication may exert these functions. Using a global model of transient ischaemia in rats, we found that pretreatment with the gap junctional blockers carbenoxolone, 18,-glycyrrhetinic acid and endothelin, applied via cannulae implanted into the hippocampus in one hemisphere, resulted in decreased numbers of TUNEL-positive neurons, as compared with the contralateral hippocampus that received saline injection. Post-treatment with carbenoxolone for up to 30 min after the stroke injury still resulted in decreased cell death, but post-treatment at 90 min after the ischaemic insult did not result in differences in cell death. However, quinine, an inhibitor of Cx36-mediated gap junctional coupling, did not result in appreciable neuroprotection. Searching for a possible mechanism for the observed protective effects, possible actions of the gap junctional blockers in the electrical activity of the hippocampus during the ischaemic insult were assessed using intracerebral recordings, with no differences observed between the saline-injected and the contralateral drug-injected hippocampus. However, a significant reduction in lipid peroxides, a measure of free radical formation, in the hippocampus treated with carbenoxolone, revealed that the actions of gap junctional coupling during injuries may be causally related to oxidative stress. These observations suggest that coupling in glial networks may be functionally important in determining neuronal vulnerability to oxidative injuries. [source] Does the pre-ischaemic administration of sevoflurane reduce myocardial stunning?ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 5 2007A porcine experimental model Background:, In a porcine model, the cardioprotective effect of sevoflurane was studied with regard to the preservation of myocardial contractility (myocardial stunning) after a myocardial ischaemic insult. Methods:, Twenty-seven pigs were randomized to receive either a dual 4% sevoflurane inhalation period as a supplement to pentobarbital anaesthesia or pentobarbital anaesthesia only before a 15-min ischaemic insult on the left anterior descending coronary artery. The ischaemic period was followed by 180 min of reperfusion. Myocardial contractility was assessed by myocardial sonomicrometry. Results:, A significant difference was found between the sevoflurane group and the control group at 5 min of reperfusion. However, subsequently, there was no overall difference between the two groups. Conclusion:, Sevoflurane administered as a pre-ischaemic bolus does not provide long-term improvement of the myocardial contractility. However, it can be speculated that sevoflurane may induce an early improvement in contractility. [source] Testosterone protects rat hearts against ischaemic insults by enhancing the effects of ,1 -adrenoceptor stimulationBRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2008S Tsang Background and purpose: Testosterone alleviates symptoms in patients with ischaemic heart disease. Androgen receptors are present in the heart, and testosterone upregulates gene expression of cardiac ,1 -adrenoceptors. We hypothesize that testosterone may confer cardioprotection by interacting with adrenoceptors. Experimental approach: In isolated perfused hearts and ventricular myocytes from orchidectomized rats without or with testosterone (200 ,g/100 g) replacement, we first determined the effect of ischaemia/reperfusion in the presence of noradrenaline (10,7 M). Then we determined the contribution of interactions between testosterone and ,1 - or ,1 -adrenoceptors in cardiac injury/protection (infarct size, release of lactate dehydrogenase, viability of myocytes, recovery of contractile function and incidence of arrhythmias) upon ischaemia/reperfusion by pharmacological manipulation using selective adrenoceptor agonists (,1 -adrenoceptor agonist: phenylephrine 10,6 M; non-selective ,-adrenoceptor agonist: isoprenaline 10,7 M) and antagonists (,1: prazosin or benoxathian 10,6 M; ,1: CGP 20712A 5 × 10,7 M). We also determined the expression of ,1 and ,1 -adrenoceptor in the hearts from rats with and without testosterone. Key results: Testosterone reduced injury induced by ischaemia/reperfusion and noradrenaline. This was achieved by enhancing the beneficial effect of ,1 -adrenoceptor stimulation, which was greater than the deleterious effect of ,1 -adrenoceptor stimulation (also enhanced by testosterone). The effects of testosterone were abolished or attenuated by blockade of androgen receptors. Testosterone also enhanced the expression of ,1A and ,1 -adrenoceptor. Conclusions and implications: Testosterone conferred cardioprotection by upregulating the cardiac ,1 -adrenoceptor and enhancing the effects of stimulation of this adrenoceptor. The effect of testosterone was at least partly mediated by androgen receptors. British Journal of Pharmacology (2008) 153, 693,709; doi:10.1038/sj.bjp.0707624; published online 24 December 2007 [source] Roles of KATP channels in delayed cardioprotection and intracellular Ca2+ in the rat heart as revealed by , -opioid receptor stimulation with U50,488HBRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2003Mai Chen The effect of preconditioning with U50,488 H (UP), a selective kappa-opioid receptor (, -OR) agonist, on infarct size and intracellular Ca2+ ([Ca2+]i) in the heart subjected to ischaemic insults were studied and evaluated. U50,488 H administered intravenously reduced the infarct size 18,48 h after administration in isolated hearts subjected to regional ischaemia/reperfusion (I/R). The effect was dose dependent. A peak effect was reached at 10 mg kg,1 U50,488 H and at 24 h after administration. The effect of 10 mg kg,1 U50,488 H at 24 h after administration was abolished by nor-binaltorphimine (nor-BNI), a selective , -OR antagonist, indicating the effect was , -OR mediated. The infarct reducing effect of U50,488 H was attenuated when a selective blocker of mitochondrial (5-hydroxydecanoic acid, 5-HD) or sarcolemmal (HRM-1098) ATP-sensitive potassium channel (KATP) was coadministered with U50,488 H 24 h before ischaemia or when 5-HD was administered just before ischaemia. U50,488 H also attenuated the elevation in [Ca2+]i and reduction in electrically induced [Ca2+]i transient in cardiomyocytes subjected to ischaemic insults. The effects were reversed by blockade of KATP channel, which abolished the protective effect of preconditioning with U50,488 H. The results indicated that mitochondrial KATP channel serves as both a trigger and a mediator, while sarcolemmal KATP channel as a trigger only, of delayed cardioprotection of , -OR stimulation. The effects of these channels may result from prevention/attenuation of [Ca2+]i overload induced by ischaemic insults. British Journal of Pharmacology (2003) 140, 750,758. doi:10.1038/sj.bjp.0705475 [source] | |||||||||||||