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Acute Ischaemia (acute + ischaemia)
Selected AbstractsEvidence that endogenous inosine and adenosine-mediated hyperglycaemia during ischaemia,reperfusion through A3 adenosine receptorsAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 4 2009D. Cortés Summary 1,The molecular mechanism underlying stress-induced hyperglycemia has not been comprehensively clarified. Recently, we demonstrated in ischaemia-reperfusion (I-R) stress-subjected liver that inosine and adenosine are mainly responsible for the hyperglycemia observed. 2,We aimed to advance in the knowledge of the role of inosine plus adenosine as mediators of hepatic-induced hyperglycemia detected after I-R in lower limbs. 3,Acute ischaemia was conducted in anesthetized rats by occluding downstream abdominal aorta and cava vein; then, reperfusion was allowed. Blood samples from hepatic or abdominal cava veins were taken throughout the experiments to measure glucose, inosine and adenosine. Antagonists to adenosine (AdoR) and adrenergic receptors (AdrR) were administered during ischaemia to analyze their effect on hepatic glucose release. 4,Ischaemia up to 60 min produced minor increase of glucose and nucleosides blood values, but 5 min of ischaemia followed by 2- (or 10-) min reperfusion increased glucose 23%, and those of inosine or adenosine by 100%. After 60 min of ischaemia and 10 min of reperfusion, glycemia rose 2-fold and blood inosine and adenosine, 3.3- and 2.7-fold, respectively. A linear positive correlation, r2, as high as 0.839 between glucose and either nucleoside blood values was calculated. The hyperglycemia response to I-R decreased by 0, 25, 33, 45 and 100% after selective inhibition of A2B AdoR, A2A AdoR, a1B AdrR, A1 AdoR, and A3 AdoR, respectively. 5,Inosine-adenosine couple through activation of hepatic A3 AdoR is the main signal for releasing glucose from liver glycogen and for promoting hyperglycemia following experimental injury of I-R from lower limbs. [source] The action of high K+ and aglycaemia on the electrical properties and synaptic transmission in rat intracardiac ganglion neurones in vitroEXPERIMENTAL PHYSIOLOGY, Issue 2 2009Jhansi Dyavanapalli We have investigated the action of two elements of acute ischaemia, high potassium and aglycaemia, on the electrophysiological properties and ganglionic transmission of adult rat intracardiac ganglion (ICG) neurones. We used a whole-mount ganglion preparation of the right atrial ganglion plexus and sharp microelectrode recording techniques. Increasing extracellular K+ from its normal value of 4.7 mm to 10 mm decreased membrane potential and action potential after-hyperpolarization amplitude but otherwise had no effect on postganglionic membrane properties. It did, however, reduce the ability of synaptically evoked action potentials to follow high-frequency (100 Hz) repetitive stimulation. A further increase in K+ changed both the passive and the active membrane properties of the postganglionic neurone: time constant, membrane resistance and action potential overshoot were all decreased in high K+ (20 mm). The ICG neurones display a predominantly phasic discharge in response to prolonged depolarizing current pulses. High K+ had no impact on this behaviour but reduced the time-dependent rectification response to hyperpolarizing currents. At 20 mm, K+ practically blocked ganglionic transmission in most neurones at all frequencies tested. Aglycaemia, nominally glucose-free physiological saline solution (PSS), increased the time constant and membrane resistance of ICG neurones but otherwise had no action on their passive or active properties or ganglionic transmission. However, the combination of aglycaemia and 20 mm K+ displayed an improvement in passive properties and ganglionic transmission when compared with 20 mm K+ PSS. These data indicate that the presynaptic terminal is the primary target of high extracellular potassium and that aglycaemia may have protective actions against this challenge. [source] Phosphate metabolite concentrations and ATP hydrolysis potential in normal and ischaemic heartsTHE JOURNAL OF PHYSIOLOGY, Issue 17 2008Fan Wu To understand how cardiac ATP and CrP remain stable with changes in work rate , a phenomenon that has eluded mechanistic explanation for decades , data from 31phosphate-magnetic resonance spectroscopy (31P-MRS) are analysed to estimate cytoplasmic and mitochondrial phosphate metabolite concentrations in the normal state, during high cardiac workstates, during acute ischaemia and reactive hyperaemic recovery. Analysis is based on simulating distributed heterogeneous oxygen transport in the myocardium integrated with a detailed model of cardiac energy metabolism. The model predicts that baseline myocardial free inorganic phosphate (Pi) concentration in the canine myocyte cytoplasm , a variable not accessible to direct non-invasive measurement , is approximately 0.29 mm and increases to 2.3 mm near maximal cardiac oxygen consumption. During acute ischaemia (from ligation of the left anterior descending artery) Pi increases to approximately 3.1 mm and ATP consumption in the ischaemic tissue is reduced quickly to less than half its baseline value before the creatine phosphate (CrP) pool is 18% depleted. It is determined from these experiments that the maximal rate of oxygen consumption of the heart is an emergent property and is limited not simply by the maximal rate of ATP synthesis, but by the maximal rate at which ATP can be synthesized at a potential at which it can be utilized. The critical free energy of ATP hydrolysis for cardiac contraction that is consistent with these findings is approximately ,63.5 kJ mol,1. Based on theoretical findings, we hypothesize that inorganic phosphate is both the primary feedback signal for stimulating oxidative phosphorylation in vivo and also the most significant product of ATP hydrolysis in limiting the capacity of the heart to hydrolyse ATP in vivo. Due to the lack of precise quantification of Piin vivo, these hypotheses and associated model predictions remain to be carefully tested experimentally. [source] MANAGEMENT OF POPLITEAL ARTERY ANEURYSMSANZ JOURNAL OF SURGERY, Issue 10 2006Maher Hamish Background: Popliteal artery aneurysms (PAA) are the most common peripheral aneurysm and are recognized as ,the silent killer of the leg circulation'. The timing and type of interventions used in their treatment is still controversial. This review examines the published data on the natural history, epidemiology, clinical presentation and management options available. The aim of this study is to try and reach a consensus with regards to the best management of PAA. Method: A systematic review of data in the English published works since 1980. Results: The authors include 53 studies containing 2854 patients with 4291 PAA. Most published data involves retrospective studies and personal experience, with one multicentre study. No randomized controlled studies exist regarding the management of PAA. Conclusions: 1. Although most PAA are of atherosclerotic origin in old patients, trauma, infection and family history are the main causes in young patients. 2. Great vigilance is needed for diagnosis as only approximately five patients are seen each year by a major vascular centre. There is no place for screening programmes to detect PAA. 3. Approximately 45% of patients are asymptomatic at the time of initial diagnosis. Aortic aneurysms are found in 40% and bilateral PAA in 50% of patients. More than 95% of patients are men with a mean age of 65 years and 45% have hypertension. 4. Surgical reconstruction is recommended for all symptomatic and asymptomatic aneurysms larger than 2 cm. Five-year graft patency rates after surgical repair range from 30 to 97%, with 5-year limb salvage ranging from 70 to 98%. Patient survival rates at 5 and 10 years are 75 and 46%, respectively. 5. If carried out carefully, intra-arterial thrombolysis can safely prepare patients presenting with acute ischaemia from occluded PAA, for surgical revascularization to restore distal run-off. 6. Endovascular repair of a PAA is a feasible option, although little evidence is yet available. 7. Lifelong, careful patient surveillance is essential to detect and treat new aneurysms at other sites. [source] Mid-term outcome of endovascular revascularization for chronic mesenteric ischaemia,BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 2 2010N. V. Dias Background: This study aimed to assess mid-term outcome after endovascular revascularization of chronic occlusive mesenteric ischaemia (CMI) and to identify possible predictors of mortality. Methods: Consecutive patients undergoing primary elective stenting for CMI between 1995 and 2007 were registered prospectively in a database. Patients with acute ischaemia were excluded. Retrospective case-note review and data analysis were performed. Results: Forty-three patients (10 men) were treated for stable (n = 30) or exacerbated (n = 13) CMI. Their median (interquartile range (i.q.r.)) age was 70 (60,79) years. Revascularization was successful in 47 of 49 vessels. The superior mesenteric artery (SMA), either alone (n = 34) or in combination with the coeliac trunk (n = 6), was the predominant target vessel. No patient died within 30 days. Median follow-up was 43 (i.q.r. 25,63) months and the estimated (s.e.) 3-year overall survival rate was 76(7) per cent. Two patients died from distal SMA occlusive disease and intestinal infarction after 6 and 18 months respectively. Previous stroke (P = 0·016), male sex (P = 0·057) and age (P = 0·066) were associated with mid-term mortality on univariable, but not multivariable analysis. Reintervention was needed in 14 patients, achieving a 3-year cumulative rate of freedom from recurrent symptoms of 88(5) per cent. Conclusion: Endovascular treatment provided high early and mid-term survival rates in this series of patients with CMI, with low complication rates. Copyright © 2009 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] | |||||||||||||