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IR Group (ir + group)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Effect of Postconditioning on Coronary Blood Flow Velocity and Endothelial Function and LV Recovery After Myocardial Infarction

JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 5 2006
XIAOJING MA
Objective: Postconditioning is a novel approach to myocardial protection during ischemia reperfusion. Our study observed the effect of postconditioning on coronary blood flow velocity and endothelial function in patients who underwent emergency percutaneous coronary intervention (PCI). Methods: Ninety-four patients with their first acute myocardial infarction who underwent revascularization within 12 hours of onset by primary PCI were recruited in the study. All the patients were randomized to two groups, IR group (PCI without postconditioning) and Postcond group (PCI with postconditioning). Corrected TIMI frame count (CTFC) was used to evaluate velocity of coronary blood after PCI. Creatine phosphokinase (CK), CK-MB, and malondialdehyde (MDA) were measured before and after PCI. Arterial endothelial function was studied noninvasively by examination of brachial artery responses to endothelium-dependent and endothelium-independent stimuli by echo Doppler technique. Wall motion score index (WMSI) was assessed by two-dimensional echocardiography before and 8 weeks after angioplasty. Results: There were no significant differences between the two groups with regard to age, sex, presence of angiographically visible collaterals, and elapsed time from the onset of symptoms until perfusion. Patients with postconditioning had much faster CTFC than patients without postconditioning (25.38 ± 5.35 vs 29.23 ± 5.54). After 8 weeks, the WMSI improved significantly in both groups, but the ,WMSI in Postcond group was significantly larger than that of IR group (1.20 ± 0.30 vs 1.04 ± 0.36, P < 0.05). There was a significant negative correlation between ,WMSI and CTFC in IR group and Postcond group (r =,0.9032, P < 0.01; r =,0.7884, P < 0.01). The peaks of CK and CK-MB of Postcond group were much lower than that of IR group (1236.57 ± 813.21 U/L vs 1697.36 ± 965.74 U/L; 116.92 ± 75.83 U/L vs 172.41 ± 92.64 U/L), and MDA-reactive products were significantly lower than that in the IR group at any same time after PCI. All patients with acute myocardial infarction had a depressed endothelium-dependent vasodilation function, while the endothelium-dependent vasodilation function was improved in Postcond group. Conclusion: Postconditioning is a simple, operative procedure for salvaging the coronary endothelial function and cardiomyocyte. It could be used widely in clinic and to better the prognosis of acute myocardial infarction. [source]

Protective Effects of Ischemic Preconditioning on the Intestinal Mucosal Microcirculation Following Ischemia,Reperfusion of the Intestine

MICROCIRCULATION, Issue 8 2005
ISMAIL H. MALLICK
ABSTRACT Objective: The small bowel villi are extremely sensitive to ischemia,reperfusion (IR) injury and a range of microcirculatory disturbances contribute to structural and functional changes. The aim of this study was to determine the protective effects of ischemic preconditioning (IPC) of the intestine on the mucosal villous microcirculation during IR injury of the intestine and whether heme oxygenase (HO) is involved in the protection. Methods: Rats were allocated into 4 groups: (1) sham, (2) IR consisting of 30 min of ischemia followed by 2 h of reperfusion, (3) IPC, as in IR group, but preceded by 10 min of ischemia and 10 min of reperfusion, and (4) with administration of zinc protoporphyrin, an HO inhibitor before IPC and IR. The mucosa of an exteriorized segment of ileum was visualized. Mucosal perfusion index (MPI), red blood cell (RBC) velocity and leukocyte,endothelial interactions during reperfusion were assessed continuously using in vivo fluorescence microscopy. HO activity in the ileum was assessed at the end of the reperfusion period. Results: IPC improved the MPI by 26% and the RBC velocity by 29% on comparison to IR. IR led to a 52% increase in leukocyte,endothelial interactions on comparison to IPC. The administration of zinc protoporphyrin reversed the beneficial effects of IPC. There was a two fold increase of HO activity in IPC compared to IR, whereas zinc protoporphyrin significantly reduced the HO activity. Conclusions: IPC conferred a protective effect on the villous microcirculation possibly via HO and might prove to be an effective strategy for the amelioration of IR injury. [source]

Hypoxic preconditioning protects rat hearts against ischaemia,reperfusion injury: role of erythropoietin on progenitor cell mobilization

THE JOURNAL OF PHYSIOLOGY, Issue 23 2008
Jih-Shyong Lin
Preconditioning, such as by brief hypoxic exposure, has been shown to protect hearts against severe ischaemia. Here we hypothesized that hypoxic preconditioning (HPC) protects injured hearts by mobilizing the circulating progenitor cells. Ischaemia,reperfusion (IR) injury was induced by left coronary ligation and release in rats kept in room air or preconditioned with 10% oxygen for 6 weeks. To study the role of erythropoietin (EPO), another HPC + IR group was given an EPO receptor (EPOR) antibody via a subcutaneous mini-osmotic pump 3 weeks before IR induction. HPC alone gradually increased haematocrit, cardiac and plasma EPO, and cardiac vascular endothelial growth factor (VEGF) only in the first two weeks. HPC improved heart contractility, reduced ischaemic injury, and maintained EPO and EPOR levels in the infarct tissues of IR hearts, but had no significant effect on VEGF. Interestingly, the number of CD34+CXCR4+ cells in the peripheral blood and their expression in HPC-treated hearts was higher than in control. Preconditioning up-regulated cardiac expression of stromal derived factor-1 (SDF-1) and prevented its IR-induced reduction. The EPOR antibody abolished HPC-mediated functional recovery, and reduced SDF-1, CXCR4 and CD34 expression in IR hearts, as well as the number of CD34+CXCR4+ cells in blood. The specificity of neutralizing antibody was confirmed in an H9c2 culture system. In conclusion, exposure of rats to moderate hypoxia leads to an increase in progenitor cells in the heart and circulation. This effect is dependent on EPO, which induces cell homing by increased SDF-1/CXCR4 and reduces the heart susceptibly to IR injury. [source]

Ischaemic preconditioning improves microvascular perfusion and oxygenation following reperfusion injury of the intestine,

BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 9 2005
I. H. Mallick
Background: Ischaemia,reperfusion (IR) injury of the intestine occurs commonly during abdominal surgery. Ischaemic preconditioning (IPC) provides a way of protecting the organ from damage inflicted by IR. This study was designed to evaluate the beneficial effect of IPC, focusing on the intestinal microcirculation and oxygenation in intestinal IR injury. Methods: Rats were allocated to three groups. Animals in the IR and IPC groups underwent 30 min of intestinal ischaemia followed by 2 h of reperfusion. In the IPC group this was preceded by 10 min of ischaemia and 10 min of reperfusion. Animals in the third group underwent laparotomy but no vascular occlusion. Intestinal microvascular perfusion, oxygenation and portal venous blood flow (PVF) were monitored continuously. At the end of the reperfusion period, blood samples were obtained for measurement of lactate dehydrogenase (LDH) and biopsies of ileum for histological evaluation. Results: IPC improved intestinal microvascular perfusion and tissue oxygenation significantly at the end of the reperfusion period (P < 0·001). PVF improved significantly in the IPC compared with the IR group (P = 0·005). The serum LDH concentration was significantly lower in the IPC than the IR group (mean(s.e.m.) 667·1(86·8) versus 1973·8(306·5) U/l; P < 0·001) Histological examination showed that ileal mucosa was significantly less injured in the IPC group. Conclusions: This study demonstrated that IPC improves intestinal microvascular perfusion and oxygenation. Copyright © 2005 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source]