The most effective ways to salvage ischemic myocardium threatened by infarction is to restore tissue perfusion as rapidly as possible. These are best accomplished by restoration of coronary flow(reperfusion) by thrombolysis, percutaneous transluminal conronary angioplasty(PTCA), coronary arterial bypass graft (CABG), or cardiac transplantation. Reperfusion of an ischemic area may result however, in paradoxical cardiomyocytes dysfunction, a phenomenon termed" reperfusion injury". Reperfusion injury has been observed in each of above situations. The myocardium can tolerate brief periods (up to 15 minutes) of severe and even total myocardial ischemia without resultant myocardial death. With increasing duration and severity of ischemia, greater cardiomyocytes damage develop with spectrum of reperfusionassociated pathologies, collectively called reperfusion injury. Here, we report a case of a sixty two-yearold female woman who was suffered cardiac surgery(bivalvular replacement and CABG) and died soon after. Post-mortem examination have revealed typical cardiac reperfusion injury in the background of diffuse myocardial infarction. So, authors report this case with literatures reviews, because we think that this is very good case of cardiac reperfusion injury, confirmed histologically by post-mortem examination.
Autopsy ; Coronary Artery Bypass* ; Coronary Vessels* ; Female ; Heart ; Heart Transplantation ; Heart Valves* ; Humans ; Infarction ; Ischemia ; Myocardial Infarction ; Myocardial Ischemia ; Myocardial Reperfusion Injury* ; Myocardial Reperfusion* ; Myocardium ; Myocytes, Cardiac ; Pathology ; Perfusion ; Reperfusion ; Reperfusion Injury ; Transplants

Humans ; Ischemia ; metabolism ; pathology ; therapy ; Ischemic Postconditioning ; methods ; Myocardial Reperfusion Injury ; metabolism ; pathology ; therapy

The concept of "ischemic postconditioning" was first raised in 2002, and the following 5 year research shows that it can protect organs from reperfusion injury. Although the mechanism of ischemic postconditioning is similar to ischemic preconditioning in many ways, it still has its own characteristics. Reperfusion injury is an inevitable problem in organ transplantation. It may accelerate the function recovery of the transplants to lessen the reperfusion injury. So ischemic postconditioning may have a fine prospect in organ transplantation for its good controllability during reperfusion. This article is going to briefly introduce the distinct mechanisms of ischemic postconditioning to protect organs from reperfusion injury and approach the possibilities of its application in organ transplantation.
Animals ; Humans ; Ischemic Preconditioning ; Ischemic Preconditioning, Myocardial ; Myocardial Reperfusion Injury ; pathology ; prevention & control ; Organ Transplantation ; adverse effects ; methods ; Reperfusion Injury ; prevention & control

Brain Ischemia ; metabolism ; pathology ; prevention & control ; Humans ; Ischemic Preconditioning ; methods ; Myocardial Reperfusion Injury ; metabolism ; pathology ; prevention & control ; Reperfusion Injury ; metabolism ; pathology ; prevention & control

Acute myocardial infarction is one of the major causes of mortality worldwide. Reperfusion in a timely fashion is the most effective way to limit infarct size. However, reperfusion can itself prompt further myocardial injury. This phenomenon is commonly known as myocardial ischemia-reperfusion (IR) injury. Mitochondrial aldehyde dehydrogenase (ALDH2) is an enzyme metabolizing acetaldehyde and toxic aldehydes. Increasing evidence has revealed a cardioprotective role of ALDH2 in myocardial IR injury. Evidence from animal studies has shown that ALDH2 diminishes acute myocardial infarct size, ameliorates cardiac dysfunction and prevents reperfusion arrhythmias. The activity of ALDH2 is severely compromised if it is encoded by the mutant ALDH2*2 gene, with an incidence of approximately 40% in Asian populations. Epidemiological surveys in the Asian population have depicted that ALDH2 polymorphism is closely associated with higher prevalence of acute myocardial infarction and coronary artery disease. Therefore, targeting ALDH2 may represent a promising avenue to protect against IR injury. This review recapitulates the underlying mechanisms involved in the protective effect of ALDH2 in cardiac IR injury. Translational potential of ALDH2 in the management of coronary heart disease is also discussed.
Aldehyde Dehydrogenase ; metabolism ; Animals ; Heart ; physiopathology ; Humans ; Mitochondria, Heart ; enzymology ; Myocardial Reperfusion Injury ; Myocardium ; pathology

Animals ; Apoptosis ; drug effects ; Ginsenosides ; pharmacology ; Myocardial Reperfusion Injury ; pathology ; Myocytes, Cardiac ; cytology ; Rats ; Rats, Wistar

OBJECTIVETo observe the alteration of cardiac myocyte nuclear inositol 1,3,4,5-tetrakisphosphate receptor (IP(4)R) binding properties in rat subjected to myocardial ischemic reperfusion in order to further make it clear whether this change is involved in the molecule mechanism of cell apoptosis of rat with myocardial ischemic reperfusion.

METHODSExtracting of cardiac myocyte nucleus was accomplished by saccharose density gradient centrifugation method, the binding properties of nuclear IP(4)R in different conditions were detected by radioligand binding assay. Apoptosis index of myocardial cell was determined by using TUNEL assay.

RESULTS(1) Myocardial cell apoptosis index in rat heart underwent 30 min regional ischemia and 3 h reperfusion increased distinctly compared with that in control group (P < 0.01). (2) There were two IP(4) binding sites located to the nuclear envelope. (3) In ischemic reperfusion injury (IRI) group, Bmax from high affinity binding site of nuclear IP(4)R significantly increased compared with that in sham-operated group, whereas Bmax from low affinity binding site didn't change. Kd values of both sites were all significantly decreased by 63% and 55%, respectively. (4) Phosphorylation of nuclear IP(4)R by PKC increased markedly its binding ability both in IRI and control group (P < 0.05), which was more apparent in IRI group. (5) In sham-operated group, the binding ability of nuclear IP(4)R increased with increasing free calcium concentrations in cytoplasm, and the binding properties of IP(4)R in IRI group were also increased in the condition of calcium overloading.

CONCLUSIONThe increasing of binding properties of nuclear IP(4)R from ischemic reperfusion heart may be one of important mechanism involved in myocardial cell apoptosis, furthermore resulting in myocardial IRI.

Animals ; Apoptosis ; Cell Nucleus ; metabolism ; Male ; Myocardial Reperfusion ; Myocardial Reperfusion Injury ; metabolism ; pathology ; Myocytes, Cardiac ; metabolism ; Rats ; Rats, Wistar ; Receptors, Cytoplasmic and Nuclear ; metabolism

OBJECTIVETo establish a flow cytometric method to detect the alteration of phenotypes and concentration of circulating microvesicles (MVs) from myocardial ischemic preconditioning (IPC) treated rats (IPC-MVs), and to investigate the effects of IPC-MVs on ischemia/reperfusion (I/R) injury in rats.

METHODSMyocardial IPC was elicited by three.cycles of 5-min ischemia and 5-min reperfusion of the left anterior descending (LAD) coronary artery. Platelet-free plasma (PFP) was isolated through two steps of centrifugation at room temperature from the peripheral blood, and IPC-MVs were isolated by ultracentrifugation from PFR PFP was incubated with anti-CD61, anti-CD144, anti-CD45 and anti-Erythroid Cells, and added 1, 2 µm latex beads to calibrate and absolutely count by flow cytometry. For functional research, I/R injury was induced by 30-min ischemia and 120-min reperfusion of LAD. IPC-MVs 7 mg/kg were infused via the femoral vein in myocardial I/R injured rats. Mean arterial blood pressure (MAP), heart rate (HR) and ST-segment of electro-cardiogram (ECG) were monitored throughout the experiment. Changes of myocardial morphology were observed after hematoxylin-eosin (HE) staining. The activity of plasma lactate dehydrogenase (LDH) was tested by Microplate Reader. Myocardial infarct size was measured by TTC staining.

RESULTSTotal IPC-MVs and different phenotypes, including platelet-derived MVs (PMVs), endothelial cell-derived MVs (EMVs), leucocyte-derived MVs (LMVs) and erythrocyte-derived MVs (RMVs) were all isolated which were identified membrane vesicles (<1 Vm) with corresponding antibody positive. The numbers of PMVs, EMVs and RMVs were significantly increased in circulation of IPC treated rats (P<0.05, respectively). In addition, at the end of 120-min reperfusion in I/R injured rats, IPC-MVs markedly increased HR (P<0.01), decreased ST-segment and LDH activity (P < 0.05, P < 0.01). The damage of myocardium was obviously alleviated and myocardial infarct size was significantly lowered after IPC-MVs treatment (P < 0.01).

CONCLUSIONThe method of flow cytometry was successfully established to detect the phenotypes and concentration alteration of IPC-MVs, including PMVs, EMVs, LMVs and RMVs. Furthermore, circulating IPC-MVs protected myocardium against I/R injury in rats.

Animals ; Cell-Derived Microparticles ; metabolism ; Coronary Vessels ; pathology ; Flow Cytometry ; Heart Rate ; Ischemic Preconditioning, Myocardial ; Myocardial Infarction ; physiopathology ; Myocardial Reperfusion Injury ; physiopathology ; Myocardium ; pathology ; Phenotype ; Rats

AIMTo investigate the effect on myocardial apoptosis and Bcl-2/Bax induced by remote preconditioning (RP) and to discuss the hypothesis from opioid receptors in pigs.

METHODSSkeletal muscle ischemia was performed in pigs by occlusion of the femoral artery (FAO) for 15 min followed by a 10 min of reperfusion. Infarction of the heart was induced by 40 min of left anterior descending coronary artery (LAD) occlusion followed by 120 min reperfusion. In the RP model induced by FAO, the role of opioid receptors was investigated by using antagonist of the opioid receptors (naloxone). The signal transduction pathway of RP was investigated by using hexamethonium. Apoptosis of left ventricular samples from nonischemic and ischemic areas was detected in situ with end-labeling (TUNEL) method and measured by flow cytometry. Bcl-2 and Bax was also measured by flow cytometry.

RESULTS(1) The apoptosis rate in ischemic myocardium in RP group measured by flow cytometry was lower (4.43% +/- 0.74%) compared with that in CONT group (15.4% +/- 1.15%), but Bcl-2/Bax was higher (1.36 +/- 0.09, CONT group: 0.56 +/- 0.08). (2) The protective effect could be prevented by naloxone used before RP protocol (apoptosis rate: 13.0% +/- 0.56% and Bcl-2/Bax: 0.69 +/- 0.18, P < 0.05). (3) Naloxone had no effect on apoptosis rate in CONT group. (4) Hexamethonium used before RP protocol had no effect on apoptosis rate and bcl-2/bax. Apoptotic cardiomyocytes detected in TUNEL correspond to the above.

CONCLUSIONRP induced by skeletal muscle ischemia could prevent myocardium from apoptosis, in which Bcl-2 and Bax might take part in regulation and control. Furthermore opioid receptors could take part in triggering the course and a neuronal signal transmission from the remote area to heart could be excluded.

Animals ; Apoptosis ; Ischemic Preconditioning ; methods ; Muscle, Skeletal ; blood supply ; Myocardial Reperfusion Injury ; pathology ; Myocardium ; pathology ; Receptors, Opioid ; Swine

OBJECTIVETo investigate the therapeutic effectiveness of intracoronary transplantation of autologous bone marrow mononuclear cells (BM-MNC) on myocardial ischemia reperfusion injury in mini-swine model.

METHODSMyocardial ischemia reperfusion injury model was established by ligating in 16 mini-swines, which were further randomized into two groups: (3.54 +/- 0.90) x 10(8) BM-MNC was intracoronarily transplanted in BM-MNC group (n = 9), and phosphate buffer saline was intracoronarily applied in the control group (n = 7). Ultrasonic cardiograhpy, hemodynamics, neovascular density, and myocardium infarction size were evaluated before and 4 weeks after transplantation.

RESULTSIn BM-MNC group, left ventricular ejection fraction (LVEF), intra-ventricular septa, lateral wall and anterior wall, cardiac output (CO) and + dp/dt(max) had no significant differences before and 4 weeks after transplantation (P > 0.05). In the control group, LVEF, intraventricular septa, lateral wall and anterior wall, CO, and + dp/dt(max) significantly decreased 4 weeks after transplantation (P < 0.05). Left ventricular end-diastolic pressure and- dp/dt(max) had no significant differences before and after cell transplantation. Capillary density was significantly larger in the BM-MNC group than in the control group [(13.39 +/- 6.96) /HP vs. (3.50 +/- 1.90) /HP]. The percentage and size of myocardial infarction was significantly lower in the BM-MNC group than in the control group.

CONCLUSIONTransplantation of BM-MNC into the myocardial ischemic reperfusion-injury area can increase capillary density and decrease infarction area, and thus remarkably improve cardiac systolic function.

Animals ; Bone Marrow Transplantation ; Coronary Vessels ; Myocardial Reperfusion Injury ; pathology ; physiopathology ; therapy ; Myocardium ; pathology ; Random Allocation ; Swine ; Swine, Miniature