OBJECTIVETo explore the effects of different oxygen flow rates during cardiopulmonary bypass (CPB) on myocardial ischemia-reperfusion (IR) injury in rabbits.

METHODSThirty rabbits were randomized equally into groups A, B and C to receive controlled oxygen reperfusion at low, normal and high flow rates (25, 50, and 80 ml.kg(-1).min(-1), respectively). Serum concentration of CK-MB and cTnT were tested by ELISA before the operation (T0) and after 30 min (T1), 2 h (T2), 12 h (T3) and 24 h (T4) of reperfusion. W/D, SOD and MDA of the myocardium were determined before and at 60 min after reperfusion. The ultrastructural alterations of the myocardium were observed.

RESULTSSerum concentration of CK-MB and cTnT in the 3 groups increased significantly after the operation, and their levels were the lowest in group A (P<0.05). W/D and MDA in the myocardium was also the lowest, while SOD the highest in group A (P<0.05). Ultrastructural pathologies were found in all the 3 groups, but relatively mild in group A.

CONCLUSIONLow oxygen flow rate during controlled reperfusion may protect the myocardium from IR injury in rabbits.

OBJECTIVEA general review was made of studies involving: (1) The experimental evidence of remote ischemic preconditioning (RIPC) and relative clinical studies, (2) The experimental and clinical evidences of remote ischemic postconditioning (RIPOC), (3) The potential mechanistic pathways underlying their protective effects.

DATA SOURCESThe data used in this review were mainly from manuscripts listed in PubMed that were published in English from 1986 to 2010. The search terms were "myocardial ischemia reperfusion injury", "ischemia preconditioning", "ischemia postconditioning", "remote preconditioning" and "remote postconditioning".

STUDY SELECTION(1) Clinical and experimental evidence that both RIPC and RIPOC produce preservation of ischemia reperfusion injury (IRI) of myocardium and other organs, (2) Studies related to the potential mechanisms, by which remote ischemic conditioning protects myocardium against IRI.

RESULTSBoth RIPC and RIOPC have been shown to attenuate myocardial IRI in laboratory animals. Also, their cardioprotective effects have appeared in some clinical studies. Except the external, the detailed internal mechanisms of remote ischemic conditioning have been generally described. Through these descriptions better protocols can be developed to provide improved cardioprotective procedures.

CONCLUSIONSRemote ischemic conditioning is an endogenous cardioprotective mechanism from outside the heart that protects against myocardial IRI and represents a general form of inter-organ protection. Remote ischemic conditioning may have an immense impact on clinical practice in the near future.

Primary percutaneous coronary intervention and thrombolysis remain therapies of choice for patients presenting with ST-segment elevation myocardial infarction (STEMI). Clinical outcome in the management of acute STEMI is dependent on myocardial reperfusion time and reperfusion strategies. Optimisation of these strategies should take into consideration logistical limitations of the local medical systems and the various patient profiles. We review the reperfusion strategies and its history in Singapore, comparing its clinical application with that in some developed Western countries.
Humans ; Myocardial Infarction ; blood ; physiopathology ; therapy ; Myocardial Reperfusion ; methods ; Singapore

Animals ; Humans ; Ischemic Preconditioning, Myocardial ; methods ; Myocardial Ischemia ; complications ; therapy ; Myocardial Reperfusion ; methods ; Myocardial Reperfusion Injury ; etiology ; prevention & control

This study examined the protective effect of ischemic postconditioning (IPoC) and minocycline postconditioning (MT) on myocardial ischemia-reperfusion (I/R) injury in atherosclerosis (AS) animals and the possible mechanism. Forty male healthy rabbits were injected with bovine serum albumin following feeding on a high fat diet for 6 weeks to establish AS model. AS rabbits were randomly divided into 3 groups: (1) I/R group, the rabbits were subjected to myocardial ischemia for 35 min and then reperfusion for 12 h; (2) IPoC group, the myocardial ischemia lasted for 35 min, and then reperfusion for 20 s and ischemia for 20 s [a total of 3 cycles (R20s/I20s×3)], and then reperfusion was sustained for 12 h; (3) MT group, minocycline was intravenously injected 10 min before reperfusion. The blood lipids, malondialdehyde (MDA), superoxide dismutase (SOD), soluble cell adhesion molecule (sICAM), myeloperoxidase (MPO), and cardiac troponin T (cTnT) were biochemically determined. The myocardial infarction size (IS) and apoptosis index (AI) were measured by pathological examination. The expression of bcl-2 and caspase-3 was detected in the myocardial tissue by using reverse transcription-polymerase chain reaction (RT-PCR). The results showed that the AS models were successfully established. The myocardial IS, the plasma levels of MDA, sICAM, MPO and cTnT, and the enzymatic activity of MPO were significantly decreased, and the plasma SOD activity was significantly increased in IPoC group and MT group as compared with I/R group (P<0.05 for all). The myocardial AI and the caspase-3 mRNA expression were lower and the bcl-2 mRNA expression was higher in IPoC and MT groups than those in I/R group (all P<0.05). It is concluded that the IPoC and MT can effectively reduce the I/R injury in the AS rabbits, and the mechanisms involved anti-oxidation, anti-inflammation, up-regulation of bcl-2 expression and down-regulation of caspase-3 expression. Minocycline can be used as an effective pharmacologic postconditioning drug to protect myocardia from I/R injury.
Animals ; Atherosclerosis ; physiopathology ; Ischemic Preconditioning, Myocardial ; methods ; Male ; Minocycline ; pharmacology ; Myocardial Reperfusion Injury ; physiopathology ; Rabbits ; Reperfusion Injury ; physiopathology

The prediction of successful recanalization following thrombolytic or endovascular treatment may be helpful to determine the strategy of recanalization treatment in acute stroke. Thrombus can be detected using noncontrast computed tomography (CT) as a hyperdense artery sign or blooming artifact on a T2*-weighted gradient-recalled image. The detection of thrombus using CT depends on slice thickness. Thrombus burden can be determined in terms of the length, volume, and clot burden score. The thrombus size can be quantitatively measured on thin-section CT or CT angiography/magnetic resonance angiography. The determination of thrombus size may be predictive of successful recanalization/non-recanalization after intravenous thrombolysis and endovascular treatment. However, cut-offs of thrombus size for predicting recanalization/non-recanalization are different among studies, due to different methods of measurements. Thus, a standardized method to measure the thrombus is necessary for thrombus imaging to be useful and reliable in clinical practice. Software-based measurements may provide a reliable and accurate assessment. The measurement should be easy and rapid to be more widely used in practice, which could be achieved by improvement of the user interface. In addition to prediction of recanalization, sequential measurements of thrombus volume before and after the treatment may also be useful to determine the efficacy of new thrombolytic drugs. This manuscript reviews the diagnosis of thrombus, prediction of recanalization using thrombus imaging, and practical considerations for the measurement of thrombus burden and density on CT.
Angiography ; Arteries ; Artifacts ; Diagnosis ; Endovascular Procedures ; Fibrinolytic Agents ; Methods ; Reperfusion* ; Stroke* ; Thrombolytic Therapy ; Thrombosis*

This study evaluated whether renal perfusion changes can be noninvasively estimated by using contrast-enhanced ultrasonography (CEUS) in renal ischemia-reperfusion injury and investigated the correlation between renal perfusion measured by CEUS and necrosis and apoptosis of renal tubular epithelial cells. In six dogs with experimentally induced renal ischemia-reperfusion injury, changes in time to peak intensity, peak intensity, and area under the curve were measured on CEUS. Peak intensity and area under the curve of the renal cortex began to decrease on day 1 (about 20% lower than baseline) and reached the lowest levels (about 50% of baseline) on day 4. They then gradually increased until day 10, at which time peak intensity was about 87% and area under the curve was about 95% of baseline; neither fully recovered. Both parameters were strongly correlated with the necrosis scores on histopathologic examination on day 4 (r = −0.810 of peak intensity and r = −0.886 of area under the curve). CEUS allowed quantitative evaluation of perfusion changes in acute renal ischemia-reperfusion injury, and CEUS results were correlated with renal tubular damage on histopathologic examination. Thus, CEUS could be a noninvasive, quantitative diagnostic method for determining progress of renal ischemia-reperfusion injury.
Animals ; Apoptosis ; Dogs* ; Epithelial Cells ; Evaluation Studies as Topic* ; Methods ; Necrosis ; Perfusion* ; Reperfusion Injury* ; Ultrasonography*

BACKGROUND: The aim of this study was to investigate the effects of remote ischemic conditioning on ischemia-reperfusion injury in rat muscle flaps histopathologically and biochemically. METHODS: Thirty albino rats were divided into 5 groups. No procedure was performed in the rats in group 1, and only blood samples were taken. A gracilis muscle flap was elevated in all the other groups. Microclamps were applied to the vascular pedicle for 4 hours in order to achieve tissue ischemia. In group 2, no additional procedure was performed. In groups 3, 4, and 5, the right hind limb was used and 3 cycles of ischemia-reperfusion for 5 minutes each (total, 30 minutes) was applied with a latex tourniquet (remote ischemic conditioning). In group 3, this procedure was performed before flap elevation (remote ischemic preconditoning). In group 4, the procedure was performed 4 hours after flap ischemia (remote ischemic postconditioning). In group 5, the procedure was performed after the flap was elevated, during the muscle flap ischemia episode (remote ischemic perconditioning). RESULTS: The histopathological damage score in all remote conditioning ischemia groups was lower than in the ischemic-reperfusion group. The lowest histopathological damage score was observed in group 5 (remote ischemic perconditioning). CONCLUSIONS: The nitric oxide levels were higher in the blood samples obtained from the remote ischemic perconditioning group. This study showed the effectiveness of remote ischemic conditioning procedures and compared their usefulness for preventing ischemia-reperfusion injury in muscle flaps.
Animals ; Extremities ; Ischemia ; Ischemic Preconditioning ; Latex ; Methods* ; Nitric Oxide ; Rats* ; Reperfusion Injury* ; Tourniquets

BACKGROUND: The aim of this study was to investigate the effects of remote ischemic conditioning on ischemia-reperfusion injury in rat muscle flaps histopathologically and biochemically. METHODS: Thirty albino rats were divided into 5 groups. No procedure was performed in the rats in group 1, and only blood samples were taken. A gracilis muscle flap was elevated in all the other groups. Microclamps were applied to the vascular pedicle for 4 hours in order to achieve tissue ischemia. In group 2, no additional procedure was performed. In groups 3, 4, and 5, the right hind limb was used and 3 cycles of ischemia-reperfusion for 5 minutes each (total, 30 minutes) was applied with a latex tourniquet (remote ischemic conditioning). In group 3, this procedure was performed before flap elevation (remote ischemic preconditoning). In group 4, the procedure was performed 4 hours after flap ischemia (remote ischemic postconditioning). In group 5, the procedure was performed after the flap was elevated, during the muscle flap ischemia episode (remote ischemic perconditioning). RESULTS: The histopathological damage score in all remote conditioning ischemia groups was lower than in the ischemic-reperfusion group. The lowest histopathological damage score was observed in group 5 (remote ischemic perconditioning). CONCLUSIONS: The nitric oxide levels were higher in the blood samples obtained from the remote ischemic perconditioning group. This study showed the effectiveness of remote ischemic conditioning procedures and compared their usefulness for preventing ischemia-reperfusion injury in muscle flaps.
Animals ; Extremities ; Ischemia ; Ischemic Preconditioning ; Latex ; Methods* ; Nitric Oxide ; Rats* ; Reperfusion Injury* ; Tourniquets

This study observed the protective effect of hypercapnic acidosis preconditioning on rabbit heart suffered from ischemia-reperfusion injury. Hypercapnic acidosis was established in animals with mechanical hypoventilation before ischemia-reperfusion. Thirty-two rabbits were randomly divided into 4 groups, with each having 8 animals in term of the degree of acidification: hypercapnic acidosis group A (group A), hypercapnic acidosis group B (group B), hypercapnic acidosis group C (group C), ischemia and reperfusion group (group IR). Animals in group IR were ventilated normally (tidal volume: 15 mL/kg, breathing rate 35 bpm). The PETCO(2) was maintained at the level of 40-50 mmHg for 30 min. Animals in groups A, B, C received low-frequency, low-volume ventilation to achieve hypercarbonic acidosis and the target levels of PETCO(2) were 75-85,65-75, 55-65 mmHg, respectively, with levels being maintained for 5 min. The animals then were ventilated normally to lower PETCO(2) to 40-50 mmHg. The left anterior branch artery of all the animals was ligated for 30 min and reperfused for 180 min. Then the infarct size was calculated. The cardiomyocytes were morphologically observed and ECG and hemodynamics were monitored on continuous basis. Acid-base balance was measured during procedure. Our results showed that the infarct size was (48.5+/-11.5)% of the risk area in the control group and (42.4+/-7.9)% in group C (P>0.05). Mean infarct size was significantly smaller in group B (34.5%+/-9.4%) (P<0.05 vs control group) and group A (31.0%+/-9.1%) (P<0.01 vs control group). It is concluded that HA-preconditioning can effectively protect the myocardium.
Acidosis, Respiratory/*physiopathology ; Hypercapnia/*physiopathology ; Ischemic Preconditioning, Myocardial/*methods ; Myocardial Reperfusion Injury/*prevention & control ; Random Allocation