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.

Animals ; Cardiopulmonary Bypass ; Myocardial Reperfusion Injury ; prevention & control ; Oxygen ; administration & dosage ; Rabbits ; Reperfusion ; methods

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.

Humans ; Ischemic Preconditioning, Myocardial ; methods ; Myocardial Reperfusion Injury ; prevention & control

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

Animals ; Disease Models, Animal ; Ischemic Preconditioning, Myocardial ; methods ; Myocardial Reperfusion Injury ; prevention & control ; Rats ; Rats, Wistar

OBJECTIVETo evaluate the efficacy and the mechanism of application of selective head cooling on neuronal morphological damage during postischemic reperfusion in a rabbit model.

METHODS168 New Zealand rabbits were randomized into three groups. Group I [n = 24, (38 +/- 0.5) degrees C, non-ischemic control]; Group II [n = 72, (38 +/- 0.5) degrees C, normothermic reperfusion]; Group III [n = 72, (28 +/- 0.5) degrees C, selective head cooling, initiated at the beginning of reperfusion). Animals in three subgroups (n = 24, each) of Group II and Group III had reperfused lasting for 30, 180 and 360 min respectively. Using computerized image analysis technique on morphological changes of nucleus, the degree of neuronal damage in 12 regions were differentiated into type A (normal), type B (mild damaged), type C (severely damaged) and type D (necrotic). Fourteen biochemical parameters in brain tissues were measured.

RESULTSAs compared with Group I, the counts of type A neuron decreased progressively, and those of type B, C and D increased significantly in Group II during reperfusion (P < 0.01). In Group II, vasoactive intestinal peptide, b-endorphine, prostacyclin, T3 and Na+, K(+)-ATPase were correlated with the changes of type A; b-endorphine and thromboxane with type B; glucose and vasopressin with type C; Na+, K(+)-ATPase, glutamic acid, T3 and vasoactive intestinal peptide with type D (P < 0.05). As compared with Group II, the counts of type A increased, and those of type C and D significantly decreased in Group III (P < 0.01). In Group III, Ca2+, Mg(2+)-ATPase were correlated with the changes of type A, C and D (P < 0.01).

CONCLUSIONSelective head cooling for sex hours during postischemic reperfusion does improve neuronal morphological outcomes in terms of morphological changes.

Animals ; Brain Ischemia ; pathology ; Cold Temperature ; Neurons ; pathology ; Rabbits ; Reperfusion Injury ; prevention & control ; Resuscitation ; methods

Female ; Humans ; Ischemic Preconditioning, Myocardial ; methods ; Male ; Myocardial Reperfusion Injury ; prevention & control

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