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 ; Myocardial Reperfusion Injury ; prevention & control ; Translational Medical Research

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

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.

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

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

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

Humans ; Myocardial Reperfusion Injury/prevention & control* ; Melatonin/therapeutic use* ; Mitochondria ; Myocardial Infarction

Ischemia/hypoxia is one of the key clinical issues following severe burns, and ischemic/hypoxic damage of tissues and organs is still hard to be prevented or minimized by various fluid resuscitation regimens. To those who suffered severe burns, even though fluid replacement therapy is delivered promptly, ischemic/hypoxic damage of organs is still inevitable. Previously, blood flow in vital organs such as heart was considered not to be reduced because of blood redistribution under the circumstance of stress. The postburn cardiac dysfunction has been mainly attributed to the reduced blood flow returned to the heart due to decreased blood volume caused by increased capillary permeability. Therefore, postburn cardiac dysfunction has been considered to be the result of burn shock. During the past two decades, we have performed serial studies on severe burns, and found that ischemic/hypoxic myocardial damage and functional impairment of myocardium due to activation of renin angiotensin system existing in the heart itself occur immediately after severe burns even before significant reduction in blood volume secondary to an increase of capillary permeability. Such prompt myocardial damage leads to cardiac deficiency, and it is also a precipitating factor for burn shock and ischemic/hypoxic injury of systemic tissues and organs. Therefore, we called it "shock heart" in our reports. The cellular and molecular mechanisms leading to myocardial damage were systematically investigated. Strategies for prevention of early postburn myocardial damage and dysfunction, and a new effective burn shock resuscitation regimen "volume replacement" plus "dynamic support" (cardiac support and myocardial protection) have been proposed based on our previous studies.
Burns ; complications ; metabolism ; Humans ; Hypoxia ; etiology ; prevention & control ; Myocardial Reperfusion Injury ; etiology ; prevention & control ; Myocardium ; metabolism

The aim of the present study was to explore the effects of two different modes of intermittent hypobaric hypoxia (IHH) on myocardial ischemia/reperfusion injury in developing rat hearts. Postnatal male sprague-Dawley rats (n=72) were divided randomly into 3 groups: intermittent hypoxia at 3 000 m (IHH3000) group, intermittent hypoxia at 5 000 m (IHH5000) group and control group. The isolated hearts were perfused in the Langendorff apparatus, undergoing 30 min of global ischemia and 60 min of reperfusion. Cardiac function, coronary flow and lactate dehydrogenase (LDH) activity were recorded at 5 min before ischemia and 1, 5, 10, 20, 30, 60 min during reperfusion, respectively. The heart weight was measured at the end of the experiment. The results showed that: (1) There was no difference in body weight gaining between IHH3000 and control groups. The gain of body weight in IHH5000 group was much lower than that in IHH3000 and control groups (P<0.01). (2) Compared with that in the control group, the recovery of cardiac function in IHH3000 group was enhanced at 60 min after ischemia/reperfusion, coronary flow was increased, and LDH activity was decreased (P<0.05), meaning a cardioprotective effect occurred. There was no significant difference in heart weight between IHH3000 and control groups. In addition, cardiac function restored better in IHH3000 group after 42 d of hypoxic exposure than that after 28 d of hypoxic exposure (P<0.05). (3) Compared with that in the control group, the recovery of cardiac function in IHH5000 group was lower, coronary flow was decreased, and LDH activity was increased (P<0.05). There was a hypertrophy in the right ventricle in IHH5000 group. All changes indicated definitely that a detrimental effect developed in IHH5000 group. The results suggest that proper IHH can protect developing rat hearts against ischemia/reperfusion injury while this effect could be affected by the modes of intermittent hypoxic exposure.
Animals ; Heart ; Heart Ventricles ; Hypoxia ; Male ; Myocardial Reperfusion Injury ; prevention & control ; Protective Agents ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury