PURPOSE: Brief myocardial ischemia evokes a cardioprotective response, referred to as "Ischemic Preconditioning", that limits injury caused by a subsequent prolonged ischemic insult. The myocardial ischemic preconditioning effect can be induced by ischemia of "distant" cardiac and noncardiac tissue, implicating the involvement of an as-yet unidentified humoral trigger. The purpose of this study was to prove the protective effect of a preconditioning ischemic trigger (PIT) obtained from coronary effluent to isolated pancreatic cells under hypoxic condition in neonatal pigs. METHODS: Isolated hearts were preconditioned 5 times with 5-min ischemia following 10-min reperfusion. Coronary effluent was collected during reperfusion, filtered by using a Sep-Pak C-18 catridge, and lyophilized after dissolving it with acetonitrile. Isolated pancreatic cells were divided into a PIT-treatment group and a control group, and each group was further divided into time-dependent and dose-dependent groups. Time-dependent groups were incubated under a hypoxic condition for durations of 1, 2, 3, and 4 hrs, and dose-dependent groups were treated with 3 different doses of PIT that had undergone hypoxic incubation for 4 hrs. Viability of the pancreatic cells after the hypoxic incubation period was evaluated by using a confocal microscope. RESULTS: In the control group, the average viability of pancreatic cells after 4 hrs of hypoxia was 60.48 +/- 1.24%, and in the PIT-treated group, the value was 71.88 +/- 1.33%, the difference in the viability between the PIT-treated group and the control group after 4 hrs of hypoxia was statistically significant. In the dose-dependent groups, the viability of pancreatic cells was significantly larger in the groups treated with original PIT and 1/10 PIT than in the control group. CONCLUSION: These data suggest that in the In-vitro pig model, PIT obtained from heart evoked ischemic tolerance to isolated pancreatic cells.
Anoxia* ; Heart* ; Ischemia ; Ischemic Preconditioning ; Ischemic Preconditioning, Myocardial ; Myocardial Ischemia ; Reperfusion ; Swine*

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.

Ischemic preconditioning is known to have protective effect on myocardial function at prolonged ischemic insult but the mechanism of the effect is not clearly known. The effect of the preconditioning on the global ischemia using cardioplegic solution is not well known. To evaluate the effect of global myocardial preconditioning on the functional recovery after cardioplegic arrest and two hours of hypothermic storage, we used the isolated rat heart and two hours cardioplegic arrest time at 0degree C. In the experimental group (n=10), after baseline functional data was obtained, ischemic preconditioning was induced with 1 min of global normothermic ischemia for three times before the arrest period. In the control group (n=10), hearts underwent no ischemic precondi- tioning. After 2 hrs of cardioplegic arrest and storage in the 0degree C cardioplegic solution reperfusion was done and hemodynamic data were collected at post-reperfusion 20 min. Heart with ischemic preconditioning showed improved functional recovery at post reperfusion 20 min in peak developed pressure and dP/dT. In percent change of the peak pressure, preconditioning group showed 93.20+/-15.7% recovery rate compared to baseline data, and control group showed 67.3+/-15.6% recovery rate. In percent change of the dP/dT, control group showed 54.7+/-18.2% recovery rate and preconditioning group showed 78.1+/-15.1% recovery rate. Percent changes in heart rate and coronary flow showed no significant difference between two groups and there was no significant differences in amount of cardioplegic delivery between groups. Our data suggest ischemic preconditioning may have protective effect on recovery state after cardioplegic arrest and 2 hr ischemic storage of isolated rat heart and its mechanism is not related to the amount of the cardioplegic delivery amount.
Animals ; Cardioplegic Solutions ; Heart Rate ; Heart* ; Hemodynamics ; Ischemia ; Ischemic Preconditioning* ; Ischemic Preconditioning, Myocardial ; Myocardial Ischemia ; Rats ; Reperfusion

Since the findings of Murry and Currie et al. that ischemic preconditioning (IPC) and heat shock response (HSR) could protect evidently myocardium against ischemia-reperfusion injury in the middle of 1980s, endogenous myocardial protection has drawn widespread attentions. A great quantity of studies completed during the past 25 years made much progress in endogenous myocardial protection. Abundant research experiences have been accumulated and a basic theoretical framework has been established in this field. However, there are still many questions need to be solved. In this review, we focused on clarifying some hot questions and important future directions in IPC, heat shock proteins (HSPs), research models and strategies in endogenous myocardial protection.
Animals ; Heat-Shock Proteins ; physiology ; Humans ; Ischemic Preconditioning ; Ischemic Preconditioning, Myocardial ; Myocardial Reperfusion Injury ; Myocardium ; Reperfusion Injury ; Time Factors

OBJECTIVE: To determine the influence of stress on myocardial apoptosis in ischemic preconditioning group (IPC). METHODS: Twenty-four Japanese white rabbits were randomly divided into 4 groups (n=6): an etomidate group (the Etom group) of depressed stress established by intravenous etomidate, an IPC group, an ischemic reperfusion group (the IR group) and a methylprednisolone group (the MP group). Myocardial apoptosis was examined by DNA-laddering, in situ nick-end labeling (TUNEL) and Hoechst dyeing. RESULTS: The DNA ladder increased in the Etom group. The percentage of apoptosis by TUNEL method was 1.7%±0.2% in the IPC group, 2.3%±0.8% in the MP group, 3.8%±1.3% in the IR group and 3.0%±0.4% in the Etom group. Hoechst dying was 4.1%±0.9% in the IPC group, 3.5%±0.4% in the MP group, 6.2%±1.6% in the IR group and 7.6%±0.4% in the Etom group. There was significant difference between the IPC group and the Etom group or IR group, and also between the MP group and the IR group. CONCLUSION A depressed stress response impairs the inhibition on myocardial apoptosis in ischemic preconditioning. Methylprednisolone may inhibit myocardial apoptosis.
Animals ; Apoptosis ; Etomidate ; pharmacology ; Heart ; drug effects ; Ischemic Preconditioning ; Ischemic Preconditioning, Myocardial ; Methylprednisolone ; pharmacology ; Myocardium ; pathology ; Rabbits

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

BACKGROUND: Ischemic preconditioning(IP) is known to be effective in the protection of myocardial necrosis, arrhythmia, and the restoration of the myocardial function in the ischemia-reperfusion state of the heart. However the exact mechanism is not clearly understood. The purpose of this study was to elucidate the trigger mechanism of IP on the restoration of the myocardial function after ischemia-reperfusion. MATERIAL AND METHOD: By connecting a Langendorff perfusion apparatus with an isolated heart of a rat, the normal temperature of the heart was maintained. The experiment was conducted in seven groups, which were divided according to the preconditioning stimuli and blockage methods: Group I(n=10) was a group without IP, Group II(n=10) a group of three-minute IP, Group III(n=10) a group of PEIP, Group IV(n=10) a group of clonidine IP, Group V(n=10) a group of IP after reserpine, Group VI(n=10) a group of PE & prazosin IP, and Group VII(n=10) a group of clonidine & yohimbine IP. Hemodynamic parameters of DP, LVEDP, +/-dP/dT and the changes of perfusion in the coronary artery were evaluated. RESULT: Developed pressure and +dP/dT changed per unit time. After 20 minutes of reperfusion, those of Group II and III were 63.1+/-3.7%, 64.8+/-4.6% and 64.5+/-4.6%, 63.8+/-4.4%, which improved more significantly than those of Group I(P<0.05). However, there were no significant differences between the Groups V and VI, and Group I. CONCLUSION: The Brief ischemic preconditioning and pharmacological preconditioning using alpha-receptor sympathomimetics have protecting effects on the restoration of myocardial function after reperfusion. And the protecting effect of preconditioning seems to be related to sympathetic neurotransmitters and to the selective action of the alpha1-adrenergic receptor.
Animals ; Arrhythmias, Cardiac ; Clonidine ; Coronary Vessels ; Heart ; Hemodynamics ; Ischemic Preconditioning ; Ischemic Preconditioning, Myocardial* ; Necrosis ; Neurotransmitter Agents ; Perfusion ; Prazosin ; Rats* ; Reperfusion ; Reserpine ; Sympathomimetics ; Yohimbine

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

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 ; Humans ; Ischemic Preconditioning, Myocardial ; MicroRNAs ; Myocardial Ischemia ; genetics ; prevention & control