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In the brain, brief episodes of ischemia induce tolerance against a subsequent severe episode of ischemia. This phenomenon of endogenous neuroprotection is known as preconditioning-induced ischemic tolerance. The purpose of this review is to summarize the current state of knowledge about mechanisms and potential applications of cerebral preconditioning and ischemic tolerance. Articles related to the terms ischemic preconditioning and ischemic tolerance were systematically searched via MEDLINE/PubMed, and articles published in English related to the nervous system were selected and analyzed. The past two decades have provided interesting insights into the molecular mechanisms of this neuroprotective phenomenon. Although both rapid and delayed types of tolerance have been documented in experimental settings, the delayed type has been found to be more prominent in the case of neuronal ischemic tolerance. Many intracellular signaling pathways have been implicated regarding ischemic preconditioning. Most of these are associated with membrane receptors, kinase cascades, and transcription factors. Moreover, ischemic tolerance can be induced by exposing animals or cells to diverse types of endogenous and exogenous stimuli that are not necessarily hypoxic or ischemic in nature. These cross-tolerances raise the hope that, in the future, it will be possible to pharmacologically activate or mimic ischemic tolerance in the human brain. Another promising approach is remote preconditioning in which preconditioning of one organ or system leads to the protection of a different (remote) organ that is difficult to target, such as the brain. The preconditioning strategy and related interventions can confer neuroprotection in experimental ischemia, and, thus, have promise for practical applications in cases of vascular neurosurgery and endo-vascular therapy.
Assuntos
Animais , Humanos , Encéfalo , Isquemia Encefálica , Hidrazinas , Isquemia , Precondicionamento Isquêmico , Membranas , Sistema Nervoso , Neurônios , Neurocirurgia , Fosfotransferases , Fatores de TranscriçãoRESUMO
Aim To study the protective effect of total flavones of rhododendra pharmacological preconditioning(TFR-PP)on myocardial ischemia and reperfusion injury and its mechanisms involved in myocardial inflammation in rats.Methods In model group the isolated perfused rat hearts set up by Langendorff system were subjected to 30 min ischemia followed by 40 min reperfusion. The hearts in TFR-PP groups were subjected to three cycles of 5 min perfusion with and without TFR before 30 min ischemia followed by 40 min reperfusion. In all groups the activities of lactate dehydrogenase (LDH), creatine phosphokinase (CK), and myeloperoxidase (MPO) in myocardium, the expressions of nuclear factor-kappa B (NF-?B), tumor necrosis factor-alpha(TNF-?), and intercellular adhersion molecule-1 (ICAM-1) were measured, and the myocardial pathomorphological changes were examined.Results TFR-PP(25、50、100 mg?L-1) could inhibit markedly the reductions of LDH and SOD activities in myocardium induced by ischemia and reperfusion injury.100 mg?L-1 TFR-PP also significantly improved the pathomorphological changes of injury. TFR-PP (25、50、100 mg?L-1) could inhibit the expressions of NF-?B, TNF-? and ICAM-1 to varying degrees.Conclusion TFR-PP has marked protective effect on ischemia and reperfusion injury in isolated rat heart via inhibiting the inflammation of myocardium.
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AIM To study the early cardioprotective effects of pharmacological preconditioning of nitroglycerin (NG) and buprenorphine (BU) used alone and in combination on myocardial ischemia in rats. METHODS Male Wistar rats were randomized to 5 groups. The ischemia and reperfusion injury was induced by ligation of the left arterior descending coronary arrery for 30 min and followed reperfusion for 2 h. The rats were subjected to different treatments before I/R. Normal saline (NS) was infused intravenously with the same volume of NG and BU in Sham group. Ischemia/preconditioning (IP) was performed by three cycles of 5 min I/R in EIP group. BU (1 0 mg?kg -1 ) and NG (0 3 mg?kg -1 ) was administered intravenously alone in BU and NG group or given together in B+N group to mimic the effects of IP, respectively. Heart rate, blood pressure, ST segment and arrhythmias were recorded continuously throughout the whole test. Plasma LDH and CK were measured on 30 min after ischemia and 2 h after reperfusion, HE and TTC staining were performed to determine myocardial necrosis at the end of test. RESULTS Compared with Sham group the onset of arrhythmias was delayed and the duration of ventricular premature contraction (VPC) was shortened remarkably ( P
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Adenosine receptor agonists can activate adenosine receptors A 1 and A 3, thus trigger delayed preconditioning signal pathway and induce high expression of protective proteins and some ionic channel opening in myocardial cells, which reduces myocardial ischemia/reperfusion injury.
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Objective To study the effects of D-Ala2-Leu5-enkephalin(DADLE) preconditioning on rabbit donor heart preservation and protective mechanism.Methods 24 rabbits were randomly divided into 4 groups. In group B, after preconditioning with DADLE(1mg?kg -1 ), the donor hearts were then arrested and preserved with Krebs-Henseleit buffer at 4℃ for 4h,and group A without conditioning as controls. Then the donor hearts were transplanted into the abdomen of recipient rabbits. Recovery situation of contraction of the donor heart was compared. The left ventricular tissues were obtained from the donor hearts after 2h of transplantation.The contents of free radicals and ATPase activity were determined and cardiac ultrastructure were observed.Results After 4h cold storage, the heart undergoing DADLE preconditioning in group B showed better recovery of left ventricular development pressure (LVDP).The activity of sodium-potassium ATPase in group B were higher than that in group A. DADLE increased free radical production 2-fold versus group A. Group B showed slighter injury in transmission electron microscopy observation than that in group A.Conclusion Our study demonstrated opioid preconditioning has protective function to rabbit heart injury caused by long term cold storage. The protective mechanism maybe related to increase of free radical content.
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Aim To observe the protective effect and possible mechanisms of Total Flavone of Abelmoschus Manihot L medic(TFA) on myocardial reperfusion injury in rabbits,when it was given as a preconditioning inducer.Method Different doses of TFA were perfused intravenously lasting for 5 min,followed by a 10 min break before 30 min ischemia and 60 min reperfusion in rabbits.Using this preconditioning method,we observed the histo-pathological changes of myocardium,the content of MDA,the activities of SOD and GSH-PX in plasma,and also,the expression of ICAM-1 in myocardium.Results TFA(16,8 and 4 mg?kg~(-1)) significantly ameliorated myocardium ischemical reperfusion injury.The activities of SOD and GSH-PX in plasma were enhanced,while the MDA level was decreased.Meanwhile,the expression of ICAM-1 mRNA in myocardium was down-regulated.Conclusion Pharmacological preconditioning of TFA could protects myocardial ischemic reperfusion injury in rabbits by inhibiting lipid peroxidation and myocardium inflammatory reaction.