Myocardial preconditioning: Basic concepts and potential mechanisms

Okubo, Seiji; Xi, Lei; Bernardo, Nelson L.; Yoshida, Kazuhiko; Kukreja, Rakesh C.

doi:10.1007/978-1-4615-5097-6_1

Cited by 33 publications

(35 citation statements)

References 126 publications

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“…Muitos pesquisadores continuam investigando os mecanismos do PCI, porém alguns passos ainda precisam ser esclarecidos. O estímulo isquêmico causa a liberação de mediadores do estresse a partir do coração, incluindo adenosina, bradicinina, catecolaminas, opióides e ROS [18][19][20] . Estes mediadores se ligam a receptores específicos da membrana celular (proteína G), que amplifica o estímulo inicial para a fosfolipase C (PLC).…”

Section: Precondicionamento Isquêmicounclassified

“…From this moment on, morphologic changes start to develop. Proteases activated especially by the sudden increase in calcium and ROS concentration start to degrade myofibrillar proteins of the cytoskeleton while lipases affect membranes causing their rupture and consequent cellular death 18 . Recovery of the production of energy by cardiomyocytes that did not undergo apoptosis during the ischemic period would be expected after perfusion is reinstituted.…”

Section: Cell Damage Secondary To Ischemia and Reperfusionmentioning

confidence: 99%

“…Several researchers continue investigating the mechanisms of IPC; however a few steps still need to be explained. The ischemic stimulus causes the release of stress mediators from the heart, including adenosine, bradykinin, catecholamines, opioids, and ROS [18][19][20] . Those mediators bind to specific receptors in the cell membrane (protein G), which amplifies the initial stimulus for phospholipase C (PLC).…”

Section: Ischemic Preconditioningmentioning

confidence: 99%

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Proteção miocárdica pelo pré- e pós-condicionamento anestésico

Pasqualin¹,

Auler²

2008

Rev. Bras. Anestesiol.

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JUSTIFICATIVA E OBJETIVO:A isquemia miocárdica perioperatória é um evento comumente observado no período perioperatório podendo aumentar significativamente a morbimortalidade pós-cirúrgica. As propriedades cardioprotetoras dos anestésicos voláteis e dos opióides têm sido estudadas durante algumas décadas e hoje constituem poderosas ferramentas no manuseio de pacientes com doença coronariana isquêmica. O objetivo desta revisão foi fornecer fundamentos da proteção miocárdica por precondicionamento. CONTEÚDO:Serão discutidos os conceitos sobre lesão celular decorrente de isquemia e reperfusão, precondicionamento isquê-mico (PCI), precondicionamento anestésico (PCA), assim como os mecanismos de proteção miocárdica. Estudos recentes em cirurgia cardíaca demonstram que a aplicação de curtos períodos de isquemia, durante a reperfusão, podem reduzir a área de infarto do miocárdio. Os anestésicos voláteis também podem apresentar efeito protetor na reperfusão miocárdica. Independentemente da via de sinalização que leva ao precondicionamento, tanto aqueles que envolvem anestésicos quanto o isquêmico, considera-se que os canais de KATP dependentes mitocondriais sejam os mediadores finais de cardioproteção por controlarem o influxo de cálcio na mitocôndria e prevenirem a indução da necrose e apoptose. Apesar do PCI e PCA efetivamente reduzirem a área de infarto do miocárdio e melhorarem a função ventricular pós-operatória, é importante salientar que esses tratamentos devem ser anteriores ao evento isquêmics no sentido de justificar sua aplicabilidade clínica. CONCLUSÕES:Os fenômenos conhecidos como precondicionamento isquêmico e precondicionamento anestésico do miocárdi, são bem conhecidos, sendo o mecanismo de proteção similar em ambas as situações, porém nem todos os passos que levam a esta proteção foram completamente esclarecidos. Mais investigações são necessária, para que as propriedades cardioprotetoras dos agentes anestésicos possam ter aplicabilidade clínica crescente.

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Section: Precondicionamento Isquêmicounclassified

Section: Cell Damage Secondary To Ischemia and Reperfusionmentioning

confidence: 99%

Section: Ischemic Preconditioningmentioning

confidence: 99%

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Proteção miocárdica pelo pré- e pós-condicionamento anestésico

Pasqualin¹,

Auler²

2008

Rev. Bras. Anestesiol.

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“…I Is sc ch he em mi ic c p pr re ec co on nd di it ti io on ni in ng g There have been many reviews on ischemic preconditioning. [20][21][22] In brief, Murry et al introduced this concept when they found, in a canine model, that four cycles of five-minute left circumflex coronary artery (Lcx) occlusion, in advance of 40-min Lcx occlusion, reduced infarct size by 75%. They named this protective effect ischemic preconditioning, 23 a phenomenon that has been extensively investigated because of its potency.…”

Section: Preconditiong 622mentioning

confidence: 99%

“…Ischemic preconditioning can be observed in a wide range of preparations: from isolated cardiomyocytes and vascular endothelial cells to hearts in situ in various species. [20][21][22]24 Although ischemic preconditioning initially referred to the ability to mitigate infarction, the definition has been extended to employ other endpoints, such as stunning 18 and coronary abnormalities. 22 In humans, ischemic preconditioning enhanced postischemic contraction in ventricular trabeculae muscle, and survival rate of isolated cardiomyocytes.…”

Section: Preconditiong 622mentioning

confidence: 99%

La protection myocardique contre les lésions d’ischémie-reperfusion par des anesthésiques: Une mise à jour pour les anesthésiologistes

Kato

Foëx

2002

Can J Anesth/J Can Anesth

194

126

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P Pu ur rp po os se e: : The aim of this review of the literature was to evaluate the effectiveness of anesthetics in protecting the heart against myocardial ischemia-reperfusion injury.S So ou ur rc ce e: : Articles were obtained from the Medline database (1980-, search terms included heart, myocardium, coronary, ischemia, reperfusion injury, infarction, stunning, halothane, enflurane, desflurane, isoflurane, sevoflurane, opioid, morphine, fentanyl, alfentanil sufentanil, pentazocine, buprenorphine, barbiturate, thiopental, ketamine, propofol, preconditioning, neutrophil adhesion, free radical, antioxidant and calcium).P Pr ri in nc ci ip pa al l f fi in nd di in ng gs s: : Protection by volatile anesthetics, morphine and propofol is relatively well investigated. It is generally agreed that these agents reduce the myocardial damage caused by ischemia and reperfusion. Other anesthetics which are often used in clinical practice, such as fentanyl, ketamine, barbiturates and benzodiazepines have been much less studied, and their potential as cardioprotectors is currently unknown. There are some proposed mechanisms for protection by anesthetic agents: ischemic preconditioning-like effect, interference in the neutrophil/platelet-endothelium interaction, blockade of Ca 2+ overload to the cytosolic space and antioxidant-like effect. Different anesthetics appear to have different mechanisms by which protection is exerted. Clinical applicability of anesthetic agent-induced protection has yet to be explored. C Co on nc cl lu us si io on n: : There is increasing evidence of anesthetic agentinduced protection. At present, isoflurane, sevoflurane and morphine appear to be most promising as preconditioning-inducing agents. After the onset of ischemia, propofol could be selected to reduce ischemia-reperfusion injury. Future clinical application depends on the full elucidation of the underlying mechanisms and on clinical outcome trials. Objectif

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Renal protection by delayed ischaemic preconditioning is associated with inhibition of the inflammatory response and NF‐κB activation

Liu

Zhang

et al. 2007

Cell Biochemistry & Function

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Brief and sublethal ischaemia renders an organ tolerant to subsequent prolonged ischaemia, which is called ischaemic preconditioning (IPC). In regard to the beneficial effects and endogenous mechanisms of renal delayed IPC, few data are available. In this study, we aim at determining reno-protective effects of delayed IPC against ischaemia-reperfusion (I/R) injury, and illustrating whether these effects are associated with suppressing inflammation and nuclear factor-kappaB (NF-kappaB) activation. I/R injury was induced by clamping both renal pedicles for 40 min, followed by 24 h of reperfusion. The rats were subjected to ischaemia for 20 min (preconditioning) or sham surgery (non- preconditioning) at day 4 before I/R. Functional and morphological parameters were evaluated at 24 h after reperfusion. At the same time, macrophage (ED-1(+)) infiltration, and the expression of intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-alpha (TNF-alpha) were assessed by immunohistochemistry. Moreover, I kappa B-alpha degradation and NF-kappaB/DNA binding activity were analyzed. Compared with rats exposed to I/R injury, preconditioned rats had a significant decrease in levels of serum creatinine (Scr, 384.3 +/- 21.8 micromol/L vs. 52.5 +/- 21.7 micromol/L; p<0.001), blood urea nitrogen (BUN, 40.4 +/- 2.7 mmol/L vs. 15.9 +/- 4.2 mmol/L; p<0.001) and serum aspartate aminotransferase (AST, 486.7 +/- 58.6 IU/L vs. 267.3 +/- 43.9 IU/L; p<0.001). Parallel to the above changes, preconditioned rats preserved structural integrity and decreased tubulointerstitial damage scores (3.4 +/- 0.3 vs. 0.2 +/- 0.05; p<0.001) and ED-1(+) cell infiltration (25.3 +/- 3.5 vs. 6.2 +/- 1.2 cells/HPF, p<0.01). Furthermore, our results showed that the expression of ICAM-1 and TNF-alpha, the degree of I kappa B-alpha degradation, and NF-kappaB/DNA binding activity were reduced by IPC. Taken together, our results demonstrated that delayed IPC offered both functional and histological protection, which may be related to suppression of inflammation in preconditioned kidneys.

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Myocardial preconditioning: Basic concepts and potential mechanisms

Cited by 33 publications

References 126 publications

Proteção miocárdica pelo pré- e pós-condicionamento anestésico

Proteção miocárdica pelo pré- e pós-condicionamento anestésico

La protection myocardique contre les lésions d’ischémie-reperfusion par des anesthésiques: Une mise à jour pour les anesthésiologistes

Renal protection by delayed ischaemic preconditioning is associated with inhibition of the inflammatory response and NF‐κB activation

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