TNF-α is required for late ischemic preconditioning but not for remote preconditioning of trauma

Ren, Xiaoping; Wang, Yan; Jones, W. Keith

doi:10.1016/j.jss.2004.03.010

Cited by 61 publications

(78 citation statements)

References 51 publications

(87 reference statements)

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“…The respiratory rate was 100 to 105 breaths per minute, and PO 2 , PCO 2 , blood pH, and body temperature were maintained within normal limits throughout the procedure as previously described. 28 ECG electrodes were placed subcutaneously, and data were recorded with a Digi-Med Sinus Rhythm Analyzer (Micro-Med). A lateral thoracotomy (1.5-cm incision between the second and third ribs) was performed to provide exposure of the left anterior descending coronary artery (LAD), while avoiding rib and sternal resection, retraction, and rotation of the heart.…”

Section: Regional Ischemia In Vivomentioning

confidence: 99%

Novel Cardioprotective Role of a Small Heat-Shock Protein, Hsp20, Against Ischemia/Reperfusion Injury

et al. 2005

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Background-Heat-shock proteins (Hsps) have been shown to render cardioprotection from stress-induced injury; however, little is known about the role of another small heat-shock protein, Hsp20, which regulates activities of vasodilation and platelet aggregation, in cardioprotection against ischemia injury. We recently reported that increased expression of Hsp20 in cardiomyocytes was associated with improved contraction and protection against ␤-agonistinduced apoptosis. Methods and Results-To investigate whether overexpression of Hsp20 exerts protective effects in both ex vivo and in vivo ischemia/reperfusion (I/R) injury, we generated a transgenic (TG) mouse model with cardiac-specific overexpression of Hsp20 (10-fold). TG and wild-type (WT) hearts were then subjected to global no-flow I/R (45 minutes/120 minutes) using the Langendorff preparation. TG hearts exhibited improved recovery of contractile performance over the whole reperfusion period. This improvement was accompanied by a 2-fold decrease in lactate dehydrogenase released from the TG hearts. The extent of infarction and apoptotic cell death was also significantly decreased, which was associated with increased protein ratio of Bcl-2/Bax and reduced caspase-3 activity in TG hearts. Furthermore, in vivo experiments of 30-minute myocardial ischemia, via coronary artery occlusion, followed by 24-hour reperfusion, showed that the infarct region-to-risk region ratio was 8.1Ϯ1.1% in TG hearts (nϭ7), compared with 19.5Ϯ2.1% in WT hearts (nϭ11, PϽ0.001). Conclusions-Our data demonstrate that increased Hsp20 expression in the heart protects against I/R injury, resulting in improved recovery of cardiac function and reduced infarction. Thus, Hsp20 may constitute a new therapeutic target for ischemic heart diseases.

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Section: Regional Ischemia In Vivomentioning

confidence: 99%

Novel Cardioprotective Role of a Small Heat-Shock Protein, Hsp20, Against Ischemia/Reperfusion Injury

et al. 2005

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“…Remote preconditioning of trauma is a nonischemic cardioprotective method, first reported in 2004 [1], and confirmed by animal studies in mouse and rat myocardial ischemia reperfusion models [15,16]. However, in previous studies, depth of anesthesia seemed insufficient, which weakened the clinical value of these studies [17].…”

Section: Discussionmentioning

confidence: 97%

“…1): 1) Sham group: intrathecal catheter placement, heart exposure, and suturing without ischemia/reperfusion; 2, 3)…”

Section: Study Groups and Experimental Protocolmentioning

confidence: 99%

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Activating mu-opioid receptors in the spinal cord mediates the cardioprotective effect of remote preconditioning of trauma

Mei

Cheng

et al. 2017

Cardiol J.

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“…Recent studies suggest that the heart can be protected from acute IRI by simply inducing surgical trauma elsewhere-a phenomenon which has been termed remote preconditioning of trauma (RPCT) [194,195]. Jones et al [195] demonstrated that an abdominal surgical incision was enough to protect the murine heart from MI.…”

Section: Novel Concepts In Ricmentioning

confidence: 99%

Cardioprotection Techniques: Preconditioning, Postconditioning and Remote Con-ditioning (Basic Science)

Hausenloy¹

2013

CPD

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Ischemic heart disease (IHD) is the leading cause of death and disability worldwide. The major pathological consequences of IHD arise from the detrimental effects of acute ischemia-reperfusion injury (IRI) on the myocardium. Therefore, in order to improve clinical outcomes in patients with IHD, novel therapeutic strategies are required to protect the myocardium from acute IRI and preserve cardiac function (cardioprotection). In this regard, endogenous cardioprotective strategies such as ischemic preconditioning (IPC), ischemic postconditioning (IPost) and remote ischemic conditioning (RIC) may provide novel approaches for protecting the heart in clinical settings in which the patient experiences acute myocardial IRI. In this review article, we provide an overview of these endogenous cardioprotective strategies with respect to the pre-clinical experimental literature, exploring their major characteristics and underlying signaling mechanisms. The application of these therapeutic strategies in the clinical setting for potential patient benefit is reviewed in another article in this special issue.

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TNF-α is required for late ischemic preconditioning but not for remote preconditioning of trauma

Cited by 61 publications

References 51 publications

Novel Cardioprotective Role of a Small Heat-Shock Protein, Hsp20, Against Ischemia/Reperfusion Injury

Novel Cardioprotective Role of a Small Heat-Shock Protein, Hsp20, Against Ischemia/Reperfusion Injury

Activating mu-opioid receptors in the spinal cord mediates the cardioprotective effect of remote preconditioning of trauma

Cardioprotection Techniques: Preconditioning, Postconditioning and Remote Con-ditioning (Basic Science)

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