Ischemic Preconditioning in Humans

Tomai, Fabrizio; Crea, Filippo; Chiariello, Luigi; Gioffrè, Pier Agostino

doi:10.1161/01.cir.100.5.559

Cited by 231 publications

(68 citation statements)

References 48 publications

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“…The preconditioning by MPTP is not intended to suggest future direct therapeutic approach, but rather aim at finding key players in the background which may help to do the best measures to alleviate the pathological alterations. The situation may be similar to ischemic preconditioning where the outcome in myocardial infarction may substantially depend on which medications were applied with an influence on preconditioning (Tomai et al, 1999). This may be especially important in light of the fact that environmental toxins could play a role in the pathogenies of idiopathic PD.…”

Section: Discussionmentioning

confidence: 99%

Effect of MPTP on mRNA expression of PGC-1α in mouse brain

et al. 2017

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The peroxisome proliferator-activated receptor-γ (PPARγ) coactivator 1α (PGC-1α) is a key regulator of mitochondrial biogenesis, respiration and adaptive thermogenesis. Beside the full-length protein (FL-PGC-1α), several other functionally active PGC-1α isoforms were identified as a result of alternative splicing (e.g., N-truncated PGC-1α; NT-PGC-1α) or alternative promoter usage (e.g., central nervous system-specific PGC-1α isoforms; CNS-PGC-1α). The achievement of neuroprotection via the CNS-targeted pharmacological stimulation is limited due to the poor penetration of the blood brain barrier (BBB) by the proposed pharmaceutical agents, so preconditioning emerged as another option. The current study aimed at the examination of how the expression levels of FL-, NT-, CNS-and reference PGC-1α isoforms change in different brain regions following various 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment regimens, including the chronic low dose treatment for preconditioning. Ninety minutes following the acute treatment regimen, the expression level of FL-, NT-and CNS-PGC-1α isoforms increased significantly in the striatum, cortex and cerebellum. However, this elevation was diminished 7 days following the last MPTP injection in this acute treatment regimen. The chronic low dose administration of MPTP, which did not cause significant toxic effect in light of the relatively unaltered dopamine levels, neither resulted in any significant change of PGC-1α expression as well. The elevation of PGC-1α levels following acute treatment may demonstrate a short-term compensatory mechanism against the mitochondrial damage induced by the complex I inhibitor MPTP. However, drug-induced preconditioning by chronic low dose MPTP seems not to induce protective responses via the PGC-1α system.

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Section: Discussionmentioning

confidence: 99%

Effect of MPTP on mRNA expression of PGC-1α in mouse brain

et al. 2017

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“…The condition of patients with a history of ACS could reflect the experimental model of MI developing tolerance to prolonged ischemic insult, namely ischemic preconditioning when the myocardium has been previously exposed to brief periods of ischemia and reperfusion [35]. Some experimental studies have investigated the effect of ischemic preconditioning on necrosis markers and the potential clinical interpretation [36][37][38].…”

Section: Discussionmentioning

confidence: 99%

New insights in the pathophysiology of acute myocardial infarction detectable by a contemporary troponin assay

Ferraro

Biganzoli

Marano

et al. 2013

Clinical Biochemistry

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Objectives: ST-elevation and non-ST-elevation myocardial infarction (STEMI, NSTEMI) are considered two distinct pathophysiologic entities. We evaluated cardiac troponin I (cTnI) release in STEMI and NSTEMI using a "contemporary" (CV > 10 to 20% at the 99th percentile concentration) cTnI assay for patients undergoing early percutaneous coronary intervention (PCI).Design and methods: 856 patients with suspected acute coronary syndrome consecutively admitted to the Emergency Department of the Maggiore Hospital of Novara (225 STEMI and 135 NSTEMI) were selected according to: 1) early (≤4 h from admission) and successful PCI; and 2) cTnI measurements at ED presentation and within 24 h. The influence of the MI type on cTnI concentrations at baseline and after PCI as well as the velocity of cTnI [cTnI V = absolute increase (after log conversion of cTnI measurements) / delay between the two measurements] was studied by multiple regression analysis, adjusting for patient parameters.Results: A statistically significant interaction between MI type and time from symptoms was reported on cTnI concentrations (p b 0.0001): STEMI and NSTEMI differed for cTnI releases at admission and after revascularization. Higher cTnI V in STEMI was detectable in patients admitted within 6 h from symptoms. Baseline cTnI concentrations were lower in patients with a history of coronary artery disease (CAD) and increased with aging (p b 0.0001). In the elderly (>75 years), the cTnI V was significantly increased.Conclusion: STEMI and NSTEMI patients have different patterns and dynamics of cTnI release influenced by the interaction with time from symptoms, by aging and history of CAD.

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“…Unfortunately, translation of these observations from animals to humans is hindered by the lack of a specific model to study ischemia-reperfusion injury in conscious humans in vivo. 15 Recently, Annexin A5 scintigraphy has been developed to detect early signs of cell death in humans in vivo. 16,17 Annexin A5 is an endogenous protein that binds with high affinity to negatively charged phosphatidylserine.…”

Section: See P 120mentioning

confidence: 99%

Annexin A5 Scintigraphy of Forearm as a Novel In Vivo Model of Skeletal Muscle Preconditioning in Humans

et al. 2005

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Background-Nonlethal ischemia and reperfusion reduce ischemia-reperfusion-induced cell death, a phenomenon called ischemic preconditioning. In animal models, this potent endogenous protection is mimicked in vivo by administration of adenosine. In humans, exploitation of ischemic preconditioning is hindered by the lack of an appropriate in vivo model to study this phenomenon. To solve this problem, we aimed to set up an easy-to-use human in vivo model to study ischemic or pharmacological preconditioning. Methods and Results-Healthy male volunteers performed unilateral ischemic handgrip. At reperfusion, we intravenously injected technetium-99m-labeled Annexin A5, a presumed marker of ischemic injury, and we imaged both forearms and hands simultaneously with a gamma camera. Region of interest analysis (counts per pixel) and subsequent calculation of the percentage difference in radioactivity between experimental and control hands (thenar muscle; meanϮSE) revealed significant uptake to the ischemically exercised tissue (26Ϯ3% at 4 hours after reperfusion; PϽ0.05). This selective localization of Annexin A5 was reduced by ischemic preconditioning (10 minutes of ischemia plus reperfusion before ischemic exercise) or by infusion of adenosine into the brachial artery to 6Ϯ1% and 10Ϯ3%, respectively (PϽ0.05 versus ischemic exercise alone), resembling observations in animal models with infarct size as an end point.Appropriate control experiments supported our conclusion. Conclusions-Annexin

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Ischemic Preconditioning in Humans

Cited by 231 publications

References 48 publications

Effect of MPTP on mRNA expression of PGC-1α in mouse brain

Effect of MPTP on mRNA expression of PGC-1α in mouse brain

New insights in the pathophysiology of acute myocardial infarction detectable by a contemporary troponin assay

Annexin A5 Scintigraphy of Forearm as a Novel In Vivo Model of Skeletal Muscle Preconditioning in Humans

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