Ventricular premature beat—driven intermittent restoration of coronary blood flow reduces the incidence of reperfusion-induced ventricular fibrillation in a cat model of regional ischemia

Na, Heung Sik; Kim, Yang In; Yoon, Young Wook; Han, Hee Chul; Nahm, Sook Hyun; Hong, Sung Yong

doi:10.1016/s0002-8703(96)90393-2

Cited by 102 publications

(69 citation statements)

References 21 publications

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“…In fact, PostC may reduce apoptosis, necrosis, and endothelial dysfunction=activation, thus leading to a reduced endothelia=leukocyte interaction and to a reduced ROS inflammatory formation. A reduced incidence of reperfusion arrhythmias has been also observed (56,96,125). Notable, already by 1994 Grech and Ramsdale (63) had reported that intermittent reperfusion may restore sinus rhythm.…”

Section: Preconditioning and Postconditioningmentioning

confidence: 86%

Cardioprotective Pathways During Reperfusion: Focus on Redox Signaling and Other Modalities of Cell Signaling

Pagliaro

Moro

Tullio

et al. 2011

Antioxidants & Redox Signaling

114

152

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Post-ischemic reperfusion may result in reactive oxygen species (ROS) generation, reduced availability of nitric oxide (NO ), Ca 2+ overload, prolonged opening of mitochondrial permeability transition pore, and other processes contributing to cell death, myocardial infarction, stunning, and arrhythmias. With the discovery of the preconditioning and postconditioning phenomena, reperfusion injury has been appreciated as a reality from which protection is feasible, especially with postconditioning, which is under the control of physicians. Potentially cooperative protective signaling cascades are recruited by both pre-and postconditioning. In these pathways, phosphorylative= dephosphorylative processes are widely represented. However, cardioprotective modalities of signal transduction also include redox signaling by ROS, S-nitrosylation by NO and derivative, S-sulfhydration by hydrogen sulfide, and O-linked glycosylation with beta-N-acetylglucosamine. All these modalities can interact and regulate an entire pathway, thus influencing each other. For instance, enzymes can be phosphorylated and=or nitrosylated in specific and=or different site(s) with consequent increase or decrease of their specific activity. The cardioprotective signaling pathways are thought to converge on mitochondria, and various mitochondrial proteins have been identified as targets of these post-transitional modifications in both pre-and postconditioning. Antioxid. Redox Signal. 14, 833-850.

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Section: Preconditioning and Postconditioningmentioning

confidence: 86%

Cardioprotective Pathways During Reperfusion: Focus on Redox Signaling and Other Modalities of Cell Signaling

Pagliaro

Moro

Tullio

et al. 2011

Antioxidants & Redox Signaling

114

152

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“…intermittent ischemia/reperfusion). In fact, acidic reperfusion reduces the incidence of ventricular fibrillation in rat heart models of regional ischemia [28,29], and there are early reports which propose intermittent ischaemia/reperfusion as a maneuver against ventricular arrhythmias in reperfusion in different species [30][31][32], including pigs [33] and humans [34].…”

Section: Clinical Considerationsmentioning

confidence: 99%

Acidic infusion in early reperfusion affects the activity of antioxidant enzymes in postischemic isolated rat heart

Penna

Perrelli

Tullio

et al. 2013

Journal of Surgical Research

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“…In this vein, another endogenous form of ischemic protection, in which a short series of repetitive cycles of brief ischemia/reperfusion are applied immediately at the onset of reperfusion, termed postconditioning, has been reported in several tissues. [15][16][17] We have shown that 7-minute ischemia applied 5 minutes after the reperfusion onset induces an almost complete protection of retinas exposed to ischemic injury. 18 On the basis of the highly effective protection induced by IPC and postconditioning against an acute ischemic episode, the aim of this work was to analyze the effect of brief ischemia pulses on retinal damage induced by experimental diabetes.…”

mentioning

confidence: 96%

Induction of Ischemic Tolerance Protects the Retina From Diabetic Retinopathy

Fernandez

Sande

Chianelli

et al. 2011

The American Journal of Pathology

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Diabetic retinopathy is a leading cause of acquired blindness. Available treatments are not very effective. We investigated the effect of a weekly application of retinal ischemia pulses (ischemic conditioning) on retinal damage induced by experimental diabetes. Diabetes was induced by an intraperitoneal injection of streptozotocin. Retinal ischemia was induced by increasing intraocular pressure to 120 mmHg for 5 minutes; this maneuver started 3 days after streptozotocin injection and was weekly repeated in one eye, whereas the contralateral eye was submitted to a sham procedure. Diabetic retinopathy was evaluated in terms of i) retinal function (electroretinogram and oscillatory potentials), ii) integrity of blood-retinal barrier (by albumin-Evans blue complex leakage and astrocyte glial fibrillary acidic protein IHC), iii) optical and electron microscopy histopathologic studies, and iv) vascular endothelial growth factor levels (using Western blot analysis and IHC). Brief ischemia pulses significantly preserved electroretinogram a-and b-wave and oscillatory potentials, avoided albumin-Evans blue leakage, prevented the decrease in astrocyte glial fibrillary acidic protein levels, reduced the appearance of retinal edemas, and prevented the increase in vascular endothelial growth factor levels induced by experimental diabetes. When the application of ischemia pulses started 6 weeks after diabetes onset, retinal function was significantly preserved. These results indicate that induction of ischemic tolerance could constitute a fertile avenue for the development of new therapeutic strategies for diabetic retinopathy treatment.

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Ventricular premature beat—driven intermittent restoration of coronary blood flow reduces the incidence of reperfusion-induced ventricular fibrillation in a cat model of regional ischemia

Cited by 102 publications

References 21 publications

Cardioprotective Pathways During Reperfusion: Focus on Redox Signaling and Other Modalities of Cell Signaling

Cardioprotective Pathways During Reperfusion: Focus on Redox Signaling and Other Modalities of Cell Signaling

Acidic infusion in early reperfusion affects the activity of antioxidant enzymes in postischemic isolated rat heart

Induction of Ischemic Tolerance Protects the Retina From Diabetic Retinopathy

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