Preconditioning with ethanol prevents postischemic leukocyte-endothelial cell adhesive interactions.

@article{Yamaguchi2002PreconditioningWE,
  title={Preconditioning with ethanol prevents postischemic leukocyte-endothelial cell adhesive interactions.},
  author={Taiji Yamaguchi and Taiji Yamaguchi and Catherine B Dayton and Takeharu Shigematsu and Patsy R. Carter and Toshikazu Yoshikawa and Dean C. Gute and Ronald J. Korthuis},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2002},
  volume={283 3},
  pages={
          H1019-30
        },
  url={https://api.semanticscholar.org/CorpusID:20016170}
}
The findings suggest that EtOH-PC induces a biphasic temporal pattern of protection against the proinflammatory effects of I/R, and are consistent with the hypothesis that the late phase of Et OH-PC is triggered by NO formed secondary to adenosine A(2) receptor-dependent activation of NOS during the period of ethanol exposure.
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Antecedent Ethanol Ingestion Prevents Postischemic Leukocyte Adhesion and P-Selectin Expression by a Protein Kinase C–Dependent Mechanism

The data indicate that antecedent ethanol exposure prevents postischemic P-selectin expression, LR, and LA by a mechanism that involves activation of calcium-dependent PKC isotypes.

Phospholipase C activation is required for cardioprotection by ethanol consumption.

It is suggested that PLC activation is required for ethanol cardioprotection against ischemia/reperfusion injury, which improves myocardial recovery after MI.

Antecedent ethanol ingestion prevents postischemic microvascular dysfunction.

Role of calcitonin gene-related peptide in the postischemic anti-inflammatory effects of antecedent ethanol ingestion.

The results indicate that the effect of antecedent ethanol ingestion to prevent postischemic LR and LA is initiated by a CGRP-dependent mechanism.

Moderate Ethanol-Preconditioning Offers Ischemic Tolerance Against Focal Cerebral Ischemic/Reperfusion: Role of Large Conductance Calcium-Activated Potassium Channel

The moderate EtOH-PC protects against I/R-induced brain damage dependent on the upregulation BKCa channels based on the expression of large conductance calcium-sensitive potassium (BKCa) channels.

Cerebral Ischemia/Reperfusion Injury and Pharmacologic Preconditioning as a Means to Reduce Stroke-induced Inflammation and Damage

The major mechanism of ischemia/reperfusion injury is discussed, an overview of preconditioning in all its various forms is provided, the underlying mechanisms are described and the recent clinical application of this emerging neuroprotective strategy is reviewed.
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53 References

Ischemic preconditioning prevents postischemic P-selectin expression in the rat small intestine.

The data indicate that P-selectin expression is a novel downstream effector target of the adenosine-initiated, PKC-dependent, anti-inflammatory signaling pathway in IPC.

Cardioprotection from ischemia by a brief exposure to physiological levels of ethanol: role of epsilon protein kinase C.

Exposure to physiologically attainable ethanol levels minutes before ischemia provides cardioprotection that is mediated by direct activation of epsilonPKC in the cardiac myocytes, and is demonstrated to provide beneficial effects of moderate ethanol consumption in ischemic heart disease.

Ischemic preconditioning attenuates postischemic leukocyte adhesion and emigration.

The ability of IPC to attenuate postischemic leukocyte adhesion and emigration may be mediated by adenosine released during IPC and during reperfusion after prolonged ischemia.

The initiating factors of late preconditioning in skeletal muscle.

Both ADO and nitric oxide contribute to initiating microvascular protection in the late phase of IPC, suggesting that up regulation of ADO is the initiating factor with secondary upregulation of Nitric oxide in late preconditioning.

Acute ethanol exposure fails to elicit preconditioning-like protection in in situ rabbit hearts because of its continued presence during ischemia.

K(ATP) channels mediate the beneficial effects of chronic ethanol ingestion.

The results indicate that K(ATP) channels mediate the protective effects of chronic consumption of ethanol, which protects the myocardium from ischemic injury by activating adenosine receptors and protein kinase C.

Acute alcohol-induced protection against infarction in rabbit hearts: differences from and similarities to ischemic preconditioning.

Recent studies reveal that brief ethanol exposure induces cardioprotection against simulated ischemia in cardiomyocytes by the activation of protein kinase C- epsilon. The present study tests the…

Chronic ethanol-induced myocardial protection requires activation of mitochondrial K(ATP) channels.

It is concluded that mitochondrial K(ATP)channel activity is required for chronic ethanol-induced protection and abolished the beneficial effects of alcohol on LV contractile recovery and myocyte necrosis.

Pharmacologic stimulation of adenosine A2 receptor supplants ischemic preconditioning in providing ischemic tolerance in rat livers.

Early and Late Preconditioning Prevent Ischemia / Reperfusion Injury: Signalling Pathways Mediating the Adaptive Metamorphosis to a Protective Phenotype in Preconditioned Tissues

Observations indicate that adaptive changes in the microvasculature play a key role in the development of the preconditioned state, and understanding the mechanisms whereby both arterial and venular endothelium enter a protective or defensive phenotype as a result of preconditionsing may lead to theDevelopment of novel therapeutic strategies to manage I/R injury.
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