John G. Krolikowski

Hyperglycemia prevents isoflurane-induced preconditioning against myocardial infarction.

Is isoflurane-induced preconditioning dose related?

The role of mitochondrial and sarcolemmal K(ATP) channels in canine ethanol-induced preconditioning in vivo.

Isoflurane-induced preconditioning is attenuated by diabetes.

Increases in coronary collateral blood flow produced by sevoflurane are mediated by calcium-activated potassium (BKCa) channels in vivo.

Isoflurane does not produce a second window of preconditioning against myocardial infarction in vivo.

Adenosine type 1 (A1) receptors mediate protection against myocardial infarction produced by chronic, intermittent ingestion of ethanol in dogs.

Atrial pacing lead location alters the hemodynamic effects of atrial-ventricular delay in dogs with pacing induced cardiomyopathy.

N-acetylcysteine restores isoflurane-induced preconditioning against myocardial infarction during hyperglycemia.

Cardioprotection by glucose-insulin-potassium: dependence on KATP channel opening and blood glucose concentration before ischemia.

Isoflurane produces delayed preconditioning against myocardial ischemia and reperfusion injury: role of cyclooxygenase-2.

Cyclooxygenase-2 mediates ischemic, anesthetic, and pharmacologic preconditioning in vivo.

Intravenous emulsified halogenated anesthetics produce acute and delayed preconditioning against myocardial infarction in rabbits.

Isoflurane protects against myocardial infarction during early reperfusion by activation of phosphatidylinositol-3-kinase signal transduction: evidence for anesthetic-induced postconditioning in rabbits.

Role of endothelial nitric oxide synthase as a trigger and mediator of isoflurane-induced delayed preconditioning in rabbit myocardium.

Morphine enhances isoflurane-induced postconditioning against myocardial infarction: the role of phosphatidylinositol-3-kinase and opioid receptors in rabbits.

Inhibition of mitochondrial permeability transition enhances isoflurane-induced cardioprotection during early reperfusion: the role of mitochondrial KATP channels.

Role of Erk1/2, p70s6K, and eNOS in isoflurane-induced cardioprotection during early reperfusion in vivo.

Inhibition of glycogen synthase kinase enhances isoflurane-induced protection against myocardial infarction during early reperfusion in vivo.

The influence of B-cell lymphoma 2 protein, an antiapoptotic regulator of mitochondrial permeability transition, on isoflurane-induced and ischemic postconditioning in rabbits.

Gender-specificity of delayed preconditioning by isoflurane in rabbits: potential role of endothelial nitric oxide synthase.

Inhibition of apoptotic protein p53 lowers the threshold of isoflurane-induced cardioprotection during early reperfusion in rabbits.

Noble gases without anesthetic properties protect myocardium against infarction by activating prosurvival signaling kinases and inhibiting mitochondrial permeability transition in vivo.

Diabetes abolishes sildenafil-induced cGMP-dependent protein kinase-I expression and cardioprotection.

Simvastatin restores ischemic preconditioning in the presence of hyperglycemia through a nitric oxide-mediated mechanism.

Reactive oxygen species and mitochondrial adenosine triphosphate-regulated potassium channels mediate helium-induced preconditioning against myocardial infarction in vivo.

The mechanism of helium-induced preconditioning: a direct role for nitric oxide in rabbits.

Inhibition of glycogen synthase kinase or the apoptotic protein p53 lowers the threshold of helium cardioprotection in vivo: the role of mitochondrial permeability transition.

Role of heat shock protein 90 and endothelial nitric oxide synthase during early anesthetic and ischemic preconditioning.

Morphine reduces the threshold of helium preconditioning against myocardial infarction: the role of opioid receptors in rabbits.

Transient metabolic alkalosis during early reperfusion abolishes helium preconditioning against myocardial infarction: restoration of cardioprotection by cyclosporin A in rabbits.

Abnormal fibrillin-1 expression and chronic oxidative stress mediate endothelial mesenchymal transition in a murine model of systemic sclerosis.

4F decreases IRF5 expression and activation in hearts of tight skin mice.

Metal ions activate vascular endothelial cells and increase lymphocyte chemotaxis and binding.

An IRF5 Decoy Peptide Reduces Myocardial Inflammation and Fibrosis and Improves Endothelial Cell Function in Tight-Skin Mice.

Inputs to medullary respiratory neurons from a pontine subregion that controls breathing frequency.

Intralipid Increases Nitric Oxide Release from Human Endothelial Cells During Oxidative Stress.