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Guochang Hu, MD, PhD
Research Assistant Professor

Research Interests
My research focus is to evaluate the role of caveolae-mediated transcellular transport in inflammation-induced increase in endothelial albumin permeability. We have shown
that activated neutrophils or exogenously applied reactive oxygen species increased pulmonary endothelial albumin permeability through Src-family kinase-dependent phosphorylation of caveolin-1.
Future studies will explore the molecular mechanisms of neutrophil-mediated increase in transendothelial albumin permeability as well as the interrelationship between the transcellular and
paracellular permeability pathways.
Another research interest is the mechanism of cardioprotection by volatile anesthetics against neutrophil-induced injury. Our studies have demonstrated that isoflurane and
sevoflurane abolish activated neutrophil-induced myocardial dysfunction, an action that occurred independent of KATP channel opening. These effects were associated with reductions in superoxide
anion production and neutrophil adherence to coronary vascular endothelium. Activation of adenosine receptors in neutrophils, but not in the heart, played a role in the preconditioning effects
of volatile anesthetics against neutrophil-induced contractile dysfunction.
E420 MSB
835 S. Wolcott Ave.
(312) 413-7866
gchu@uic.edu
Selected Publications
- Hu G, Salem, MR, and Crystal GJ. Isoflurane prevents platelet-induced enhancement of coronary endothelial dysfunction by neutrophils. Anesthesia and Analgesia 2005;101:(In press)
- Hu G, Salem, MR, and Crystal GJ. Role of adenosine receptors in volatile anesthetic preconditioning against neutrophil-induced contractile dysfunction in isolated rat hearts. Anesthesiology 2005;103: 287-95.
- Hu G, Salem, MR, and Crystal GJ. Isoflurane and sevoflurane precondition against neutrophils-induced contractile dysfunction in isolated rat hearts. Anesthesiology 2004;100: 489-97.
- Hu G, Vasiliauskas T, Salem, MR, Rhone DP, and Crystal GJ. Neutrophils pretreated with volatile anesthetics lose ability to cause cardiac dysfunction. Anesthesiology 2003;98: 712-8.
- Hu G, Vinten-Johansen J, Salem MR, Zhao ZQ, and Crystal GJ. Isoflurane inhibits neutrophil-endothelium interactions in the coronary circulation: lack of a role for adenosine triphosphate-sensitive potassium channels. Anesthesia and Analgesia 2002;94: 849-56.
- Crystal GJ, Zhou X, Alam S, Piotrowski A, and Hu G. Lack of role for nitric oxide in cholinergic modulation of myocardial contractility in vivo. American Journal of Physiology 2001;281:H198-H206.
- Crystal GJ, Zhou X, Gurevicius J, Czinn EA, Salem MR, Alam S, Piotrowski A, and Hu G. Direct coronary vasomotor effects of sevoflurane and desflurane in in situ canine hearts. Anesthesiology 2000;92:1103-13.
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