Gabriel J. Hauser, M.D.

Professor and Vice Chairman, Department of Pediatrics
Professor, Department of Physiology and Biophysics

• M.D., Sackler School of Medicine, 1979

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There has been significant progress in recent years in our understanding of the mechanisms underlying hypotension in patients with Septic Shock as more information on protein and molecular pathways became available. Our laboratory focused on several steps along the pathway of endotoxin-immune cells-cytokines-nitric oxide-vascular smooth muscle cell function. We have studied the role of oxygen free radicals in TNF toxicity in mice, role of Neuropeptide Y and its inhibitors in vasoconstrictor response to endotoxin in rats with septic and hemorrhagic shock, and the role of heat-shock protein induction on iNOS induction and its protective role in endotoxin-induced hypotension and vascular smooth muscle hypocontraction. These studies were conducted in animal models of i.v. endotoxin and cecal ligation and puncture. We also studied the role of tyrosine kinase inhibitors on these pathways, demonstrating that TK inhibitors play a role in nitric-oxide-mediated vascular smooth muscle dysfunction.

Representative Publications:

• Hauser GJ, Myers AK, Dayao EK and Zukowska-Grojec Z: Neuropeptide Y infusion improves hemodynamics and survival in rat endotoxic shock. Am J Physiol, 270:H796-H800, 1996.
• Hauser GJ, Dayao EK, Wasserloos K, Pitt BR and Wong H: HSP Induction inhibits iNOS mRNA expression and attenuates hypotension in endotoxin-challenged rats. Am J Physiol, 271:H2529-H2535, 1996.
• Klein SM, Wong HR, Dayao EK and Hauser GJ: Tyrosine kinase inhibition attenuates sepsis-induced vasoplegia and iNOS mRNA expression in rats but does not affect NF-kB nuclear translocation. Shock, 14:544-549, 2000

More Publications at PubMed

Related Links:

• Division of Pediatric Critical Care and Pulmonary Medicine