William M. Armstead
Research Associate Professor of Anesthesiology and Critical Care
Department: Anesthesiology and Critical Care
Graduate Group Affiliations
Contact information
Department of Anesthesiology and Critical Care
3620 Hamilton Walk, JM3
Philadelphia, PA 19104-4283
3620 Hamilton Walk, JM3
Philadelphia, PA 19104-4283
Office: 215-573-3674
Fax: 215-349-5078
Fax: 215-349-5078
Email:
armsteaw@uphs.upenn.edu
armsteaw@uphs.upenn.edu
Publications
Links
Search PubMed for articles
Pharmacological Sciences Graduate Group Faculty
Department of Anesthesiology and Critical Care
Search PubMed for articles
Pharmacological Sciences Graduate Group Faculty
Department of Anesthesiology and Critical Care
Education
B.A. (Biochemistry)
University of Pennsylvania, 1979.
M.S. (Pharmacology)
Tulane University, 1983.
Ph.D. (Pharmacology)
Tulane University, 1985.
Permanent linkB.A. (Biochemistry)
University of Pennsylvania, 1979.
M.S. (Pharmacology)
Tulane University, 1983.
Ph.D. (Pharmacology)
Tulane University, 1985.
Description of CVI Expertise
CVI Program Unit(s):Cardiovascular Development / Congenital Heart Disease
Channel Biology / Electrophysiology
Thrombosis / Hemostasis
CVI Research Description:
I am interested in the control of cerebral hemodynamics, particularly in the perinate, during physiologic and pathologic conditions such as traumatic brain injury and cerebral hypoxia/ischemia. Recent topic areas include the contribution of plasminogen activators and K channels to such control of cerebral hemodynamics as a function of age.
Selected Publications
Jagolino AL and WM Armstead: PTK, MAPK, and NOC/oFQ impair hypercapnic cerebrovasodilation after hypoxia/ischemia. Am J Physiol 284: H101-H107, 2003.Armstead WM: ET-1 contributes to age dependent G protein impairment after brain injury J Neurotrauma 20: 105-110, 2003.
Philip S and WM Armstead.: Newborn pig nociceptin/orphanin FQ activates protein tyrosine kinase and mitogen activated protein kinase to impair NMDA cerebrovasodilation after ischemia. Neuro Report 14: 201-203, 2003.
Armstead WM: Protein kinase C activation generates superoxide and contributes to impairment of cerebrovasodilation induced by G protein activation after brain injury. Brain Res 971: 153-160, 2003.
Armstead WM: COX-2 dependent superoxide generation contributes to age dependent impairment of G protein mediated cerebrovasodilation. Anesthesiology 98: 1378-1383, 2003.
Ross J and Armstead WM: Differential role of PTK and ERK MAPK in superoxide impairment of KATP and Kca channel cerebrovasodilation. Am J Physiol 285: R149-R154, 2003.
Armstead WM: NOC/oFQ activates PKC and generates superoxide to impair hypotensive cerebrovasodilation after hypoxia/ischemia. Med Sci Monit 8: BR8-14, 2002.
Armstead WM: Protein tyrosine kinase and mitogen activation protein kinase activation contribute to KATP and Kca channel impairment after brain injury. Brain Res 943: 276-282, 2002.
Armstead WM: NOC/oFQ and NMDA contribute to piglet hypoxic ischemic hypotensive cerebrovasodilation impairment. Ped Res 51: 586-591, 2002.
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