Eric R. Gross
Academic Appointments
- Instructor, Anesthesia
Key Documents
Contact Information
-
Clinical Offices
Department of Anesthesia 300 Pasteur Dr H3580 MC 5640 Stanford, CA 94305 Tel Work (650) 497-8000 Fax (650) 725-8544
- Academic Offices
Not for medical emergencies or patient use
Professional Overview
Clinical Focus
- Anesthesia
Administrative Appointments
- Director, Stanford Anesthesia Research Seminars (FNR) (2012 - present)
- Member, Stanford Society of Physician Scholars (2010 - present)
- Member, Stanford Pharmacy and Therapeutics Committee (2009 - present)
Honors and Awards
- Kosaka Award Finalist, International Anesthesia Research Society (IARS) Annual Meeting (2010)
- Resident Research Award, 1st Place, New York Society of Anesthesiologists (2010)
- Young Investigator Award, Runner-Up, International Society For Heart Research (ISHR) Annual Meeting (2005)
Professional Education
| Residency: | Stanford University CA (2011) |
| Internship: | St. Joseph's Regional Medical Center WI (2008) |
| Medical Education: | Medical College of Wisconsin WI (2007) |
| Anesthesiology: | Stanford University, Anesthesiology (2011) |
| MD: | Medical College of Wisconsin, Medicine (2007) |
| PhD: | Medical College of Wisconsin, Pharmacology (2005) |
Graduate & Fellowship Program Affiliations
Scientific Focus
Current Research Interests
I am an anesthesiologist working in the laboratory of Dr. Daria Mochly-Rosen. My interest is in TRPV1 channels, the ion channel which gives you the hot sensation in your mouth after you eat that chili pepper.
What's interesting is that this channel opening may be a natural pathway for the organs to protect themselves from ischemia-reperfusion injury. In time, this lack of or repeated stimulus may change the TRPV1 receptor to make it more sensitive or less sensitive to pain.
I have a few projects that I am presently working on:
1. How does TRPV1 activation reduce myocardial cellular injury?
2. How does TRPV1 modulate the sensitivity of the pain sensation?
3. Why does capsaicin, the TRPV1 activator, have different pain responses in different ethnic populations (Asian, Caucasians, African Americans)?
4. How does hyperglycemia or diabetes decrease TRPV1 expression and function and is this why many diabetic patients have peripheral neuropathy and silent myocardial infarctions?
My previous basic science research background involves examining the mechanism of how opioids and volatile anesthetics protect tissue from ischemia-reperfusion injury and what are the molecular mechanisms involved both through in vivo and cellular models of ischemia-reperfusion injury. I believe that TRPV1 receptors have an integral role in this protection. Send me an email if you are interested.
Publications
- Factors mediating remote preconditioning of trauma in the rat heart: central role of the cytochrome p450 epoxygenase pathway in mediating infarct size reduction. J Cardiovasc Pharmacol Ther. 2013; (1): 38-45
- Hunter syndrome in an adult: beware of tracheal stenosis. Anesth Analg. 2010; (2): 642-3
- Acute methadone treatment reduces myocardial infarct size via the delta-opioid receptor in rats during reperfusion. Anesth Analg. 2009; (5): 1395-402
- Activation of kappa-opioid receptors at reperfusion affords cardioprotection in both rat and mouse hearts. Basic Res Cardiol. 2008; (5): 454-63
- Delayed cardioprotection afforded by the glycogen synthase kinase 3 inhibitor SB-216763 occurs via a KATP- and MPTP-dependent mechanism at reperfusion. Am J Physiol Heart Circ Physiol. 2008; (3): H1497-500
- Diabetes abolishes morphine-induced cardioprotection via multiple pathways upstream of glycogen synthase kinase-3beta. Diabetes. 2007; (1): 127-36
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