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Loren P. Thompson, PhD

Academic Title:

Adjunct Associate Professor

Primary Appointment:

Obstetrics, Gynecology and Reproductive Sciences

Secondary Appointment(s):



655 West Baltimore St. BRB 11-040

Phone (Primary):

(410) 706-4422


(410) 706-5747

Education and Training

B.A., Biology, AugustanaCollege, Rockville, IL, 1973-77

M.S., Physiology, Univ. of Minn, Duluth, MN, 1977-79

Ph.D., Physiology, MichiganStateUniversity, E.Lansing, MI, 1979-84

Research Fellow, Dept. of Physiology, Univ. of MI, Ann Arbor, MI, 1984-86

Postdoct. Assoc., Dept. of Pharmacology, Univ. of VT, Burlington, VT, 1986-90



I received my Ph.D. in cardiovascular physiology from Michigan State University in East Lansing, MI in 1984.  I spent 2 years at the University of Michigan in Ann Arbor, MI and 5 years at the University of Vermont in Burlington, VT as a post-doctoral fellow studying vascular mechanisms in hypertensive diseased models.  I spent 5 years at the University of Iowa in Iowa City, IA as a Research Scientist.  I joined the faculty at the University of Maryland, Baltimore in 1996 in the Dept. of Obstetrics, Gynecology and Reproductive Sciences as an Asst. Professor and am currently an Assoc. Professor.  I also have a secondary appointment in the Dept. of Physiology as an Assoc. Professor where my duties are to teach in the Physiology Section of the Medical School Curriculum.  I am a member of the The American Physiological Society, The Perinatal Research Society and The Society for Reproductive Investigation. 

Research/Clinical Keywords

fetus, heart, mitochondria, hypoxia, placenta, cardiovascular programming

Highlighted Publications

Dong Y and Thompson LP.  Differential expression of eNOS in coronary and cardiac tissue of hypoxic fetal guinea pig hearts.  J. Soc. Gynecol. Invest. 13: 483-90, 2006.

Thompson LP, Al-Hasan Y.  Impact of oxidative stress in fetal programming.  J Pregnancy.  vol. 2012  doi:10.1155/2012/582748.

Evans, LC, Liu H, Pinkas G, Thompson LP. Chronic hypoxia increases peroxynitrite, MMP9 expression, and collagen accumulation in fetal guinea pig hearts.  Pediatr Res 71 (1): 25-31, 2012.

Al-Hasan YM, Pinkas GA, Thompson LP. Prenatal hypoxia reduces mitochondrial protein expression and cytochrome c oxidase activity in guinea pig offspring hearts.Reproductive Sciences. Jan 9;21(7):883-891, 2014.

Thompson LP, Crimmins S, Telugu B, Turan S. Intrauterine hypoxia: clinical consequences and therapeutic perspectives.  Research and Reports in Neonatalogy. 5:79-89, 2015.

Research Interests

Prolonged exposure to reduced oxygen levels (hypoxic stress) is the leading cause of fetal morbidity and mortality.  Under normal conditions, the fetus develops in a relatively reduced oxygen environment.  Yet, it has undergone cardiovascular adaptations that favor delivery of its oxygen and nutrient needs.  Under conditions of intrauterine hypoxia (where oxygen levels are further reduced from normal), the fetus is vulnerable to hypoxic stress.  The fetus’s ability to adapt to this stress depends on the length and severity of the exposure, although may result in intrauterine growth restriction, fetal brain damage and altered cardiac function.  Epidemiological studies and animal models have now identified a strong association between reduced fetal growth and an increased risk of disease in the adult, suggesting the importance of fetal health on adult well-being.    

A reduction in oxygen levels has been shown to stimulate the expression of a variety of oxygen-sensitive genes (such as HIF-1, iNOS, and VEGF) and as an adaptive mechanism for cell survival.  We have identified that prolonged exposure to hypoxia increases gene expression of some of these factors, contributing to both adaptive and maladaptive responses in the fetal cardiovascular system.  Thus, our research interest focuses on the effect of hypoxic stress on the expression of oxygen-sensitive genes and how altered gene expression influences cardiac function and blood vessel reactivity in both the fetus and the affected offspring through cardiovascular programming.  Further, we are also interested in the effect of hypoxia on trophoblast invasion of the placenta and its impact on spiral artery remodeling, placental perfusion, and maternal and fetal consequences.

Awards and Affiliations

American Physiological Society, 1986-present

Society of Reproductive Investigation, 1994-presen

Perinatal Research Society, 1995-present

Excellence in Teaching Award, Dept. of Physiology, UMB SOM, Cardiovascular and Integrative Lectures, 2007-12

Grants and Contracts

NIH RO1 (PI)  Impact of prenatal hypoxia on mitochondrial funciton of offspring hearts, 9/1/15-5/31/19

UMB-Dept. of Ob/Gyn/Repro Sci. Seed Grant Award (Thompson/Turan) Detection of fetal cardiac biomarkers in congenital heart defects by small RNA sequencing, 10/1/14-9/30/

Completed Grants

UMB-UMCP Seed Grant (Co-PI)  Development of a novel animal model for human preeclampsia, 8/1/13-7/31/14

NIH RO1 HL49999-17 (PI) Fetal hypoxemia and endothelium-derived nitric oxide,  5/1/1995 - 4/30/12

NIH NRSA Predoctoral Fellowship Grant for Promoting Diversity in Health Related Research (Mentor) 7/1/08-6/30/11


Lab Techniques and Equipment

We have developed an animal model of chronic fetal hypoxia using the pregnant guinea pig.  We use a combination of techniques to investigate the effect of hypoxia on gene expression in the fetal heart and blood vessels.  We utilize the wire myograph and isolated, perfused heart preparations to quantify effects on vascular and cardiac function.  mRNA expression is quantified using qPCR, protein expression by Western blot analysis and protein localization by immunocytochemistry.  We utilize a variety of commercially available kits to assess enzymatic activity and protein levels in tissues and isolated cells.  We also isolate mitochondria, quantitate mitochondrial protein expression and measure cardiomyocyte respiration as indices of mitochondrial function in isolated heart cells and placenta.