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VMI
 


Vascular Medicine Institute
University of Pittsburgh
BST E1240
200 Lothrop Street
Pittsburgh, PA 15261
Phone: 412-383-5853
Fax: 412-648-5980

Small Animal Hemodynamic Core

The Small Animal Hemodynamic core, led by Dr. Ana Mora, specializes in acquisition and analysis of hemodynamic data obtained during survival and terminal studies of rat and murine models. Our team consists of surgeons, bioengineers, and technicians who have extensive experience with the design, implementation, analysis, and reporting of such studies.

Our core has streamlined the small animal hemodynamic study process, from protocol conception to final printout, to ensure generation of traceable and reproducible analysis of complex data.

Common survival procedures performed by our surgeons include pulmonary artery banding and transverse aorta constriction.  Terminal procedures include open- and closed-chest hemodynamic assessment of the right ventricle, left ventricle, pulmonary artery, and aorta. Pressure -volume loop measurements acquired via our EMKA system and high-fidelity admittance catheters, along with Doppler velocities acquired via Indus Industries system, can produce in-depth and customized characterization of a rodent’s hemodynamic phenotype. 




 

For further consultation, please contact Dr. Ana Mora

For procedure scheduling, please contact Jeffrey Baust.

 

Personnel

Director/Coordinator

Surgical Component

Bio-analytic Component



Facilities

The Hemodynamic Sub-Core is located within the Vascular Medicine Institute, Department of Medicine at the University of Pittsburgh on the 12th floor of the Biomedical Science Tower East. The Core Facility has the technology and infrastructure in place necessary to acquire direct pressure-volume measurements using Transonic catheters and Doppler flow analyses. The core has two full-equipped stations dedicated exclusively to hemodynamic studies in rodents. The Core has binocular Stereo Zoom Microscopes with Single Arm Boom Stand with halogen dissection lights, rodent ventilators (Harvard Instruments), Advantage Pressure Volume Measurement Systems (Science) with dedicated computers, and Doppler Signal Processing Workstation (Indus Instruments).


Institutional Animal Care and Use

All procedures are performed in accordance with guidelines set forth by the University of Pittsburgh Institutional Animal Care and Use Committee.


Rodent Models of PH, PAH, and Heart Remodeling

The Core has been instrumental for the establishment of multiple models of PAH in mice and rats including PA banding, Hypoxia exposure, Monocrotaline, Sugen/Hypoxia that closely recapitulate the pathogenesis and clinical outcome of human disease, and more importantly, have proven value in evaluating novel therapies

  Chronic Hypoxia Monocrotaline Sugen Hypoxia PA Banding Transverse Aortic constriction PH-HFpEF
Species Mouse Rat Rat/Mouse Rat/Mouse Rat/Mouse Rat/Mouse
Increased PAP + ++ +++ - - ++
Increased RV pressures + ++ +++ +++ - ++
Increased AO pressures - - - - - +
Increased LV pressures - - - - +++ ++
Medial Thickening Distal Muscularization ++ ++ +++ - - +
Intimal Lesions - +/- ++ - - -
RV Hypertrophy + +++ +++ +++ - ++
LV Hypertrophy - - - - +++ +
 

Support


Publications/Abstracts that involved the Core

Sharifi-Sanjani M, Shoushtari AH, Quiroz M, Baust J, Sestito SF, Mosher M, Ross M, McTiernan CF, St Croix CM, Bilonick RA, Champion HC, Isenberg JS. (2014). Cardiac CD47 drives left ventricular heart failure through Ca2+-CaMKII-regulated induction of HDAC3. J Am Heart Assoc. 3(3):e000670. PMID 24922625. PMC4309049.

Frazziano G, Al Ghouleh I, Baust J, Shiva S, Champion HC, Pagano PJ. (2014).  Nox-derived ROS are acutely activated in pressure overload pulmonary hypertension: indications for a seminal role for mitochondrial Nox4. Am J Physiol Heart Circ Physiol. 306(2):H197-205. PMID 24213612. PMC3920131. DOI:10.1152/ajpheart.00977.2012 

Kelley EE, Baust J, Bonacci G, Golin-Bisello F, Devlin JE, St Croix CM, Watkins SC, Gor S, Cantu-Medellin N, Weidert ER, Frisbee JC, Gladwin MT, Champion HC, Freeman BA, Khoo NK. (2014). Fatty acid nitroalkenes ameliorate glucose intolerance and pulmonary hypertension in high-fat diet-induced obesity. Cardiovasc Res. 101(3):352-63. PMID 24385344. PMC3928004. DOI:10.1093/cvr/cvt341

Ratt NJ, Taabima DM, Specht PA, Tejero J, Champion HC, Kim-Shapiro DB, Baust J, Mik EG, Hildesheim M, Stasch JP, Becker EM, Truebel H, Gladwin MT. (2013). Direct sGC activation bypasses NO scavenging reactions of intravascular free oxy-hemoglobin and limits vasoconstriction. Antioxid Redox Signal. PMID 23697678. PMIC3869448. DOI:10.1089/ars.2013.5181 

Weidert ER, Cantu-Medellin N, Schoenborn, SO, Khoo NK, CHampion HC, Baust J, Devlin J, Tarpey MM, St Croix CM, Kelley EE. (2013). P4: Nitrite-mediated, xanthine oxidase-dependent diminution of obesity-related hyperglycemia and cardiopulmonary dysfunction. Nitric Oxide. 31:S14–S15. DOI:10.1016/j.niox.2013.02.006 

Lai YC, Tabima DM, Baust J, Dube JJ, Chacon A, Alvarez-Perez JC, Goodpaster BH, Garcia-Ocaña A, Tofovic S, Mora AL, Gladwin MT. (2013). P47: AMPK activation by nitrite and metformin increases glut-4 mediated glucose uptake and normalizes pulmonary venous hypertension in a rat model of severe metabolic syndrome. Nitric Oxide. 31:S33–S34. DOI:10.1016/j.niox.2013.02.049 

Gor S, Kelley EE, Baust J, Bonnaci GR, Golin-Bisello F, Cantu-Medellin N, Devlin J, St Croix SM, Watkins SC, Champion HC, Freeman BA, Khoo NK. (2012). Inhibition of Obesity-Induced Pulmonary Arterial Hypertension by Electrophilic Fatty Acids. Free Radical Biology and Medicine. 53:S96. DOI:10.1016/j.freeradbiomed.2012.10.174

Cantu-Medellin N, Khoo NK, Shoenborn CJ, Weidert ER, Baust J, Champion HC, Tarpey MM, Kelley EE. (2012). Manipulation of Xanthine Oxidase-Derived Reactive Species Reduces Obesity-Induced Inflammation and Impairment of Glucose Tolerance. Free Radical Biology and Medicine. 53:S95-S96. DOI:10.1016/j.freeradbiomed.2012.10.173

Hill MR, Simon MA, Valdez-Jasso D, Zhang W, Champion HC, Sacks MS. (2014). Structural and mechanical adaptations of right ventricle free wall myocardium to pressure overload. Ann Biomed Eng. 42(12):2451-65. PMID:25164124. PMC4241140. doi: 10.1007/s10439-014-1096-3.