Assistant Professor of Medicine
Bryan McVerry received his M.D. from Georgetown University School of Medicine in 1997. Following internship in Internal Medicine and Pediatrics, he completed residency in Internal Medicine at the University of Chicago. He then went on to study out of hospital cardiac arrest during a one-year research fellowship in the Emergency Resuscitation Center at the University of Chicago. He subsequently completed clinical and research fellowships in Pulmonary and Critical Care Medicine at Johns Hopkins University under the mentorship of Joe G.N. Garcia and Brett A. Simon. In August of 2005, Dr. McVerry joined the faculty of the Division of Pulmonary, Allergy, and Critical Care Medicine at the University of Pittsburgh where he currently serves as Assistant Professor.
Dr. McVerry’s clinical interest and expertise focuses on the care of critically ill patients in the medical ICU, specifically those with acute lung injury and ARDS. In addition, he has developed an interest in endocrine dysregulation in critical illness.
Dr. McVerry’s research interest focuses primarily on basic and translational investigation of the role(s) of the pulmonary circulation in the development of, compensation for, and resolution of acute lung injury.
Acute lung injury (ALI) is characterized by endothelial permeability and subsequent leakage of protein and fluid into the extravascular compartment and alveoli. Dr. McVerry’s initial work applied basic discoveries from the Garcia laboratory and demonstrated the protective effects of the endothelial barrier enhancing agent sphingosine 1-phosphate (S1P) in a translationally relevant canine model of inflammatory ALI using quantitative CT analysis to characterize regional lung edema accumulation after intratracheal endotoxin administration (McVerry et al Amer J Resp Crit Care Med 2004, Szczepaniak et al Transl Res 2008). The figure below demonstrates the improvement in regional alveolar edema formation in endotoxin injured canine lungs (panels A,D) after treatment with intravenous S1P either prophylactically (panels B,E) or as rescue therapy (panels C,F).
Endothelial dysfunction in ALI is not limited solely to the dysregulation of barrier function. Disruption of the control of vasomotor tone in the acutely injured lung may have profound effects on regional edema formation as well as ventilation and perfusion matching and gas exchange. The figure below adapted from Easley et al (Acad Radiol 2006; 13:916) demonstrates the impairment in blood flow redistribution away from consolidated lung regions in a sheep injured with intravenous endotoxin in contrast to a sheep injured with large volume saline lung lavage. As demonstrated in the accompanying table, despite worse dependent air space consolidation, the lavaged animal displays improved oxygenation when compared to the endotoxin injured animal as a result of blood flow redistribution to better aerated regions of lung.
Dr. McVerry’s laboratory is dedicated to examining the manifestations of and mechanisms underlying endothelial dysfunction in acute lung injury and understanding the physiological ramifications thereof. Specifically, Dr. McVerry’s NIH Mentored Career Development Award (K08) focuses on the investigation of vasomotor function in the normal and injured lung using relevant in vivo model systems, a sophisticated isolated perfused mouse lung, and S1P as a pharmacological platform. In addition, the role of endothelial nitric oxide synthase and its product nitric oxide on the regulation of vascular tone and endothelial barrier integrity in the injured lung is a focus of current investigations.
Szczepaniak WS, Pitt BR, McVerry BJ. S1P2 receptor-dependent Rho-kinase activation mediates vasoconstriction in the murine pulmonary circulation induced by sphingosine 1-phosphate. Am J Physiol Lung Cell Mol Physiol. 2010 Jul;299(1):L137-45.
Szczepaniak WS, Zhang Y, Hagerty S, Crow MT, Kesari P, Garcia JG, Choi AM, Simon BA, McVerry BJ. Sphingosine 1-phosphate rescues canine LPS-induced acute lung injury and alters systemic inflammatory cytokine production in vivo. Transl Res. 2008 Nov;152(5):213-24.
McVerry BJ, Peng X, Hassoun PM, Sammani S, Simon BA, Garcia JG. Sphingosine 1-phosphate reduces vascular leak in murine and canine models of acute lung injury. Am J Respir Crit Care Med. 2004 Nov 1;170(9):987-93.
McVerry BJ, Garcia JG. In vitro and in vivo modulation of vascular barrier integrity by sphingosine 1-phosphate: mechanistic insights. Cell Signal. 2005 Feb;17(2):131-9.