Assessing Post‐Stroke Cardiac Dysfunction in the Insular Ischemic Stroke Rat Model

Abstract

Patients who have suffered an ischemic stroke with damage to the right insular cortex (IC) often develop post‐stroke cardiac complications. However, the pathophysiology and time course of these post‐stroke myocardial changes require further investigation which is complicated by a lack of pre‐clinical models. The purpose of this work is to assess the time course of post‐stroke cardiac fibrosis and inflammation in a rat model of selective insular ischemic stroke. IC ischemic stroke was induced in six‐month‐old Wistar rats via unilateral stereotaxic injection of endothelin‐1 into the right IC (n=6/surgical group). Control rats received a phosphate‐buffered saline (PBS) injection into the right IC (n=6/surgical group). To establish a time course of cardiac dysfunction, hearts were histologically examined at 6, 24 hours, 7, 14 and 28 days post‐stroke for fibrosis (Masson's Trichrome stain), inflammation (CD45+, myeloperoxidase, CD3+, CD45R, CD68+ immunostaining) and endothelial dysfunction (phosphorylated endothelial nitric oxide synthase (eNOS)). Areas of interest included the 4 heart chambers and pulmonary vein/left atrium border (PV‐LA border). Results from this study showed that focal IC ischemic stroke led to neutrophil infiltration at 6 hours, followed by T lymphocyte infiltration at 7 days at the PV‐LA border. Left atrial tissue experienced long‐term fibrosis at 28 days following focal IC stroke. Further, B lymphocyte infiltration was seen at 28 days post‐stroke in left ventricular tissue. These findings provide insight into the progression of post‐stroke cardiac changes and suggest that inflammation is a treatable target to prevent post‐stroke myocardial injury.Support or Funding InformationThis study is funded by the Kathleen & Dr Henry Barnett Research Chair in Stroke Research (Western University, London, Ontario, Canada), the Western University Medical and Health Sciences Research Board Seed Research Grant, and the Edward and Alma Saraydar Neurosciences Fund (London Health Sciences Foundation).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.