Cerebral blood flow alteration following acute myocardial infarction in mice

Author:

Kaplan Abdullah1,Yabluchanskiy Andriy2,Ghali Rana1,Altara Raffaele345,Booz George W.6,Zouein Fouad A.1

Affiliation:

1. Department of Pharmacology and Toxicology, American University of Beirut Faculty of Medicine, Beirut, Lebanon

2. Translational Geroscience Laboratory, Reynold’s Oklahoma Center on Aging, Department of Geriatric Medicine, Oklahoma City, OK, U.S.A.

3. Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway

4. KG Jebsen Center for Cardiac Research, Oslo, Norway

5. Department of Pathology, School of Medicine, University of Mississippi Medical Center, Jackson, MS, U.S.A.

6. Department of Pharmacology and Toxicology, University of Mississippi Medical Center, School of Medicine, Jackson, MS, U.S.A.

Abstract

Heart failure is associated with low cardiac output (CO) and low brain perfusion that imposes a significant risk for accelerated brain ageing and Alzheimer’s disease (AD) development. Although clinical heart failure can emerge several years following acute myocardial infarction (AMI), the impact of AMI on cerebral blood flow (CBF) at early stages and up to 30 days following MI is unknown. Sixteen months old male mice underwent left anterior descending (LAD) coronary artery ligation. Hemodynamics analyses were performed at baseline and at days 1, 7, and 30 post-MI. Left ventricular (LV) ejection fraction (EF), LV volumes, CO, and right common carotid artery (RCCA) diameter were recorded by echocardiography. RCCA flow (RCCA FL) was measured by Doppler echocardiography. LV volumes consistently increased (P<0.0012) and LV systolic function progressively deteriorated (P<0.0001) post-MI. CO and RCCA FL showed a moderate but significant decrease over the course of MI with similar fluctuation pattern such that both variables were decreased at day 1, increased at day 7, and decreased at 30 days post-MI. Correlation and regression analyses between CO and RCCA FL showed a strong correlation with significance at baseline and day 30 post-MI (R = 0.71, P=0.03, and R = 0.72, P=0.03, respectively). Days 1 and 7 analyses between CO and RCCA FL showed moderate correlation with non-significance post-MI (R = 0.51, P=0.2, and R = 0.56, P=0.12, respectively). In summary, CBF significantly decreased following AMI and remained significantly decreased for up to 30 days, suggesting a potential risk for brain damage that could contribute to cognitive dysfunction later in life.

Publisher

Portland Press Ltd.

Subject

Cell Biology,Molecular Biology,Biochemistry,Biophysics

Reference61 articles.

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