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The Splenic Vascular Response Following a Myocardial Infarction

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Title: The Splenic Vascular Response Following a Myocardial Infarction
Author: Ruggiero, Sara
Department: Department of Human Health and Nutritional Sciences
Program: Human Health and Nutritional Sciences
Advisor: Simpson, Jeremy
Abstract: Introduction: This thesis is an investigation into the splenic vascular response to heart failure (HF) following a myocardial infarction (MI). The spleen is the largest secondary lymphoid organ in the human body and its immunological role is well described. Previous findings suggest that the spleen plays a role in cardiac health. However, splenic physiology has never been characterized during the progression of HF. The principle aim of this thesis is to determine if splenic blood flow and/or splenic size changes during HF. We hypothesize that blood flow will be preferentially maintained to the spleen with no change in spleen size post-MI. The secondary aim of this thesis is to investigate arteriolar smooth muscle and endothelial structures within the spleen during the development of HF. We hypothesize that the splenic vasculature will not be altered during HF. Methods: At 5wks of age, rats were randomly assigned for either MI (n=58) or sham (n=56) surgery. At 2, 5 and 9wks post surgery, Doppler ultrasound measurements of the splenic, left renal, left common carotid and left femoral arteries were performed. Cardiac function was assessed at all time-points via echocardiography and at 9wks post-surgery via invasive hemodynamic analysis of the left ventricle. Immunohistochemistry was performed on the spleen, soleus and extensor digitorum longus muscles to characterize endothelial and smooth muscle vascular changes in the spleen post-MI compared to the lower limb. Results: Blood flow to the spleen and brain was preferentially maintained by 9wks post-MI, whereas blood flow to the lower limb and kidney was reduced. On further analysis of the spleen, spleen size increased by 5wks post-MI and remained elevated at 9wks. Splenic blood flow was increased with increasing organ size post-MI, whereas no association was found in sham animals. Surprisingly, vascular smooth muscle thickness increased in the spleen 9wks post-MI, despite the increase in splenic blood flow. No changes in the splenic endothelial organization or endothelial cell types within the spleen were observed. Conclusions: Blood flow to the spleen increases, vascular smooth muscle thickness increases and splenomegaly occurs during HF suggesting a greater unrealized role for the spleen during HF-induced hemodynamic compromise.
Date: 2017-04
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