"Mesenteric Vascular Dysregulation and Intestinal Inflammation Accompan" by Emily Swartz Besecker, Gina M. Deiter et al.

Health Sciences Faculty Publications

Title

Mesenteric Vascular Dysregulation and Intestinal Inflammation Accompanies Experimental Spinal Cord Injury

Authors

Emily Swartz Besecker, Gettysburg CollegeFollow
Gina M. Deiter, Penn State College of MedicineFollow
Nicole Pironi, Muhlenberg College
Timothy K. Cooper, The Pennsylvania State University College of Medicine
Gregory Michael Holmes, Penn State College of MedicineFollow

Document Type

Article

Publication Date

11-9-2016

Department 1

Health Sciences

Abstract

Cervical and high thoracic spinal cord injury (SCI) drastically impairs autonomic nervous system function. Individuals with SCI at thoracic spinal-level 5 (T5) or higher often present cardiovascular disorders that include resting systemic arterial hypotension. Gastrointestinal (GI) tissues are critically dependent upon adequate blood flow and even brief periods of visceral hypoxia triggers GI dysmotility. The aim of this study was to test the hypothesis that T3-SCI induces visceral hypoperfusion, diminished postprandial vascular reflexes and concomitant visceral inflammation. We measured in vivo systemic arterial blood pressure and superior mesenteric artery (SMA) and duodenal blood flow in anesthetized T3-SCI rats at 3 days and 3 weeks post-injury either fasted or following enteral feeding of a liquid mixed-nutrient meal (Ensure™). In separate cohorts of fasted T3-SCI rats, markers of intestinal inflammation were assayed by qRT-PCR. Our results show that T3-SCI rats displayed significantly reduced SMA blood flow under all experimental conditions (p<0.05). Specifically, the anticipated elevation of SMA blood flow in response to duodenal nutrient infusion (postprandial hyperemia) was either delayed or absent after T3-SCI. The dysregulated SMA blood flow in acutely-injured T3-SCI rats coincides with abnormal intestinal morphology and elevation of inflammatory markers, all of which resolve after 3 weeks. Specifically, Icam1, Ccl2 (MCP-1) and Ccl3 (MIP-1α) were acutely elevated following T3-SCI. Our data suggest that arterial hypotension diminishes mesenteric blood flow necessary to meet mucosal demands at rest and during digestion. The resulting GI ischemia and low-grade inflammation may be an underlying pathology leading to GI dysfunction seen following acute T3-SCI.

Copyright Note

This is the author's version of the work. This publication appears in Gettysburg College's institutional repository by permission of the copyright owner for personal use, not for redistribution.

Recommended Citation

Besecker, Emily Swartz, Gina M. Deiter, Nicole Pironi, Timothy K. Cooper, and Gregory Michael Holmes. "Mesenteric Vascular Dysregulation and Intestinal Inflammation Accompanies Experimental Spinal Cord Injury." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (2016).