Abstract
BackgroundSpinal cord injury (SCI) disrupts autonomic pathways and consequently perturbs cardiovascular homeostasis. Injuries above T6 results in loss of descending sympathetic control of the splanchnic vasculature. Blood pressure regulation is impaired resulting in resting hypotension and episodic hypertension, the latter of which is known as a life threatening condition called autonomic dysreflexia (AD). These fluctuations in arterial blood pressure following SCI may also result in dysfunction and maladaptive remodelling at the level of the splanchnic resistance vasculature.ObjectiveTo examine the time course of structural and functional adaptations of resistance mesenteric vasculature in a complete T3 transection rodent model.Design/Method15 male Wistar rats were randomly assigned to three groups: T3 SCI 1 Week (n=5), T3 SCI 1 Month (n=5), and Uninjured Control (n=5). Functional and structural assessment of primary mesenteric arteries were assessed ex vivo using a pressure myograph system. In addition to vessel morphology and myogenic tone, functional assessment of vasocontractility was assessed using α1 adrenoceptor agonist phenylephrine (PE) and methoxamine (MET).ResultsMyogenic tone is significantly impaired in the T3 SCI 1 Week and T3 SCI 1 Month groups compared to the Uninjured Control group (p = 0.0212 and p=0.0059, respectively). EC50 values were extrapolated from PE dose response curves and were lower for both the T3 SCI 1 Week and T3 SCI 1 Month groups compared to the Uninjured Control group (p<0.0001 and p=0.0004, respectively). There are no significant differences found between EC50 values determined for MET. Wall thickness is decreased and vessel diameter is increased in the T3 SCI 1 Month group compared to the Uninjured Control group (p=0.0221 and p=0.066, respectively).ConclusionHypersensitivity to the α1 adrenoceptor agonist PE but not MET suggest deficiency in the reuptake of norepinephrine in resistance mesenteric vasculature. Decreased wall thickness, in addition to an increased vessel diameter may suggest chronic outward hypotrophic remodelling.Support or Funding InformationThis research was funded by the Canadian Institute of Health Research and the Heart and Stroke Foundation of BC and Yukon.
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