reproducable-paraplegia-thoracic-aortic-occlusion-murine-model-spinal

Reproducable Paraplegia by Thoracic Aortic Occlusion in a Murine Model of Spinal Cord Ischemia-reperfusion

Background
Lower extremity paralysis continues to complicate aortic interventions. The lack of understanding of the underlying pathology has hindered ...

University of Colorado

A reduction in stature (shrinkage) has been used as a measure of the load on the spine. Musculoskeletal effects of ageing may influence individual responses to compressive loading on the spine and the resultant loss in stature. The aim was to apply the technique of precision stadiometry for assessment of spinal shrinkage in a comparison of responses of two different age groups performing a regimen of circuit weight training. In all, 20 subjects (10 aged 18-25 and 10 aged 47-60 years) participated in the study. Each performed two sets of a 12-station circuit of exercises, the loading being established relative to individual capabilities. Recovery procedures using a semi-supine posture intervened between the two sets and again post-exercise; altogether seven measures of change in stature were obtained using precision stadiometry. The two groups showed a similar pattern of spinal shrinkage, losses in stature being greater for the first set compared to the later set of exercises. Subjects gained height whilst in the formal recovery posture, but responses were inconsistent during warm-up, cool-down and active recovery. Irrespective of age, the spine was less responsive to loading as the duration of activity was increased. It was concluded that provided loading is related to individual capability, healthy older operators are not necessarily compromised by their age in activities that include handling and lifting weights.

Effects of loading on spinal shrinkage in males of different age groups.

Despite investigation into preventable pharmacologic adjuncts, paraplegia continues to complicate thoracoabdominal aortic interventions. The alpha 2a adrenergic receptor agonist, dexmedetomidine, has been shown to preserve neurologic function and neuronal viability in a murine model of spinal cord ischemia reperfusion, although the mechanism remains elusive. We hypothesize that dexmedetomidine will blunt postischemic inflammation in vivo following thoracic aortic occlusion with in vitro demonstration of microglial inhibition following lipopolysaccharide (LPS) stimulation.

Interruption of spinal cord microglial signaling by alpha-2 agonist dexmedetomidine in a murine model of delayed paraplegia.

Paraplegia continues to complicate thoracoabdominal aortic interventions. The elusive mechanism of spinal cord ischemia-reperfusion injury has delayed the development of pharmacological adjuncts. Microglia, the resident macrophages of the central nervous system, can have pathological responses after a variety of insults. This can occur through toll-like receptor 4 (TLR-4) in stroke models. We hypothesize that spinal cord ischemia-reperfusion injury after aortic occlusion results from TLR-4-mediated microglial activation in mice.

Kirsten A. Freeman

Department of Surgery,
Division of Cardiothoracic Surgery,
Department of Surgery, Division of Cardiothoracic Surgery

University of Colorado

Reproducable Paraplegia by Thoracic Aortic Occlusion in a Murine Model of Spinal Cord Ischemia-reperfusion

Kirsten A. Freeman

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Department of Surgery,Division of Cardiothoracic Surgery,Department of Surgery, Division of Cardiothoracic Surgery

University of Colorado

Reproducable Paraplegia by Thoracic Aortic Occlusion in a Murine Model of Spinal Cord Ischemia-reperfusion

Department of Surgery,
Division of Cardiothoracic Surgery,
Department of Surgery, Division of Cardiothoracic Surgery