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  • Title: The effects of nimodipine on ischemic injury of the spinal cord during thoracic aortic cross-clamping.
    Author: Rhee RY, Gloviczki P, Cambria RA, Lowell RC, Okazaki H.
    Journal: Int Angiol; 1996 Jun; 15(2):153-61. PubMed ID: 8803641.
    Abstract:
    BACKGROUND: The purpose of this study was to evaluate the protective effects of a neuroselective calcium antagonist, nimodipine on spinal cord ischemia during and after thoracic aortic cross-clamping. METHODS: Thirty adult dogs underwent 60 minutes of thoracic aortic cross-clamping via a left thoracotomy. The dogs were randomized into 3 groups (n = 10) and received either intravenous control (normal saline), sham (polyethylene glycol) or nimodipine solution during a period of 150 minutes. Spinal cord perfusion (SCP) was directly monitored using a laser doppler flowmeter. After 48 hours, neurologic status was assessed using Tarlov scores and the spinal cords evaluated histologically for evidence of ischemia (grades 1-4: severe to mild ischemia). RESULTS: Twenty-six dogs survived the operation. Proximal (carotid) blood pressure increased 30-40% and cerebrospinal fluid (CSF) pressure increased 50% during cross-clamping for all 3 groups. The SCP decreased predictably during cross-clamping in all dogs but after unclamping, the nimodipine group had significantly less hyperperfusion than the saline and sham control groups (30 min after unclamping, control: 74.1 +/- 12.6 ml/min, sham: 51.8 +/- 4.15 ml/min, nimodipine: 33.1 +/- 3.9 ml/min, p = 0.04). This hyperperfusion phenomenon correlated with adverse neurologic (Tarlov score) outcome (p = 0.01). Paraplegia rates were 78% (control), 70% (sham) and 71% (nimodipine) (p = NS). The histologic grades of the spinal cords from those dogs which received nimodipine tended to correspond to better tissue preservation (control: 1.72 +/- 0.49, sham: 1.75 +/- 0.46, nimodipine: 2.14 +/- 0.56, p = NS). CONCLUSIONS: Nimodipine used as single agent therapy failed to show a statistically significant clinical neurologic benefit. However, nimodipine significantly decreased postischemic reperfusion hyperemia in the spinal cord as measured by laser doppler flowmetry. This reduced hyperperfusion, which significantly correlated with functional outcome, may be responsible for dampening neural cell damage. Thus, nimodipine should be considered as an adjunct to a multimodality approach in the prevention of spinal cord ischemia during thoracic and thoracoabdominal aortic reconstructions.
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