Intravenous hydrogen sulfide does not induce neuroprotection after aortic balloon occlusion-induced spinal cord ischemia/reperfusion injury in a human-like porcine model of ubiquitous arteriosclerosis

Bibliographic Details
Title: Intravenous hydrogen sulfide does not induce neuroprotection after aortic balloon occlusion-induced spinal cord ischemia/reperfusion injury in a human-like porcine model of ubiquitous arteriosclerosis
Authors: Andre Bredthauer, Karla Lehle, Angelika Scheuerle, Hubert Schelzig, Oscar McCook, Peter Radermacher, Csaba Szabo, Martin Wepler, Florian Simon
Source: Intensive Care Medicine Experimental, Vol 6, Iss 1, Pp 1-14 (2018)
Publisher Information: SpringerOpen, 2018.
Publication Year: 2018
Collection: LCC:Medical emergencies. Critical care. Intensive care. First aid
Subject Terms: Hydrogen sulfide, I/R injury, Ubiquitous arteriosclerosis, Aortic aneurysm, Neuro protection, Medical emergencies. Critical care. Intensive care. First aid, RC86-88.9
More Details: Abstract Objective In rodents, intravenous sulfide protected against spinal cord ischemia/reperfusion (I/R) injury during aortic balloon occlusion. We investigated the effect of intravenous sulfide on aortic occlusion-induced porcine spinal cord I/R injury. Methods Anesthetized and mechanically ventilated “familial hypercholesterolemia Bretoncelles Meishan” (FBM) pigs with high-fat-diet-induced hypercholesterolemia and atherosclerosis were randomized to receive either intravenous sodium sulfide 2 h (initial bolus, 0.2 mg kg body weight (bw)−1; infusion, 2 mg kg bw−1 h−1; n = 4) or vehicle (sodium chloride, n = 4) prior to 45 min of thoracic aortic balloon occlusion and for 8 h during reperfusion (infusion, 1 mg kg bw−1 h−1). During reperfusion, noradrenaline was titrated to maintain blood pressure at above 80% of the baseline level. Spinal cord function was assessed by motor evoked potentials (MEPs) and lower limb reflexes using a modified Tarlov score. Spinal cord tissue damage was evaluated in tissue collected at the end of experiment using hematoxylin and eosin and Nissl staining. Results A balloon occlusion time of 45 min resulted in marked ischemic neuron damage (mean of 16% damaged motoneurons in the anterior horn of all thoracic motor neurons) in the spinal cord. In the vehicle group, only one animal recovered partial neuronal function with regain of MEPs and link motions at each time point after deflating. All other animals completely lost neuronal functions. The intravenous application of sodium sulfide did not prevent neuronal cell injury and did not confer to functional recovery. Conclusion In a porcine model of I/R injury of the spinal cord, treatment with intravenous sodium sulfide had no protective effect in animals with a pre-existing arteriosclerosis.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2197-425X
Relation: http://link.springer.com/article/10.1186/s40635-018-0209-y; https://doaj.org/toc/2197-425X
DOI: 10.1186/s40635-018-0209-y
Access URL: https://doaj.org/article/b5008412a9114809a4eb502b1fce41be
Accession Number: edsdoj.b5008412a9114809a4eb502b1fce41be
Database: Directory of Open Access Journals
More Details
ISSN:2197425X
DOI:10.1186/s40635-018-0209-y
Published in:Intensive Care Medicine Experimental
Language:English