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

URN to cite this document:

urn:nbn:de:bvb:355-epub-384072 Copy

DOI to cite this document:

10.5283/epub.38407 Copy

Bredthauer, Andre ; Lehle, Karla ; Scheuerle, Angelika ; Schelzig, Hubert ; McCook, Oscar ; Radermacher, Peter ; Szabo, Csaba ; Wepler, Martin ; Simon, Florian

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Date of publication of this fulltext: 01 Mar 2019 12:18

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Details

Item type:	Article
Journal or Publication Title:	Intensive Care Medicine Experimental
Publisher:	Springer Open
Volume:	6
Number of Issue or Book Chapter:	1
Page Range:	pp. 1-14
Date:	24 October 2018
Institutions:	Medicine > Lehrstuhl für Herz-, Thorax- und herznahe Gefäßchirurgie
Projects:	Open Access Publizieren (DFG)
Identification Number:	Value Type 10.1186/s40635-018-0209-y DOI
Keywords:	Hydrogen sulfide; I/R injury; Ubiquitous arteriosclerosis; Aortic aneurysm; Neuro protection
Dewey Decimal Classification:	600 Technology > 610 Medical sciences Medicine
Status:	Published
Refereed:	Yes, this version has been refereed
Created at the University of Regensburg:	Yes
Item ID:	38407

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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 ...

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.

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Metadata last modified: 29 Sep 2021 07:41

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