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Investigating a Model for Acute Ischemic Pain in Humans | OMICS International | Abstract
ISSN: 2167-0846

Journal of Pain & Relief
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Research Article

Investigating a Model for Acute Ischemic Pain in Humans

Freiberg FJ1, Abahji T2, Kreth S1, Irnich D1, Kuhlencordt PJ2, Crispin A3, Mussack T4, Hoffmann U2, Thiel M1,5 and Lang PM1*
1Department of Anaesthesiology, Ludwig Maximilians University, Munich, Germany
2Department of Angiology, Ludwig Maximilians University, Munich, Germany
3Department of Biometry, Epidemiology and Medical Informatics, Ludwig Maximilians University, Germany
4Department of Surgery, Ludwig Maximilians University, Munich, Germany
5Department of Anaesthesiology and Intensive Care Medicine, University Medical Centre Mannheim, Medical Faculty Mannheim, Ruprecht Karls University Heidelberg, Mannheim, Germany
Corresponding Author : Philip M. Lang
Department of Anaesthesiology
Ludwig Maximilians University
Marchioninistr. 15, 81377 München, Germany
Tel: +49 89 4400 73429
Fax: +49 89 4400 78886
E-mail: philip. [email protected]
Received December 19, 2014; Accepted February 10, 2015; Published February 12, 2015
Citation: Freiberg FJ, Abahji T, Kreth S, Irnich D, Kuhlencordt PJ, et al. (2015) Investigating a Model for Acute Ischemic Pain in Humans. J Pain Relief 4:172. doi: 10.4172/2167-0846.1000172
Copyright: © 2015 Freiberg JF, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Background:

The pathophysiology of acute ischemic pain is not well established. The aim of the present study was to investigate acute ischemic pain in humans with a view to establish a scientific model to perform future studies. We examined whether peripheral nerve damage and acute inflammation occur during short episodes of acute ischemia.

Methods: Eleven patients with unilateral peripheral arterial disease (PAD) performed treadmill exercise until intolerable ischemic pain urged them to stop. Blood samples were taken before, immediately after treadmill exercise and after a period of recovery. S100B-serum was detected via Elecsys® S100B Immunoassay and IL-6 levels determined via COBAS® IL6 Elecsys 2010.

Results: Treadmill exercise led to intolerable exercise-induced ischemic pain (Numeric Rating Scale) 9 ± 0.3 (0- 10, mean ± SEM)) in the PAD affected leg. Reduced ankle/brachial-index (ABI) (0.13 ± 0.05 mean ± SEM) with a mean ankle pressure of 26 ± 9 mmHg, pO2, pH and increased serum lactate indicated that severe ischemia occurred in the PAD affected leg. The inflammation marker IL-6 increased locally and systemically post exercise (n.s.).

Conclusion: We present an effective method to examine acute ischemic pain in humans. By focusing on changes in metabolic parameters in the affected limb, this model could potentially help to evaluate and detect changes during acute ischemic pain and thus contribute to the understanding of the underlying pathophysiology.

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