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Freiberg FJ, Abahji T, Kreth S, Irnich D, Kuhlencordt PJ, Crispin A, Mussack T, Hoffmann U, Thiel M and Lang PM*
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.