Impairment of neurogenic inflammatory and anti-inflammatory responses in diabetic rats

József Németh, Márta Thán, Réka Sári, Barna Peitl, Gábor Oroszi, Beatrix Farkas, János Szolcsányi, Zoltán Szilvássy

Research output: Article

10 Citations (Scopus)


The effect was studied of a primary (preconditioning) neurogenic inflammatory challenge induced by electrical stimulation of the peripheral stump of the sciatic nerve (20 V, 0.5 ms, 5 Hz, for 5 min) on neurogenic oedema (5 min later) induced by stimulation of the contralateral sciatic nerve. Plasma extravasation due to the second stimulation was decreased by 52.7 ± 3.1% (P < 0.01) in normal animals and by 29.7 ± 2.2 and 18.1 ± 1.5% with 50 mg/kg streptozotocin pretreatment i.v. 4 and 8 weeks previously, respectively. Subsequently, bilateral sciatic nerve stimulation increased baseline plasma somatostatin levels from 6.4 ± 0.3, 11.7 ± 1.4, and 16.8 ± 3.8 to 28.3 ± 2.9 (P < 0.01), 17.9 ± 3.7, and 25.1 ± 1.7 pmol/l in normal, and 4- and 8-week diabetic animals, respectively. We conclude that experimental diabetes impairs the capability of a preconditioning neurogenic inflammatory episode to elicit a systemic anti-inflammatory effect. This is accompanied by a deficiency in elevation of the plasma somatostatin level in response to nerve stimulation, although the baseline plasma somatostatin level increases proportionally to the duration of experimental diabetes.

Original languageEnglish
Pages (from-to)83-88
Number of pages6
JournalEuropean Journal of Pharmacology
Issue number1
Publication statusPublished - dec. 10 1999

ASJC Scopus subject areas

  • Pharmacology

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