Abstract.
The study was designed to investigate whether gastric microcirculation is involved in mechanisms of gastroprotective action of glucocorticoids during desensitization of capsaicin-sensitive sensory neurons (CSN). The effects of desensitization of CSN on gastric microcirculation and gastric erosions after indomethacin administration (35 mg/kg) were compared in sham-operated rats and adrenalectomized animals without and with corticosterone replacement (4 mg/ kg sc). Desensitization of CSN (by capsaicin, 100 mg/kg s. c.) and adrenalectomy or sham-operation was performed 2 or 1 weeks before experiment, respectively. An in vivo microscopy technique for the direct visualization of gastric microcirculation and the analysis of red blood cell (RBC) velocity was employed. The results obtained indicate that desensitization of capsaicin-sensitive sensory neurons potentiate indomethacin-induced microvascular disturbances in gastric submucosa and mucosa and gastric injury. These potentiated effects of the desensitization are profoundly promoted by concomitant glucocorticoid deficiency. The results suggest that protective action of glucocorticoids against indomethacin- induced injury during desensitization of CSN is provided by their maintenance of gastric blood flow.
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Received 28 July 2006; accepted 21 August 2006
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Bobryshev, P., Podvigina, T., Maltcev, N. et al. Gastric microcirculation as target of gastroprotective action of glucocorticoid hormones in rats with desensitization of capsaicin-sensitive sensory neurons. Inflammopharmacol 14, 236–242 (2006). https://doi.org/10.1007/s10787-006-1546-0
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DOI: https://doi.org/10.1007/s10787-006-1546-0