Background: Interventions that reduce the generation or the effects of reactive oxygen species exert beneficial effects in a variety of models of septic shock. We investigatedthe effect of tempol, a low-molecular-weight membrane-permeable radical scavenger, on mesenteric blood flow and organ injury in a murine cecal ligation and puncture (CLP) model of septic shock. Materials and Methods: Forty-four Swiss albino mice were anesthetized with chloral hydrate (400 mg/kg, i.p.) and subjected to CLP (except for the sham-operated animals). The animals were divided randomly into 4 groups: the 1st group was sham operated (sham-operated group, n = 10); the 2nd group underwent CLP and was injected with saline (CLP + saline group, n = 12); the 3rd group was sham operated and treated with tempol (10 mg/kg, i.p., sham-treated + tempol group, n = 10); the 4th group underwent CLP and was treated with tempol (10 mg/kg, i.p., CLP + tempol group, n = 12). Mesenteric arterial blood flow (MABF) was measured by Doppler ultrasound. Poly(adenosine 5′-diphosphate-ribose) polymerase (PARP) activity was examined in the liver, lung, and kidneys. Results: In the CLP + saline group, the MABF was significantly lower than in the sham-operated group (p < 0.001). After tempol administration, MABF values significantly increased (p < 0.05). We observed significantly stronger PARP-positive staining in the lungs and kidney glomeruli in the CLP + saline group than in those of the sham-operated group (plung = 0.0148, pglomeruli = 0.0025). A marked reduction in PARP activity was found in the lung and kidney glomeruli of the CLP + tempol group (plung = 0.0026, pglomeruli = 0.0085). There was no significant effect of CLP on PARP activity in the liver and kidney tubuli (pliver > 0.05, ptubuli > 0.05). Conclusion: Tempol improved MABF in a CLP-induced septic shock model. Although tempol could not prevent the activation of PARP in the liver and kidney tubuli, it did attenuate PARP activation in the lung and kidney glomeruli.

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