Abstract Objective: Periodontitis is associated with endothelial dysfunction, which is clinically characterized by a reduction in endothelium-dependent relaxation. However, we have previously shown that impairment in endothelium-dependent relaxation is transient. Therefore, we evaluated which mediators are involved in endothelium-dependent relaxation recovery. Material and methods: Rats were subjected to ligature-induced experimental periodontitis. Twenty-one days after the procedure, the animals were prepared for blood pressure recording, and the responses to acetylcholine or sodium nitroprusside were obtained before and 30 minutes after injection of a nitric oxide synthase inhibitor (L-NAME), cyclooxygenase inhibitor (Indomethacin, SC-550 and NS- 398), or calcium-dependent potassium channel blockers (apamin plus TRAM- 34). The maxilla and mandible were removed for bone loss analysis. Blood and gingivae were obtained for C-reactive protein (CRP) and myeloperoxidase (MPO) measurement, respectively. Results: Experimental periodontitis induces bone loss and an increase in the gingival MPO and plasmatic CRP. Periodontitis also reduced endothelium-dependent vasodilation, a hallmark of endothelial dysfunction, 14 days after the procedure. However, the response was restored at day 21. We found that endothelium-dependent vasodilation at day 21 in ligature animals was mediated, at least in part, by the activation of endothelial calcium-activated potassium channels. Conclusions: Periodontitis induces impairment in endothelial-dependent relaxation; this impairment recovers, even in the presence of periodontitis. The recovery is mediated by the activation of endothelial calcium-activated potassium channels in ligature animals. Although important for maintenance of vascular homeostasis, this effect could mask the lack of NO, which has other beneficial properties.

OBJETIVO: Avaliar a cicatrização colônica em ratos espontaneamente hipertensos. MÉTODOS: Cinquenta ratos machos, jovens e isogênicos. Vinte e cinco ratos da linhagem Wistar Kyoto (WKY) como controle e vinte e cinco ratos espontaneamente hipertensos (SHR) como grupo experimento. Realizou-se colotomia e colorrafia a 2,5 cm da reflexão peritoneal. Alocaram-se os animais aleatoriamente em sub-grupos para avaliação no terceiro, sétimo e décimo quarto dias de pós-operatório. Foram avaliados a concentração de angiotensina II, a resistência da anastomose à insuflação, a epitelização, a organização das túnicas da parede intestinal, a reação inflamatória e a deposição de colágeno. RESULTADOS: A avaliação da resistência da anastomose, epitelização, organização das túnicas e deposição de colágeno não foi significativa entre os grupos. A reação inflamatória foi mais intensa no grupo controle na avaliação do terceiro dia de pós-operatório (p=0,023) igualando-se ao grupo experimento nos demais tempos. CONCLUSÃO: A hipertensão arterial sistêmica, em ratos, não influenciou de forma significante no processo cicatricial de anastomoses do cólon.

PURPOSE: Evaluation of colonic healing in spontaneously hypertensive rats. METHODS: Fifty male, young and inbred rats were used. Twenty-five Wistar Kyoto rats (WKY) as control and twenty-five spontaneously hypertensive rats (SHR) as an experimental group. Colotomy and bowel suture at 2.5 cm from the peritoneal reflection were performed. All animals were allocated randomly into sub-groups for review at the third, seventh and fourteenth days after surgery. We evaluated the concentration of angiotensin II, the burst pressure, epithelialization, the organization of the tunics of the bowel wall, inflammatory response and collagen deposition. RESULTS: The burst pressure, epithelialization, organization of the tunics and collagen deposition was not significant between groups. The inflammatory reaction was more intense in the control group on the third postoperative day (p=0.023) as the experimental group on the remaining time. CONCLUSION: Systemic arterial hypertension in rats did not influence significantly the healing process of colonic anastomoses.