Role of nitric oxide in post-ischemic gingival hyperemia in anesthetized dogs

The possible involvement of nitric oxide ( * NO) in the preservation of blood flow to the canine gingiva after compression of gingival tissue was studied. Gingival blood flow, gingival tissue oxygen partial pressure (PO 2 ), external carotid arterial blood pressure and external carotid arterial blood flow were monitored before, during, and after compression of gingival tissue in the presence and absence of the nitric oxide synthase inhibitor, N ω -nitro-L-arginine-methyl-ester (L-NAME). Compression of gingival tissue resulted in an immediate decrease in gingival blood flow and tissue PO 2 . After the compression of gingival tissue, hyperemia was observed in the gingiva, which depended on the duration of ischemia. Gingival tissue PO 2 slowly recovered during hyperemia. Pretreatment with L-NAME (60 mg/kg, i.a.) significantly suppressed reactive hyperemia in gingival tissue. The L-NAME-suppressed reactive hyperemia was partially reversed by treatment with L-arginine (60 mg/kg, i.a.). In addition, * NO was detected using an * NO selective electrode during interruption of blood flow and during reactive hyperemia in the gingiva. These results suggest that * NO contributes to the vasodilation during reactive hyperemia in gingival tissue, and aids in the maintenance of homeostasis in gingival circulation.