No abstract

I Prostaglandin E2 dose-dependently and reversibly inhibited the noradrenaline overflow resulting from nerve stimulation of the rabbit kidney. 2 The magnitude of this inhibition varied inversely with the frequency of stimulation employed. 3 The prostaglandin synthesis inhibitors, indomethacin and meclofenamic acid, both increased the transmitter overflow resulting from renal nerve stimulation, suggesting that endogenous prostaglandin has a role in the regulation of transmitter release. 4 In the presence of indomethacin, the inhibitory effect of exogenous prostaglandin E2 was enhanced. 5 The prostaglandin precursor, arachidonic acid, also caused a significant, dose-dependent and reversible inhibition of transmitter overflow. This inhibition became insignificant when arachidonic acid was applied in the presence of indomethacin, suggesting that the inhibition was mediated by newly formed prostaglandin rather than by arachidonic acid itself. 6 It is proposed that newly formed prostaglandin controls noradrenaline release primarily from inner cortical nerve endings, thereby maintaining juxtamedullary blood flow under periods of increased sympathetic nerve activity.

A six-month-old Labrador retriever presented for investigation of a colonic mass identified as an incidental finding during exploratory coeliotomy. Computed tomography identified a lesion in the colon which occupied part of its lumen and shared blood supply with the remainder of the colon. The lesion was suspected to be a colonic duplication and it was excised by segmental colectomy during exploratory coeliotomy. Histopathology from the excised colon confirmed the diagnosis of a colonic duplication. The dog recovered uneventfully and had no complications. To the authors' knowledge, this is the first report of an asymptomatic, spherical, communicating colonic duplication and the first report to describe segmental colectomy for the management of this condition in veterinary patients.

No abstract