The Study On Secretory Hypofunction Of Rat Submandibular Glands Resulted From Ischemia/reperfusion

PurposeDry eye syndrome is a multifactorial disease of the ocular surface and tears film that results in ocular discomfort, visual disturbances, and tear instability, with potential damage to the cornea and conjunctiva. Although some therapeutical options are adopted according to the severity of the syndrome, inadequate tear production makes it difficult for further ophthalmological treatment for patients with severe keratoconjunctivitis sicca. The procedure of autotransplantation of the submandibular gland (SMG) has been reported as an effective treatment method. However, the early-phase dysfunction of the transplanted SMGs challenges the prognosis of the surgery.Previous studies have identified that denervation of the transplanted glands, following substantial reduction of neurotransmitter release, could lead to secretion dysfunction of the transplanted SMGs. However, the possible effect of ischemia/reperfusion (I/R) occurring during the transplantation has not been studied clearly yet. Our study aimed at a detailed investigation of structural and functional changes in I/R model of rat SMGs without denervation.Materials and MethodsAn in-situ ischemia/reperfusion experimental model of rat SMGs was conducted. The rat SMGs were subjected to90min ischemia without denervation, following by reperfusion for1h,12h,24h, and72h respectively. After reperfusion, salivary secretion, histological changes, tight junctions (TJs) alterations, reactive oxygen species (ROS) levels, and cellular apoptosis of the involved SMGs were detected in our study.ResultsThe secretory function of the involved glands was decreased dramatically at1h and12h after reperfusion; then, the saliva secretion gradually tended to the level of the control at72h after reperfusion. A rising cellular atrophy, inflammatory cells infiltration, and tissue edema were found after reperfusion, especially after reperfusion for12h. Ultra-structurally, after1h and12h post-reperfusion, I/R caused the collapse of TJs, with less electron-dense materials present between the adjoining cells, which seemed to be improved after reperfusion for24h and72h. ROS level and the number of apoptotic cells were observed shown the same tendency, with higher ROS levels and more TUNEL-positive cells at1h and12h after reperfusion.ConclusionOur study suggested that ischemia/reperfusion could cause a series of injury-stress responses in rat SMGs, along with the hypofunction of the involved glands. So we concluded that injury-stress responses caused by I/R might play an important role in the early-phase dysfunction of the transplanted SMGs.