Alterations in hypothalamic synaptophysin and death markers may be associated with vasopressin impairment in sepsis survivor rats

Author(s)

Santos-Junior, N. N. ; Catalao, C. H. R. ; Costa, L. H. A. ; Rossignolli, B. B. ; Dos-Santos, R. C. ; Malvar, D. C. ; Mecawi, A. S. ; Rocha, M. J. A.

• Document type: Journal article
• Source: Journal of Neuroendocrinology; v. 30, n. 8, p. 8-pg., 2018-08-01.

Abstract

The impairment in arginine vasopressin (AVP) secretion during sepsis is described in clinical and experimental studies and has been associated with oxidative stress, apoptosis and diminished activation of hypothalamic neurones. However, few studies have assessed these abnormalities in sepsis survivors. In the present study, we performed 2 sets of experiments on Wistar rats that had been subjected to sepsis by cecal ligation and puncture (CLP) or nonmanipulated (naive) as a control. In the first set, tissues and blood were collected from survivor rats 10 days after CLP to quantify hypothalamic Bcl-2, cleaved caspase-3 and synaptophysin contents, as well as bacterial load. In the second set, survivor rats were submitted to an acute osmotic stimulus (hypertonic saline) and, after 30 minutes, water intake and AVP secretion were analysed. The sepsis-surviving rats did not show bacterial load in tissues, although their hypothalamic synaptophysin and Bcl-2 levels were decreased and the cleaved caspase-3 level was increased compared to the control group. However, AVP secretion was significantly attenuated in the CLP survivor animals submitted to an acute osmotic stimulus. These results suggest that the persistent AVP impairment in sepsis survivor animals may be the result hypothalamic dysfunction associated with a synaptic deficit and decreased anti-apoptotic protein expression. (AU)

• FAPESP's process: 15/12152-5 - Hormonal, behaviour alterations and brain oxidative stress in sepsis survival animals
• Grantee: Maria José Alves da Rocha
• Support Opportunities: Regular Research Grants