O papel do córtex pré-frontal medial ventral no controle das respostas cardiovasculares induzidas por neuropatia em ratos

Abstract

The medial ventral prefrontal cortex (vCPFM) is a structure of the limbic system involved in the modulation of autonomic responses. The physiological and structural changes in the neurons of this necleus are related to hyperalgesia induced by neuropathy. The aim of this study was to evaluate the participation of vCPFM in cardiovascular alterations induced by neuropathy in rats. Male Wistar rats weighing 160-180g were used. They underwent surgery to induce neuropathy, after seven days stereotaxy was performed for cannula implantation in vCPFM for injection of Cobalt Chloride (CoCl2). The surgery for cannulation of the femoral artery was done 5 days after stereotactic and one day after the nociceptive tests were performed to evaluate the Heart Rate (HR) and Mean Blood Pressure (MAP). Innovative thermal stimuli ("Cold"), mechanical ("Brush"), punctual ("VonFrey") and the thermal stimuli ("Heat") and mechanical stimuli ("Pin") were used. Thus, assessed their HR and MAP. The HR and MAP values were increased by nociceptive stimulation and the findings of the present study demonstrate that this behavior is dependent on the type of estimate. The innocuous thermal stimulus, the "cold" acetone cooling method, is not able to generate pain in false-operated animals, so it is also expected to not affect HR and MAP. Using the real-time estimation model with the "Von Frey" method or dynamic with the "Brush" method, in false-operated animals, such as MAP and HR amplitudes were small, consistent with a low intensity of originals that can not Generate nociception and pain. The noxious mechanical stimulus "Pin" increased MAP and HR. It is already recommended that "Heat" caused a sustained increase in HR and was also able to provide a greater cardiovascular response than mechanical stimulation. The results suggested that vCPFM involvement is important in the cardiovascular responses required in the hyperalgesic responses induced by harmful and innocuous stimuli in a model of nerve ligation neuropathy.