The systemic inflammatory response syndrome (SIRS) is an inflammatory condition which affects the whole body and represents a serious threat. Endotoxemia, sepsis and its complications (septic shock and multiple organ failure) are the major cause of death in intensive care units worldwide, despite recent major technological advances. In spite of endotoxemia, hypertension is also a disease which may lead to a significant medical and social impact, being characterized by elevated and sustained blood pressure levels and associated with changes in the reflex mechanisms that regulate the cardiovascular system. There is an experimental similarity between the pathophysiology of essential hypertension in men with spontaneously hypertensive rats (SHR). These animals, as well as hypertensive humans, have a marked sympathetic overactivity and decreased vagal cardiac tone. Clinical studies have shown that in situations where there is less parasympathetic activity, the inflammatory processes seems to be more pronounced. The aim of this study is to test the hypothesis that, in the face of the immune challenge caused by LPS, SHR will be particularly more sensitive to vagal stimulation (induced by pyridostigmine treatment), since these animals have reduced vagal tonus compared to normotensive rats. To better study this mechanism, we will quantify the plasma concentration of PGE2 and PGD2 and also cytokines (IL-1, IL-6 and TNF-± and IL-10) in these animals. We suggest that there is an inversely proportional relationship between vagal tone and PGE2 and a directly proportional parallel between vagal tone and PGD2, considering that they are pro and antipyretic mediators, respectively.
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