Abstract
In vitro, the contractile activity of rat mesenteric lymphatic vessels (LV) and lymph nodes (LN) was studied in abdominal experimental sepsis caused by ligation-puncture of the cecum. It was found that sepsis leads to a pronounced decrease in tone and a decrease in the frequency and amplitude of phase contractions of LV and LN. It is shown that in sepsis the main causes leading to inhibition of the contractile function of LV and LN are increased expression of iNOS and COX-2. In the LV, the mechanism of hyperproduction of NO predominates, which leads to the opening of ATP-sensitive K+-channels of the smooth muscle cell (SMC) membrane, hyperpolarization of the membrane, and relaxation of the SMC. In LN, COX-2 is predominantly expressed, which is accompanied by an increase in the production of PGI2, which causes relaxation of the SMC capsule of LN. Endogenous and exogenous glucocorticoids in sepsis have a protective effect on the transport function of LV and LN by inhibiting the expression of iNOS and COX-2.
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