Immune potential of lymph node-derived lymphocytes in uncontrolled hemorrhagic shock.

The state of T cell immunity was evaluated in rats in early (1-4 h) hemorrhagic shock induced by a massive splenic injury. T cell subpopulations from treated and untreated shocked animals were tested by flow cytometry and the results were compared with healthy controls. A fall in CD4+ T lymphocyte and natural killer (NKR-P1+) cell number, marked decline in the T helper (CD4+) to T suppressor (CD8+) ratio, and decrease of interleukin-2 receptor (IL-2R) bearing cells in peripheral blood, mesenteric, and popliteal lymph nodes of rats was found in the early stages of hemorrhagic shock. The same phenotype profile was also revealed in lymphocytes of rats in hemorrhagic shock following massive splenic injury treated with Ringer's lactate. The number of TCRalpha beta and TCR-gamma delta positive cells, as well as the percentage of CD4 and CD8 positive cells in the thymus, was similar in all groups of rats. Culture of lymph node cells taken from rats following hemorrhage in the presence of 100 U/mL hrIL-2 resulted in a marked increase in the number of NKR-PI+ positive cells from 4.2% to 30.5% (P < 0.001). Magnet separated NKR-P1+ fractions lysed the allogeneic fibroblasts in the same manner as IL-2-activated NKR-P1 cells from the control rats. Popliteal lymph node (PLNi) CD8b+ lymphocytes from rats in hemorrhagic shock preinfected into the footpad with cytomegalovirus (CMV) 6 days prior to injury lost their ability to lyse the CMV-infected fibroblasts and protect the monolayer from CMV infection when compared with PLNi cells from control infected rats. The possible mechanisms for the observed cellular dysfunction following hemorrhage are discussed.