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) hemorrh agic 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 a nd natural killer (NKR-P1+) cell number, marked decline in the T helper (CD 4+) to T suppressor (CD8+) ratio, and decrease of interleukin-2 receptor (I L-2R) bearing cells in peripheral blood, mesenteric, and popliteal lymph no des of rats was found in the early stages of hemorrhagic shock. The same ph enotype profile was also revealed in lymphocytes of rats in hemorrhagic sho ck following massive splenic injury treated with Ringer's lactate. The numb er of TCR alpha beta and TCR gamma delta positive cells, as well as the per centage of CD4 and CD8 positive cells in the thymus, was similar in all gro ups of rats. Culture of lymph node cells taken from rats following hemorrha ge in the presence of 100 U/mL hrIL-2 resulted in a marked increase in the number of NKR-P1+ positive cells from 4.2% to 30.5% (P < 0.001). Magnet sep arated NKR-P1+ fractions lysed the allogeneic fibroblasts in the same manne r as IL-2-activated NKR-P1 cells from the control rats. Popliteal lymph nod e (PLNi) CD8b+ lymphocytes from rats in hemorrhagic shock preinfected into the footpad with cytomegalovirus (CMV) 6 days prior to injury lost their ab ility to lyse the CMV-infected fibroblasts and protect the monolayer from C MV infection when compared with PLNi cells from control infected rats. The possible mechanisms for the observed cellular dysfunction following hemorrh age are discussed.