Hematologic disturbances during sepsis: platelets and leukocytes.
This brief review summarizes recent observations about leukocyte and platelet involvements during sepsis and septic shock. Endotoxins are known to exert significant effects on leukocytes and platelets as well as monocytes, macrophages, endothelial, and mast cells. The presence of endotoxin itself is reported to enhance the phagocytic and killing capacity of neutrophils. Transfusion of additional white blood cells has been shown to increase the probability of recovery from sepsis. Defects in neutrophil function, impaired opsonization, sequestration of neutrophils in pulmonary capillaries, and depressed metabolic states adversely affecting neutrophils may significantly contribute to the lethal outcome of septic shock. Platelet responses in septic shock are reported to include aggregation accompanied by release of several agents, including vasoactive amines, ADP, and platelet factor 3. In summary, leukocytes and platelets are known to perform significant roles in sepsis and septic shock although the precise mechanisms of their involvement remain to be clearly defined.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology*; D004731:Endotoxins / Q000494:pharmacology; D006801:Humans; D008253:Macaca mulatta; D009503:Neutropenia / Q000139:chemically induced; D009504:Neutrophils / Q000187:drug effects / Q000502:physiology*; D010587:Phagocytosis; D011817:Rabbits; D012772:Shock, Septic / Q000097:blood*
D001786:Blood Glucose; D004731:Endotoxins