Next, we investigated the role of intracellular Ca2+ in TNF-induced SIRS in vivo by [Ca2+]i chelation with ester-loaded BAPTA-AM (2 mM i.v.)34, and found that it did not protect mice against mortality, but significantly ameliorated body temperatures (Fig. 6a,b), and protected against renal vascular leakage (Fig. 6c). This evidence concerns the gene TNF and systemic inflammatory response syndrome.