Early-phase endotoxic shock-induced myocardial injury increases iNOS and selectin expression in macaque primate.

Background Our previous study has established a macaque model with early-phase endotoxic shock. The present study further investigated myocardial and blood vessel injury in Macaques by examining the subsequent expression of ACP, selectins, iNOS, and cTnI in response to LPS treatment. Methods In an experiment with anaesthetised, instrumental macaques, eleven animals were randomised into: an En group ( n =6), receiving a dose of 2.8mgkg −1 lipopolysaccharides (LPS) by i.v.; and a Co group ( n =5), injected with normal saline of 1mlkg −1 . Cytochemistry of acid phosphatase (ACPase) in heart was performed by electron microscope at 120min following endotoxin injection. Three immunochemical stains, namely, L-selectin, P-selectin and iNOS protein in heart, were studied. In addition, cardiac troponin I (cTnI), L-selectin and P-selectin in plasma were detected. Results In the early phase of endotoxic shock, LPS caused myocardial lysosome damage. The data of immunochemical staining showed the thrombus formation in vessels and the increase of iNOS, L-Selectin and P-Selectin expression in heart, but LPS challenge did not change L-selectin, P-selectin and cTnI in plasma. Conclusion The increase of iNOS, L-selectin and P-selectin protein expression following endotoxin administration may have caused vessel injury and myocardial damage in macaques.