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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Animals, Disease Models, Animal, Escherichia coli, Female, L-Selectin, Lipopolysaccharides, Macaca, Male, Myocardium, Nitric Oxide Synthase Type II, P-Selectin, Shock, Septic, Troponin I.
user
Does early-phase endotoxic shock-induced myocardial injury increase iNOS and selectin expression in macaque primate? Context: 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. In an experiment with anaesthetised, instrumental macaques, eleven animals were randomised into: an En group (n=6), receiving a dose of 2.8 mg kg(-1) lipopolysaccharides (LPS) by i.v.; and a Co group (n=5), injected with normal saline of 1 ml kg(-1). Cytochemistry of acid phosphatase (ACPase) in heart was performed by electron microscope at 120 min 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. 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.
assistant
The increase of iNOS, L-selectin and P-selectin protein expression following endotoxin administration may have caused vessel injury and myocardial damage in macaques. Final Decision: yes