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Early-phase endotoxic shock-induced myocardial injury increases iNOS and selectin expression in macaque primate
Guo Qing Yin1, Kai He Du, Fei Rong Gu
1College of Veterinary Medicine, Nanjing Agricultural University, 6 Tongwei Road, Nanjing, Jiangsu 210095, PR China. yinguoq@jlonline.com
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 2.8 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.
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.
Insights
Lipopolysaccharide (LPS) administration in macaques induced early endotoxic shock, causing myocardial lysosome damage and increased expression of inducible nitric oxide synthase (iNOS), L-selectin, and P-selectin, leading to vascular injury.
Area of Science:
- Cardiovascular Research
- Pathology
- Immunology
Background:
- Established macaque model for early-phase endotoxic shock.
- Investigated myocardial and vascular injury following lipopolysaccharide (LPS) administration.
- Examined expression of acid phosphatase (ACP), selectins, inducible nitric oxide synthase (iNOS), and cardiac troponin I (cTnI).
Purpose of the Study:
- To further investigate myocardial and blood vessel injury in macaques during early-phase endotoxic shock.
- To examine the expression of specific proteins in response to LPS treatment.
- To understand the molecular mechanisms underlying endotoxic shock-induced organ damage.
Main Methods:
- Used an anesthetized macaque model, randomized into endotoxin (LPS) and control groups.
- Performed cytochemistry for acid phosphatase (ACPase) in the heart via electron microscopy.
- Utilized immunochemical staining for L-selectin, P-selectin, and iNOS protein in heart tissue and plasma.
Main Results:
- LPS induced myocardial lysosome damage in the early phase of endotoxic shock.
- Observed thrombus formation in vessels and increased expression of iNOS, L-selectin, and P-selectin in the heart.
- No significant changes in plasma L-selectin, P-selectin, or cTnI levels were detected post-LPS challenge.
Conclusions:
- Increased expression of iNOS, L-selectin, and P-selectin following endotoxin administration is implicated in vessel and myocardial damage.
- Findings suggest these proteins play a critical role in the pathogenesis of endotoxic shock in macaques.
- The macaque model provides insights into endotoxic shock-induced cardiovascular complications.
