Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

Impact of beta-adrenoceptor blockade on systemic inflammation and coagulation disturbances in rats with acute traumatic coagulopathy.

Authors: Xu, L  Yu, WK  Lin, ZL  Tan, SJ  Bai, XW  Ding, K  Li, N 
Citation: Xu L, etal., Med Sci Monit. 2015 Feb 12;21:468-76. doi: 10.12659/MSM.893544.
Pubmed: (View Article at PubMed) PMID:25676919
DOI: Full-text: DOI:10.12659/MSM.893544

BACKGROUND: Sympathetic hyperactivity occurs early in acute traumatic coagulopathy (ATC) and is closely related to its development. beta-adrenoceptor antagonists are known to alleviate adverse sympathetic effects and improve outcome in various diseases. We investigated whether beta-blockers have protective effects against inflammation and endothelial and hemostatic disorders in ATC. MATERIAL AND METHODS: ATC was induced in male Sprague-Dawley rats by trauma and hemorrhagic shock. Rats were randomly assigned to the sham, ATCC (ATC control), and ATCB (ATC with beta-adrenoceptor blockade) groups. Rats were injected intraperitoneally with propranolol or vehicle at baseline. Heart rate variability (HRV) and markers of inflammation, coagulation, and endothelial activation were measured, and Western blotting analysis of nuclear factor (NF)-kappaB was done after shock. Separate ATCC and ATCB groups were observed to compare overall mortality. RESULTS: HRV showed enhanced sympathetic tone in the ATCC group, which was reversed by propranolol. Propranolol attenuated the induction of pro-inflammatory cytokines TNF-alpha and IL-6, as well as fibrinolysis markers plasmin antiplasmin complex and tissue-type plasminogen activator. The increased serum syndecan-1 and soluble thrombomodulin were inhibited by propranolol, and the NF-kappaB expression was also decreased by propranolol pretreatment. But propranolol did not alter overall mortality in rats with ATC after shock. CONCLUSIONS: Beta-adrenoceptor blockade can alleviate sympathetic hyperactivity and exert anti-inflammatory, anti-fibrinolysis, and endothelial protective effects, confirming its pivotal role in the pathogenesis of ATC. Its mechanism in ATC should be explored further.


Disease Annotations
Objects Annotated

Additional Information

RGD Object Information
RGD ID: 11554180
Created: 2016-10-20
Species: All species
Last Modified: 2016-10-20
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.