Abstract
We hypothesized that pharmacologic blockade of Cyclooxygenase 2(COX 2) using Nimesulide (Nime) prevents maladaptive changes in the LV structure/function secondary to pressure overload. In vivo LV structure/function was assessed by pressure/volume catheter at 14 days post surgery in 3 groups(n ≥ 6 per group); Sham-operated (Sham), Untreated pressure overload (PO) and PO + Nime (10 mg/kg/d). Relative to sham, LV mass index was significantly increased in PO group(P≤0.05). End diastolic volume, an indicator of chamber size, was significantly decreased in the PO animals compared to sham (202 ± 17 vs. 143 ± 16 Sham vs. PO, Nime + PO: 226 ± 9). Hydroxyproline analysis demonstrated collagen levels in PO rats were significantly elevated relative to Sham. Nime treatment significantly prevented the increase in LV mass index, reduction in end diastolic volume and increase in collagen levels. In summary, COX 2 inhibition with Nime prevented the maladaptive changes in the LV after pressure overload. This suggests that acute cardiac remodeling during pathological stress occurs by COX 2 mediated inflammatory pathway and can be attenuated by COX 2 inhibitors. Acknowledging the clinical failure of chronic COX 2 inhibitor use, we propose that acute treatment with COX 2 inhibitors during the initial stages of cardiac remodeling can be beneficial in maintaining normal cardiac structure and function. AHA 09BGIA2090065
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.