الفهرس 
Review Of LiteratureOnly 14 pages are availabe for public view
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Abstract
Current clinical practices combine CSA and NSAIDs for the treatment of severe arthritic conditions including rheumatoid arthritis, psoriatic arthritis, systemic lupus erythematosus and chronic polyarthritis.
However, few reports are available regarding the hemodynamic influences of the concurrent exposure to CSAINSAlDs.
The experimental pharmacological studies undertaken in the current study opted to provide more insights into the understanding of the hemodynamic, baroreflex, cardio-autonomic and left ventricular effects evoked by acute or chronic treatments with CSA, NSAlDs, or their combinations in female rats.
The differential contributions of NADPH-oxidase and Rho-kinases pathways in the chronic CSA/diclofenac
hemodynamic effects were also investigated. Other unique aspects of the current study pertained to the evaluation of the role of HO/CO signaling, and its crosstalk with the NOSINO pathway in the detrimental hemodynamic and cardiac influences of chronic CSA/diclofenac. Experiments were performed in conscious female Wistar rats pre-instrumented with femoral intravascular cannulas.
A summary of the main results and conclusions of the study is outlined below.
<1.Intravenous administration of a single dose of CSA caused significant (i) increases in
systolic and diastolic BP, (ii) decreases in PP! and HR, (iii) enhancement of systolic contractility (increased dP/dtmax) and altered diastolic function (reduced tau), (iv)
elevations in time- and frequency- domain values of HRY and (v) shifts in cardiac autonomic balance towards parasympathetic dominance.
<2.Whereas the acute CSA effects disappeared upon concurrent i.v. treatment with celecoxib,they were intensified (SBP and DBP) or preserved (other parameters) in rats eo-treated with diclofenac. The failure of diclofenac to reverse the detrimental hemodynamic and
autonomic actions of CSA was echoed after replacing diclofenac with SC560, a selective
COX-l inhibitor, suggesting an important role for COX-l inhibition in mediating the interaction of CSA with diclofenac or SC560.