Inhibition of prostaglandins does not reduce the cardiovascular changes during endotoxemia in rats

Abed Azab, Sergio Kobal, Mazal Rubin, Jacob Kaplanski

Research output: Contribution to journalArticlepeer-review

9 Scopus citations


Vasodilatory prostanoids, such as prostacyclin and PGE2, and pro-inflammatory cytokines are known to play a central role in the pathogenesis of endotoxemia. This study was undertaken to elucidate whether indomethacin (INDO), a non-selective COX inhibitor, has protective effects against the cardiovascular alterations that occur during endotoxemia. Sprague-Dawley rats were injected intraperitoneally with 15 mg/kg lipopolysaccharide (LPS). LPS injection led to a prominent decrease in cardiac left ventricular end diastolic area (LVEDA) and increased LV fractional shortening (FS), as measured by echocardigraphy. LPS also led to a significant increase in plasma and myocardial TNF-α and IL-1β levels, and elevated plasma and hypothalamic levels of PGE2. Neither the decrease in LVEDA and the increase in FS, nor the elevation in plasma and myocardial cytokine levels were altered by INDO (10 mg/kg). On the other hand, pretreatment with INDO significantly reduced the elevation in PGE2 and the hypothermia induced by LPS. Taken together, this study demonstrates that solely inhibiting the production of PGE 2 is not sufficient to reduce the cardiovascular alteration seen in endotoxemia.

Original languageEnglish
Pages (from-to)135-142
Number of pages8
JournalProstaglandins Leukotrienes and Essential Fatty Acids
Issue number2
StatePublished - 1 Feb 2006

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology


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