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Vol. 303, Issue 3, 1007-1013, December 2002
University of Michigan Medical School, Departments of Pharmacology
(T.D.B., J.K.H., B.R.L.) and Internal Medicine (R.M.M.), Ann Arbor,
Michigan
C-Reactive protein (CRP), a marker for acute inflammation, is
associated with increased risk of cardiovascular events. The mechanism
underlying this association is uncertain. An acute inflammatory response was induced in rabbits by subcutaneous injection of croton oil
(CO) 1 to 3 days before 30 min of regional myocardial ischemia/180 min
of reperfusion. CO treatment increased plasma CRP from below the limit
of detection to 2.5 ± 0.5 mg/dl and was associated with an
increase in infarct size expressed as percentage of risk region [32 ± 6% vehicle controls (n = 7) to
47 ± 9% CO-treated rabbits (n = 7;
P < 0.05]. After 10 min of ischemia and 180 min
reperfusion, no infarct was found in controls; however, an infarct of
7 ± 1% was found in CO-treated rabbits (P < 0.05; CRP, 2.3 ± 0.4 mg/dl). The CRP-related increase in infarct
size was not observed in croton oil-treated, C6-deficient rabbits
(n = 5/group), indicating the involvement of
complement. In these rabbits, infarct size was 22 ± 2%
(P < 0.05) despite having plasma CRP of 4.3 ± 0.4 mg/dl. The CRP-associated increase in infarct size was
ameliorated by pretreatment with heparin (n = 7;
infarct size 33 ± 3%; CRP, 2.3 ± 0.3 mg/dl;
P < 0.05) or N-acetylheparin
(n = 7; infarct size 23 ± 4%; CRP, 3.1 ± 0.5 mg/dl; P < 0.05). These observations may explain why increased serum CRP is associated with an augmented risk
for cardiovascular events.
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