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in myocardial dysfunction after hemorrhagic
shock and lower-torso ischemia
Divisions of Vascular and Cardiac Surgery, Toronto General Hospital; and The Department of Surgery, University of Toronto, Ontario, Canada M5G 2C4
Ruptured abdominal
aortic aneurysm (RAAA) repair, a combination of hemorrhagic shock and
lower-torso ischemia, is associated with a 50-70%
mortality. Myocardial dysfunction may contribute to the high rate of
mortality after aneurysm repair. We attempted to determine whether RAAA
repair results in cardiac dysfunction mediated by tumor necrosis
factor-
(TNF-). We modeled aortic rupture and repair in the rat
by inducing hemorrhagic shock to a mean blood pressure of 50 mmHg for 1 h, followed by supramesenteric clamping of the aorta for 45 min. After
90 min of reperfusion, cardiac contractile function was assessed with a
Langendorff preparation. Myocardial TNF-, ATP and creatine phosphate
(CP) levels, and markers of oxidant stress
(F2-isoprostanes) were measured. Cardiac function in the
combined shock and clamp rats was significantly depressed compared with
sham-operated control rats but was similar to that noted in animals
subjected to shock alone. Myocardial TNF- concentrations increased
10-fold in the combined shock and clamp rats compared with sham rats,
although there was no difference in myocardial ATP, CP, or
F2-isoprostanes. TNF- neutralization improved cardiac
function by 50% in the combined shock and clamp rats. Hemorrhagic
shock is the primary insult inducing cardiac dysfunction in this model
of RAAA repair. An improvement in cardiac contractile function after
immunoneutralization of TNF- indicates that TNF- mediates a
significant portion of the myocardial dysfunction in this model.
ruptured abdominal aortic aneurysm; left ventricular function; cytokines; neutrophils; oxidant stress
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