Biology Reference
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Boucher et al. (
35
) subjected rats to ischemia-reperfusion and
treated them with IGF-1, DA, and a combination of IGF-1 and
DA 30 mg/kg i.v., or vehicle at the start of 30 min ischemia. Both
IGF-1 and DA reduced infarct size and improved cardiac function
3 days after ischemia-reperfusion compared to vehicle. In the rep-
erfused heart, apoptosis was reduced with either or both IGF-1
and DA treatments as measured by reduced TUNEL staining and
caspase-3 activity.
Prunier et al. (
36
) examined the thrombogenic effects of a
chronic EPO therapy after MI. Rats underwent coronary occlusion
followed by reperfusion. They were assigned to one of the following
groups: EPO-A, single i.p. injection of EPO 5,000 U/kg at the time
of reperfusion; EPO-C, injection of EPO 5,000 U/kg at the time of
reperfusion followed by 300 U/kg/week; PBS-C, injection of vehi-
cle only. After 8 weeks of treatment they were exposed to a pre-
thrombotic test based on partial stenosis of the inferior vena cava. As
compared to the rats receiving vehicle only, the rats treated with
EPO exhibited a significant reduction in MI size, the hematocrit was
significantly increased in EPO-C, but the proportion of rats in which
a thrombus occurred was similar in all groups.
Shan et al. (
37
) subjected mice to 45 min ischemia followed by
4 h reperfusion; EPO 1,000 U/kg, administered right before rep-
erfusion, reduced infarct size assessed by TTC staining.
Echocardiography examination suggested that EPO administra-
tion significantly improved cardiac function following ischemia-
reperfusion. TUNEL assay indicated that EPO treatment decreased
apoptosis. EPO administration also significantly increased the level
of nuclear GATA-4 phosphorylation in the myocardium which was
positively correlated with the reduction of MI. Activation of
GATA-4 may be one of the mechanisms by which EPO induced
protection against myocardial ischemia-reperfusion injury.
Doue et al. (
38
) studied rats with left coronary artery occlu-
sion randomized to receive either an intravenous injection of
200 U/kg of EPO or saline immediately after release of the occlu-
sion. This study demonstrated that a single treatment with EPO
immediately after release of coronary ligation suppressed cardiac
remodeling and functional deterioration. (99m)Tc-annexin V
autoradiographs and TUNEL staining confirmed that this change
was due to a decrease in the extent of myocardial apoptosis in the
ischemic-reperfused region.
A model of murine cardiac arrest was employed by Huang
et al. (
39
). Cardiopulmonary resuscitation was started after 6.5 or
9.5 min of asphyxia-induced cardiac arrest. The resuscitated ani-
mals received either erythropoietin (1,000, 3,000, or 5,000 U/kg)
or placebo intravenously 3 min after return of spontaneous circulation.
Erythropoietin 5,000 U/kg improved post-resuscitation myocar-
dial dysfunction and short-term survival only when cardiac arrest
lasted 6.5 min.
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