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Vol. 294, Issue 2, 722-727, August 2000
1-Adrenoceptor mRNA1
Departments of Medicine (H.C., D.L., M.S., J.L.M.), Physiology
(Y.C.Z., M.I.P.), and Pediatrics (P.M.), University of Florida College
of Medicine, and the Veterans Affairs Medical Center (H.C., D.L., M.S.,
J.L.M.), Gainesville, Florida
Plasma catecholamine levels rise, and myocardial
1-adrenoceptor (1-AR) sensitivity
increases during ischemia. These factors enhance myocardial injury and
cardiac dysfunction. 1-AR blockers are clinically used
to protect heart against ischemia and to improve cardiac dysfunction in
patients with ischemic heart disease, but these agents often cause
intolerable side effects. To examine the potential cardioprotective
effect of therapy with antisense-oligodeoxynucleotides directed at
1-AR mRNA (1-AS-ODNs) during myocardial
ischemia-reperfusion, Sprague-Dawley rats were treated with
1-AS-ODNs or inverted-oligodeoxynucleotides (IN-ODNs),
each 200 µg/rat. Hearts were excised, perfused, and subjected to
global ischemia (30 min) followed by reperfusion (30 min). Other rats
were given selective 1-AR blocker atenolol (2 mg/kg) or
saline before excising the hearts. Ischemia-reperfusion resulted in
cardiac dysfunction, indicated by an increase in coronary perfusion
pressure and left ventricular end-diastolic pressure and a decrease in
developed left ventricular pressure, as well as evidence of lipid
peroxidation in saline-treated rats (all P < .05 versus control values). Administration of AS-ODNs or atenolol, but not
IN-ODNs, protected hearts against functional deterioration and lipid
peroxidation (P < .05 versus saline or IN-ODNs
treatment). AS-ODNs therapy appeared to be equivalent to atenolol in
these effects. Expression of 1-AR protein as well as
mRNA in the myocardium were markedly up-regulated after
ischemia-reperfusion, and treatment with 1-AS-ODNs, but
not atenolol, decreased the rise in enhanced expression of
1-AR. These observations imply that
1-AS-ODNs can ameliorate cardiac dysfunction after
ischemia-reperfusion by reducing the expression of 1-AR
in the ischemic-reperfused myocardium.
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