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1 Department of Physiology, Shanghai Medical University, Shanghai 200032, People's Republic of China; 3 Division of Cardiovascular Medicine, Department of Internal Medicine and Human Physiology, University of California, Davis, California 95616; and 2 Department of Medicine, University of California, Irvine, California 92868
Acupuncture and
electroacupuncture (EA) have been used in traditional Chinese medicine
to treat a wide range of diseases and conditions, including angina
pectoris and myocardial infarction. In a feline model of reflex-induced
reversible myocardial ischemia, electrical stimulation of the
median nerves to mimic EA (Neiguan acupoint) significantly improved
ischemic dysfunction, secondary to an inhibitory effect of EA on reflex
pressor effects evoked by bradykinin (BK). The central mechanism of
EA's inhibitory effect in this model is unknown. Accordingly, in
-chloralose-anesthetized cats, BK (10 µg/ml) was applied to the
gallbladder to elicit a cardiovascular reflex response that
significantly (P < 0.05) increased arterial blood pressure and heart rate; normalized systolic wall thickening (%WTh) of the left ventricle, measured by ultrasonic single-crystal sonomicrometer, increased by 31 ± 11%
(P < 0.05). After ligation of a side
branch of the left anterior descending coronary artery, the reflex
pressor response to BK resulted in a significant decrease of %WTh
(
32 ± 6%) in the ischemic region. When bilateral
EA of the Neiguan acupoints was performed, the pressor response to BK
was inhibited and regional myocardial function was significantly
improved (+19 ± 20%). The inhibitory effects of EA on blood
pressure and %WTh were reversed by intravenous injection of naloxone
(0.4 mg/kg; n = 9) or microinjection
of naloxone (10 nM in 0.1 µl/site; n = 14) into the rostral ventrolateral medulla (rVLM). Thus %WTh with
intravenous naloxone was reduced to
13 ± 29%
(P<0.05) during stimulation of the
gallbladder. Our results indicate that the inhibitory effect of EA on
the BK-induced pressor response and the consequent improvement of
ischemic dysfunction is dependent on the activation of opioid
receptors, specifically receptors located in the rVLM.
pressor response; myocardial ischemia; rostral ventrolateral medulla; systolic wall thickening
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