摘要
Aim: To observe the effect of electroacupuncture (EA) on acute myocardial ischemia (AMI) induced changes of cardiac sympathetic discharges and the effects of some related receptors in the spinal cord. Methods: A total of 53 rabbits anesthetized with mixture solution of 25% urethane (420 mg/kg) and 1.5% chloralose (50 mg/kg) were used in this study. AMI was induced by occlusion of the ventricular branch of the left coronary artery. Discharges of the left cardiac sympathetic nerve were recorded by using a bipolar platinum electrode. Bilateral "Ximen"(PC 40) and "Kongzhui"(LU 6) were stimulated electrically by using an EA therapeutic apparatus or an electrical stimulator. DPDPE δ opiate receptor agonist, 20 nmol, 10 μL, n=8), Naltrindole Hydrochloride (δ opiate receptor antagonist, 20 nmol, 10 μL, n=8), DAP5 (NMDA receptor antagonist, 5 nmol, 10 μL, n=9) and CNQX (non NMDA receptor antagonist, 5 nmol, 10 μL, n=8) were respectively injected into the thoracic subarachnoid space of the spinal cord in different groups, followed by observing their effects on changes of sympathetic activity evoked by EA of the abovementioned acupoints. Results: ① After AMI, sympathetic discharges increased (200.56±79.89%) in 10 cases and decreased (-59.34 ±7.06%) in other 9 cases in comparison with their individual basal values. After EA of "Ximen" (PC 4) and "Kongzhui"(LU 6), AMI induced increase and decrease changes of the sympathetic activity were suppressed significantly, but the effect of EA of LU 6 was weaker than that of EA of PC 4. ② Following EA of PC 4 and LU 6, sympathetic discharges increased significantly in 2 and 4 cases, decreased apparently in 7 and 3 cases, and had no striking changes in 1 and 3 cases respectively. The mean reaction threshold of sympathetic activity after EA of PC 4 and LU 6 were 2.1±0.65 mA and 3.28±1.13 mA separately. ③ After pre treatment with DPDPE, the reaction threshold of the cardiac sympathetic activity to EA of PC 4 elevated significantly (35.89±6.12%); while after pre treatment with Naltrindole, this reaction threshold decreased considerably (84.88±26.58%). Following intrathecal injection of DAP5 (n=9) and CNQX (n=9) , the reaction thresholds of the cardiac sympathetic activity to EA of PC 4 increased obviously (142.06±60.27% and 112.54±28.58% separately). It suggests that spinal δ opioid receptor, NMDA and non NMDA receptors are involved in EA induced changes of sympathetic activity. Conclusion: ① EA could regulate AMI induced changes of cardiac sympathetic activity; and ② spinal δ opioid receptors, NMDA and non NMDA receptors participate in the effect of EA on the cardiac sympathetic activity.
Aim: To observe the effect of electroacupuncture (EA) on acute myocardial ischemia (AMI) induced changes of cardiac sympathetic discharges and the effects of some related receptors in the spinal cord. Methods: A total of 53 rabbits anesthetized with mixture solution of 25% urethane (420 mg/kg) and 1.5% chloralose (50 mg/kg) were used in this study. AMI was induced by occlusion of the ventricular branch of the left coronary artery. Discharges of the left cardiac sympathetic nerve were recorded by using a bipolar platinum electrode. Bilateral 'Ximen'(PC 40) and 'Kongzhui'(LU 6) were stimulated electrically by using an EA therapeutic apparatus or an electrical stimulator. DPDPE δ opiate receptor agonist, 20 nmol, 10 μL, n=8), Naltrindole Hydrochloride (δ opiate receptor antagonist, 20 nmol, 10 μL, n=8), DAP5 (NMDA receptor antagonist, 5 nmol, 10 μL, n=9) and CNQX (non NMDA receptor antagonist, 5 nmol, 10 μL, n=8) were respectively injected into the thoracic subarachnoid space of the spinal cord in different groups, followed by observing their effects on changes of sympathetic activity evoked by EA of the abovementioned acupoints. Results: ① After AMI, sympathetic discharges increased (200.56±79.89%) in 10 cases and decreased (-59.34 ±7.06%) in other 9 cases in comparison with their individual basal values. After EA of 'Ximen' (PC 4) and 'Kongzhui'(LU 6), AMI induced increase and decrease changes of the sympathetic activity were suppressed significantly, but the effect of EA of LU 6 was weaker than that of EA of PC 4. ② Following EA of PC 4 and LU 6, sympathetic discharges increased significantly in 2 and 4 cases, decreased apparently in 7 and 3 cases, and had no striking changes in 1 and 3 cases respectively. The mean reaction threshold of sympathetic activity after EA of PC 4 and LU 6 were 2.1±0.65 mA and 3.28±1.13 mA separately. ③ After pre treatment with DPDPE, the reaction threshold of the cardiac sympathetic activity to EA of PC 4 elevated significantly (35.89±6.12%); while after pre treatment with Naltrindole, this reaction threshold decreased considerably (84.88±26.58%). Following intrathecal injection of DAP5 (n=9) and CNQX (n=9) , the reaction thresholds of the cardiac sympathetic activity to EA of PC 4 increased obviously (142.06±60.27% and 112.54±28.58% separately). It suggests that spinal δ opioid receptor, NMDA and non NMDA receptors are involved in EA induced changes of sympathetic activity. Conclusion: ① EA could regulate AMI induced changes of cardiac sympathetic activity; and ② spinal δ opioid receptors, NMDA and non NMDA receptors participate in the effect of EA on the cardiac sympathetic activity.
