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The Study on Effects and Mechanisms of the Non-Invasive Limb Ischemic Preconditioning on Ischemic Ventricular Arrhythmias in Rabbits

Author: HouLiFang
Tutor: PanQiangWen
School: Luzhou Medical College
Course: Physiology
Keywords: Noninvasive limb ischemic preconditioning Arrhythmia Monophasic action potential ATP-sensitive potassium channel inhibitor p38 mitogen- activated protein kinase
CLC: R541.7
Type: Master's thesis
Year: 2010
Downloads: 22
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Abstract


Objective: To study the noninvasive limb ischemic preconditioning effect and mechanism of rabbit ischemic ventricular arrhythmias experimental theoretical basis for its clinical application. Methods: Japanese white rabbits 27 weight (1.8 ± 0.4) kg, male or female, ischemia randomized to the control group (Ctr, n = 8), non-invasive limb ischemic preconditioning group (LIP, n = 7 ), LIP glibenclamide glibenclamide group (LG, n = 6) and groups LIP SB203580 (LSB, n = 6). Animal is anesthetized, the right external jugular vein to insert the electrode into the right ventricle to record the endocardial MAP; needle electrode II lead ECG extremities subcutaneous record is inserted standards; open 1-2mm2 holes after the 4th or 5th intercostal space of the left sternal insert the the contact electrode Zhixin outdoor parietal pericardium little pressure to record the epicardial MAP. Ctr group were not given special treatment, pending ECG and heart, the adventitia the MAP graphics stability, blade element (2U/kg) after intravenous injection of pituitary myocardial ischemia background caused intravenous epinephrine (0.2ml/kg). Induced arrhythmias ; simultaneous recording of the relationship between the ECG and heart, adventitia MAP observed heart, adventitia MAP changes and arrhythmia; LIP group: tourniquet ligation rabbit double hindlimb ischemia 5min Loosen make again perfusion 5min, repeated four times, more than with the Ctr group; the LG groups: the first intravenous glibenclamide the urea (0.16mg/kg) 30min underwent the same treatment as the LIP group; LSB group: first intravenous SB203580 (0.1 mg / kg) 30min succeeding LIP group the same processing. RM6280 biological signal acquisition and processing system for dynamic observation of changes in the ECG and heart outer membrane of MAP. After the end of the experiment, air embolism animals were killed, the removal of the heart with 4% paraformaldehyde for morphological observation, some stored at -70 ℃ refrigerator stand. Results: ① ischemia before and after, the the Ctr group of endocardial APD90, respectively (130.66 ± 13.36) ms and (135.23 ± 10.24) ms epicardial APD90 (132.56 ± 16.27) ms and (141.90 ± 16.37) ms; LIP group endocardial APD90 respectively (122.47 ± 13.94) ms and (130.26 ± 17.12) ms epicardial APD90 (124.16 ± 9.72) ms and (148.02 ± 12.78) ms; the the LG group endocardial APD90, respectively ( 127.19 ± 36.78) ms and (134.72 ± 46.01) ms epicardial APD90 were (146.20 ± 16.21) ms and (160.78 ± 22.73) ms; the LSB group endocardial APD90 were (100.88 ± 13.36) ms and (104.56 ± 28.46) ms, epicardial APD90 were (105.77 ± 18.59) ms and (104.10 ± 20.69) ms. Postischemic ventricular arrhythmias were mainly for premature ventricular contractions bigeminy and triple law. The Ctr group of 3 cases of ventricular tachycardia, ventricular fibrillation, and none of the LIP, LG and LSB group ventricular tachycardia and ventricular fibrillation. The duration of arrhythmia (s), respectively (231.54 ± 15.78) (1,676,100 ± 16.13), (159.38 ± 29.56) (209.83 ± 26.39). ② myocardial tissue SOD activity (U / mgprot) were (263.78 ± 61.51), (322.63 ± 50.46), (280.56 ± 37.01) and (314.52 ± 44.72); the content of MDA (nmol / mgprot) (14.01 ± 6.23, respectively. ), (5.34 ± 2.17), (6.25 ± 2.57) and (5.94 ± 2.13); the content of NO (μmol / gprot) were (30.85 ± 10.13), (242.17 ± 48.84), (68.18 ± 31.26) and (65.18 ± 22.55). ③ ischemia groups endocardial APD90 were prolonged, LIP and LSB group endocardial the APD90 short in the Ctr group (P lt; 0.05); ischemia the Ctr, LIP and LG groups epicardial APD90 extend the LSB group APD90 shortening the LSB group the epicardial APD90 short Ctr LIP group (P lt; 0.05). LIP and LG group arrhythmia duration shorter than the CTR group (P LT; 0.05). The LIP group SOD activity is higher than the Ctr group (P lt; 0.05), LG and LSB group SOD activity Ctr and LIP group was no difference (P gt; 0.05); LIP, LG and LSB MDA content were lower than Ctr group (P lt; 0.01), LG and LSB group MDA content LIP group were no differences (P gt; 0.05); the LIP group of NO content is higher than the the Ctr group of (P lt; 0.01), LG and LSB group NO content below LIP group (P lt; 0.01), LG and LSB group NO content Ctr group were no differences (P gt; 0.05). The ④ HSP70 mRNA relative expression levels were (3.04 ± 0.20), (3.14 ± 0.20), (2.65 ± 0.18) and (2.61 ± 0.31), LIP group HSP70 mRNA relative expression amount Ctr group, no difference (P gt; 0.05), while LG and LSB groups relative HSP70 mRNA expression were lower than Ctr and LIP group (P lt; 0.01); relative expression of COX-2 mRNA, respectively (1.36 ± 0.16), (1.61 ± 0.22), (1.47 ± 0.19) and (1.14 ± 0.09), the the LIP group of COX-2 mRNA relative expression was higher than the Ctr group (P lt; 0.05), less than the LSB group of COX-2 mRNA relative expression the Ctr and LIP group (P lt ; 0.05), LG group of COX-2 mRNA relative expression compared to the amount Ctr LIP group were not different (P gt; 0.05); relative expression levels of iNOS mRNA were (1.32 ± 0.08), (1.75 ± 0.12), (1.40 ± 0.14) and (1.34 ± 0.07), the LIP group iNOS mRNA relative expression levels higher than the the Ctr group of (P lt; 0.01) LG and LSB group iNOS mRNA relative expression level lower than the LIP group (P lt; 0.01 ); the TNFa mRNA relative expression levels were (0.57 ± 0.03), (0.38 ± 0.03), (0.55 + 0.06) and (0.54 ± 0.04), the LIP group of TNFa mRNA relative expression level lower than the Ctr group (P lt; 0.01), LG and LSB group TNFa mRNA relative expression level is higher than the LIP group (P lt; 0.01); relative expression levels of NF-κB mRNA were (0.62 ± 0.05), (0.51 ± 0.03), (0.59 ± 0.04 ) and (0.60 ± 0.04), the the LIP group of NF-κB mRNA relative expression level lower than the Ctr group (P lt; 0.01), LG and LSB group of NF-κB mRNA relative expression level higher than the LIP group (P lt; 0.01 ). To ⑤ p-of p38MAPK protein positive expression in the Ctr group (0.08 ± 0.02), LIP group (0.15 ± 0.03), the LG group (0.12 ± 0.02), p-p38MAPK protein expression the LIP and LG group were higher than the Ctr group ( P lt; 0.05), while the positive expression of p-p38MAPK protein in the LSB group (0.05 ± 0.02), compared with Ctr, LIP and LG group were reduced (P lt; 0.05). Conclusion: 1.LIP reducing myocardial oxidative damage and improve myocardial blood supply, thus enhancing the rabbit ischemic myocardial electrical stability; 2.p38MAPK LIP important way to enhance the electrical stability of ischemic myocardium, KATP antioxidant and improve play the role of myocardial blood supply, etc.; 3. LIP I / R myocardial protective effect of possible mechanisms and signal transduction pathways first \activate downstream mitogen-activated protein kinase (MAPK) system, thus causing the transmission and amplification of the signal, and activation of nuclear transcription factors and produce effector the final play myocardial protective effect.

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CLC: > Medicine, health > Internal Medicine > Heart, blood vessels ( circulatory ) disease > Heart disease > Arrhythmia
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