CAJ | 학술논문

目的通过离体及在体实验评价右美托咪定对家兔心率(HR)的影响,探讨其减慢HR的机制.方法离体实验健康成年家兔,体重2.0～2.5 kg,8～10周龄,雌雄不拘.成功建立Langendorff离体灌注模型的24个心脏,采用随机数字表法,将其分为3组(n=8):对照组(C组)、3、30 ng/ml右美托咪定组(D1组和D2组).C组持续灌注K-H液45 min,D1组和D2组K-H液平衡灌注15 min时,分别灌注含相应浓度右美托咪定的K-H液30 min.分别于K-H液平衡灌注15 min、灌注含右美托咪定的K-H液15、30 min时记录HR和左心室收缩压.在体实验健康成年家兔25只,体重2.0～ 2.5 kg,8～10周龄,雌雄不拘,采用随机数字表法,将其分为5组(n=5):右美托咪定3、6、9、12、15 μg/kg组(D3组、D6组、D9组、D12组和D15组),经10 min静脉输注相应剂量的右美托咪定.分别于给药前(T0)、给药后15、40 min(T1,2)时记录HR和MAP.右美托咪定剂量与HR变化率之间进行Spearman相关分析.结果离体实验与C组比较,D1组和D2组各时点HR和左心室收缩压差异无统计学意义(P＞0.05).在体实验与T0时比较,D6组和D9组T1时HR降低,D12组和D15组T1,2时HR降低,D6组、D9组和D12组T12时MAP降低(P＜0.05),D3组各时点HR差异无统计学意义(P＞0.05).右美托咪定剂量与HR变化率之间的相关系数为0.944(P＜0.05).结论右美托咪定减慢家兔HR的机制与对窦房结的直接抑制作用无关,而与自主神经调节有关.
목적 통과리체급재체실험평개우미탁미정대가토심솔(HR)적영향,탐토기감만HR적궤제.방법 리체실험 건강성년가토,체중2.0～2.5 kg,8～10주령,자웅불구.성공건립Langendorff리체관주모형적24개심장,채용수궤수자표법,장기분위3조(n=8):대조조(C조)、3、30 ng/ml우미탁미정조(D1조화D2조).C조지속관주K-H액45 min,D1조화D2조K-H액평형관주15 min시,분별관주함상응농도우미탁미정적K-H액30 min.분별우K-H액평형관주15 min、관주함우미탁미정적K-H액15、30 min시기록HR화좌심실수축압.재체실험건강성년가토25지,체중2.0～ 2.5 kg,8～10주령,자웅불구,채용수궤수자표법,장기분위5조(n=5):우미탁미정3、6、9、12、15 μg/kg조(D3조、D6조、D9조、D12조화D15조),경10 min정맥수주상응제량적우미탁미정.분별우급약전(T0)、급약후15、40 min(T1,2)시기록HR화MAP.우미탁미정제량여HR변화솔지간진행Spearman상관분석.결과 리체실험여C조비교,D1조화D2조각시점HR화좌심실수축압차이무통계학의의(P＞0.05).재체실험 여T0시비교,D6조화D9조T1시HR강저,D12조화D15조T1,2시HR강저,D6조、D9조화D12조T12시MAP강저(P＜0.05),D3조각시점HR차이무통계학의의(P＞0.05).우미탁미정제량여HR변화솔지간적상관계수위0.944(P＜0.05).결론 우미탁미정감만가토HR적궤제여대두방결적직접억제작용무관,이여자주신경조절유관.
Objective To evaluate the effect of dexmedetomidine on heart rate (HR) of rabbits through in vitro and in vivo experiments, and investigate the mechanism by which dexmedetomidine lowered HR.Methods In vitro experiment Healthy adult rabbits of both sexes, weighing 2.0-2.5 kg, aged 8-10 weeks, were studied.The 24 isolated hearts passively perfused in a Langendorff apparatus were randomly divided into 3 groups (n =8 each) using a random number table: control group (group C) , and dexmedetomidine 3 and 30 ng/ml groups (D1 and D2 groups).The isolated hearts were continuously perfused with K-H solution for 45 min in group C.After 15 min of equilibration, the isolated hearts were perfused for 30 min with K-H solution containing dexmedetomidine 3 and 30 ng/ml in D1 and D2 groups, respectively.At 15 min of equilibration, and at 15 and 30 min of perfusion with K-H solution containing dexmedetomidine, HR and left ventricular systolic pressure (LVSP) were recorded.In vivo experiment Twenty-five healthy adult rabbits of both sexes, weighing 2.0-2.5 kg, aged 8-10 weeks, were randomly divided into 5 groups (n=5 each) using a random number table: dexmedetomidine 3, 6, 9, 12, and 15 μg/kg groups (D3, D6, D9, D12, D15groups), to receive the corresponding doses of dexmedetomidine which was intravenously infused over 10 min.HR and mean arterial pressure were monitored and recorded before administration (T0) , and at 15 and 40 min after administration (T1,2).The correlation between doses of dexmedetomidine and change rate of HR was tested by Spearman correlation analysis.Results In vitro experiment Compared with group C, no significant changes were found in HR and LVSP at each time point in D1 and D2 groups (P＞0.05).In vivo experiment Compared with those at T0 , HR at T1 in D6 and D9 groups, HR at T1,2 in D12 and D15 groups, and mean arterial pressure at T1,2in D6, D9, and D12 groups were significantly decreased (P＜0.05) , and no significant change was found in HR at each time point in group D3 (P＞0.05).The correlation coefficient between doses of dexmedetomidine and change rate of HR was 0.944 (P＜0.05).Conclusion The mechanism by which dexmedetomidine lowers HR of rabbits is not related to direct inhibition of sinoatrial nodes, but associated with the balance of autonomic nervous system.