中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2010年
1期
28-32
,共5页
封英%费佳谦%钱小伟%周宏斌%徐谷峰%王琳琳%鲁惠顺%陈新忠
封英%費佳謙%錢小偉%週宏斌%徐穀峰%王琳琳%魯惠順%陳新忠
봉영%비가겸%전소위%주굉빈%서곡봉%왕림림%로혜순%진신충
罗哌卡因%血管收缩%钙离子%脐动脉
囉哌卡因%血管收縮%鈣離子%臍動脈
라고잡인%혈관수축%개리자%제동맥
Ropivacaine%Vasoconstriction%Calcium%Umbilical artery
目的 研究不同浓度罗哌卡因对离体人脐动脉平滑肌的收缩作用,并分析其可能的机制.方法 采用离体脐动脉环灌流模型,用MedLab生物信号采集系统测定并记录血管的张力变化情况,观察累积浓度罗哌卡因对去内皮血管环的收缩效应,并同时观察细胞外Ca~(2+)"浓度、L-型Ca~(2+)通道阻滞剂维拉帕米、内质网三磷酸肌醇受体阻滞剂肝素和兰尼定受体阻滞剂钌红对罗哌卡因血管效应的影响.结果 罗哌卡因诱发剂量关联性双相脐血管反应:在低浓度(1.0×10~(-5)~1.0 × 10(~4)moL/L)时收缩张力逐渐升高,较高浓度(3.0×10~(-4)~3.0×10~(-3)mol/L)时收缩张力依次回落.在无钙液中罗哌卡因未能诱发脐动脉环收缩,而随细胞外液钙离子浓度增加较低浓度罗哌卡因致脐动脉收缩张力增加.维拉帕米可显著抑制罗哌卡因对脐动脉环的收缩反应,而维拉帕米+钌红、维拉帕米+肝索并不增加维拉帕米的抑制作用.结论 罗哌卡因可诱发离体人脐动脉剂量关联性双相收缩效应.细胞外Ca~(2+)通过L-型钙通道内流,而非肌质网Ca~(2+)释放,使细胞内[Ca~(2+)]升高介导了罗哌卡因诱发的血管平滑肌收缩反应.
目的 研究不同濃度囉哌卡因對離體人臍動脈平滑肌的收縮作用,併分析其可能的機製.方法 採用離體臍動脈環灌流模型,用MedLab生物信號採集繫統測定併記錄血管的張力變化情況,觀察纍積濃度囉哌卡因對去內皮血管環的收縮效應,併同時觀察細胞外Ca~(2+)"濃度、L-型Ca~(2+)通道阻滯劑維拉帕米、內質網三燐痠肌醇受體阻滯劑肝素和蘭尼定受體阻滯劑釕紅對囉哌卡因血管效應的影響.結果 囉哌卡因誘髮劑量關聯性雙相臍血管反應:在低濃度(1.0×10~(-5)~1.0 × 10(~4)moL/L)時收縮張力逐漸升高,較高濃度(3.0×10~(-4)~3.0×10~(-3)mol/L)時收縮張力依次迴落.在無鈣液中囉哌卡因未能誘髮臍動脈環收縮,而隨細胞外液鈣離子濃度增加較低濃度囉哌卡因緻臍動脈收縮張力增加.維拉帕米可顯著抑製囉哌卡因對臍動脈環的收縮反應,而維拉帕米+釕紅、維拉帕米+肝索併不增加維拉帕米的抑製作用.結論 囉哌卡因可誘髮離體人臍動脈劑量關聯性雙相收縮效應.細胞外Ca~(2+)通過L-型鈣通道內流,而非肌質網Ca~(2+)釋放,使細胞內[Ca~(2+)]升高介導瞭囉哌卡因誘髮的血管平滑肌收縮反應.
목적 연구불동농도라고잡인대리체인제동맥평활기적수축작용,병분석기가능적궤제.방법 채용리체제동맥배관류모형,용MedLab생물신호채집계통측정병기록혈관적장력변화정황,관찰루적농도라고잡인대거내피혈관배적수축효응,병동시관찰세포외Ca~(2+)"농도、L-형Ca~(2+)통도조체제유랍파미、내질망삼린산기순수체조체제간소화란니정수체조체제조홍대라고잡인혈관효응적영향.결과 라고잡인유발제량관련성쌍상제혈관반응:재저농도(1.0×10~(-5)~1.0 × 10(~4)moL/L)시수축장력축점승고,교고농도(3.0×10~(-4)~3.0×10~(-3)mol/L)시수축장력의차회락.재무개액중라고잡인미능유발제동맥배수축,이수세포외액개리자농도증가교저농도라고잡인치제동맥수축장력증가.유랍파미가현저억제라고잡인대제동맥배적수축반응,이유랍파미+조홍、유랍파미+간색병불증가유랍파미적억제작용.결론 라고잡인가유발리체인제동맥제량관련성쌍상수축효응.세포외Ca~(2+)통과L-형개통도내류,이비기질망Ca~(2+)석방,사세포내[Ca~(2+)]승고개도료라고잡인유발적혈관평활기수축반응.
Objective To investigation the effect of ropivacaine on the contraction of the isolated human umbilical artery and the mechanisms involved. Methods Endothelium-denuded human umbilical artery rings obtained from healthy full-term paturients were prepared. Using isometric force transducers and a fluorometer, the effect of ropivacaine in cumulative concentration on the contraction response induced by KCl in the presence or absence of verapamil, or verapamil plus ruthenium red or verapamil plus heparin was observed. Furthermore, the effect of ropivacaine on the contraction response of the artery rings incubated in different concentrations of extracellular Ca~(2+) was also observed. Results Ropivacaine induced a dose-dependent biphasic contractile response of human umbilical artery rings; increasing at concentrations of 1.0 × 10~(-5) to 1.0 ×10~(-4) mol/Land decreasing from 3. 0 × 10~(-4) to 3.0×10~(-3) mol/L, which was inhibited by verapamil, or verapamil plus ruthenium red, or verapamil plus heparin. No difference was found between pre-treatment of verapamil, verapamil plus ruthenium red and verapamil plus heparin. Ropivacaine induced no contractile response in Ca~(2+) -free solution and a extracellular Ca~(2+) dose-dependent increasing contractile response(1.0 × 10~( -4) to 3.0 × 10 ~(-2)mol/L ). Conclusion Ropivacaine induced a dose-dependent biphasic contractile response of human umbilical artery rings. The increase in intracellular Ca~(2+) concentrations by the extracellular Ca~(2+) influx, not by the release from the sarcoplasmic reticulum, is involved in ropivacaine-induced vasoconstriction of human umbilical artery smooth muscle.