中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2011年
2期
245-247
,共3页
降钙素基因相关肽%去甲肾上腺素%钙通道,L型%肌细胞,心脏
降鈣素基因相關肽%去甲腎上腺素%鈣通道,L型%肌細胞,心髒
강개소기인상관태%거갑신상선소%개통도,L형%기세포,심장
Calcitonin gene-related peptide%Norepinephrine%Calcium channels,L-type%Myocytes,cardiac
目的 探讨降钙素基因相关肽(CGRP)混合去甲肾上腺素(NE)对大鼠心肌细胞L-型钙电流(ICa-L)的影响.方法 SD大鼠,雌雄不拘,体重260~280 g,急性分离其心肌细胞,用全细胞膜片钳方法记录ICa-L.采用随机数字表法,将心肌细胞随机分为3组(n=6):CGRP组用含CGRP 1×10-7mol/L的台氏液灌流;NE组用含NE 1×10-6mol/L的台氏液灌流;CGRP+NE组(CN组)用含NE 1×10-6mol/L+CGRP 1×10-7mol/L的台氏液灌流.各组均灌流1 min,流速2 ml/min;然后用台氏液洗脱1 min.于灌流前1 min、灌流1 min和洗脱1 min时,记录ICa-L峰值,并绘制CGRP或NE灌流后ICa-L的电流-电压曲线.结果 CGRP可抑制心肌细胞ICa-L(P<0.05).NE可促进心肌细胞ICa-L(P<0.05).与CN组比较,灌流1 min时CGRP组ICa-L降低,NE组ICa-L升高(P<0.05).CGRP使心肌细胞ICa-L的电流-电压曲线明显上移;NE使心肌细胞ICa-L的电流一电压曲线明显下移.结论 CGRP可削弱NE对大鼠心肌细胞ICa-L的促进作用.
目的 探討降鈣素基因相關肽(CGRP)混閤去甲腎上腺素(NE)對大鼠心肌細胞L-型鈣電流(ICa-L)的影響.方法 SD大鼠,雌雄不拘,體重260~280 g,急性分離其心肌細胞,用全細胞膜片鉗方法記錄ICa-L.採用隨機數字錶法,將心肌細胞隨機分為3組(n=6):CGRP組用含CGRP 1×10-7mol/L的檯氏液灌流;NE組用含NE 1×10-6mol/L的檯氏液灌流;CGRP+NE組(CN組)用含NE 1×10-6mol/L+CGRP 1×10-7mol/L的檯氏液灌流.各組均灌流1 min,流速2 ml/min;然後用檯氏液洗脫1 min.于灌流前1 min、灌流1 min和洗脫1 min時,記錄ICa-L峰值,併繪製CGRP或NE灌流後ICa-L的電流-電壓麯線.結果 CGRP可抑製心肌細胞ICa-L(P<0.05).NE可促進心肌細胞ICa-L(P<0.05).與CN組比較,灌流1 min時CGRP組ICa-L降低,NE組ICa-L升高(P<0.05).CGRP使心肌細胞ICa-L的電流-電壓麯線明顯上移;NE使心肌細胞ICa-L的電流一電壓麯線明顯下移.結論 CGRP可削弱NE對大鼠心肌細胞ICa-L的促進作用.
목적 탐토강개소기인상관태(CGRP)혼합거갑신상선소(NE)대대서심기세포L-형개전류(ICa-L)적영향.방법 SD대서,자웅불구,체중260~280 g,급성분리기심기세포,용전세포막편겸방법기록ICa-L.채용수궤수자표법,장심기세포수궤분위3조(n=6):CGRP조용함CGRP 1×10-7mol/L적태씨액관류;NE조용함NE 1×10-6mol/L적태씨액관류;CGRP+NE조(CN조)용함NE 1×10-6mol/L+CGRP 1×10-7mol/L적태씨액관류.각조균관류1 min,류속2 ml/min;연후용태씨액세탈1 min.우관류전1 min、관류1 min화세탈1 min시,기록ICa-L봉치,병회제CGRP혹NE관류후ICa-L적전류-전압곡선.결과 CGRP가억제심기세포ICa-L(P<0.05).NE가촉진심기세포ICa-L(P<0.05).여CN조비교,관류1 min시CGRP조ICa-L강저,NE조ICa-L승고(P<0.05).CGRP사심기세포ICa-L적전류-전압곡선명현상이;NE사심기세포ICa-L적전류일전압곡선명현하이.결론 CGRP가삭약NE대대서심기세포ICa-L적촉진작용.
Objective To investigate the effects of calcitonin gene-related peptide (CGRP) combined with norepinephrine (NE) on L-type calcium current (LCa-l) in rat ventricular myocytes. Methods Ventricular myocytes were isolated from SD rats (weighing 260-280 g) by retrograde perfusion of the heart via the aorta with an enzyme-containing solution as previously described. Whole-cell patch-clamp recording was made using Axopatch 200B amplifier. The cells were perfused for 1 min with Tyrode solution containing CGRP 1 × 10-7 mol/L (group CGRP) , NE 1 × 10-6 mol/L (group NE), or CGRP 1 × 10-7 mol/L + NE 1 × 10-6 mol/L (group CN) and again washed with Tyrode solution. ICa-L was recorded 1 min before and 1 min after the cells were perfused and 1 min after the cells were washed. I-V curve of ICa-L was made after the cells were perfused with solution containing CGRP or NE alone. Results CGRP significantly inhibited the peak of ICa-L, while NE significantly promoted the peak of ICa-L(P < 0.05) . The peak of ICa-L was significantly decreased 1 min after the cells were perfused in group CGRP,while increased 1 min after the cells were perfused in group NE compared with group CN ( P < 0.05). CGRP made the I-V curve of ICa-L move up-ward, while NE made the I-V curve of ICa-L move down-ward. Conclusion CGRP can weaken the promotion of ICa-L induced by NE in rat ventricular myocytes.