多塞平对离体兔基底动脉环和隐动脉环的作用

AIM: To study the effects of doxepin (Dox) on cerebral artery. METHODS: The effects of Dox were observed using the isolated basilar and saphenous artery rings of rabbits. RESULTS: Dox inhibited the constriction of the basilar and saphenous artery rings evoked by KCl with IC50 5.75 mumol.L-1 (95% confidence limits were 2.3-14 mumol.L-1, n = 8) and 34.6 mumol.L-1 (95% confidence limits were 3.8-316 mumol.L-1, n = 8), respectively. Dox also inhibited the constriction of the basilar and saphenous artery rings of the rabbits stimulated by 5-hydroxytryptamine (5-HT), IC50 were 6.3 mumol.L-1 (95% confidence limits were 1.7-23.3 mumol.L-1, n = 7) and 8.0 mumol.L-1 (95% confidence limits were 6.3-10.3 mumol.L-1, n = 6), respectively. In both samples (basilar and saphenous artery rings) CaCl2 evoked, the pD2 of Dox was 5.28 +/- 0.40 and 4.76 +/- 0.14, respectively (n = 6, P < 0.01). Dox 5.8 mumol.L-1 inhibited the constriction of the saphenous artery evoked by norepinephrine (NE) in Ca(2+)-free medium. Dox 30 mumol.L-1 inhibited the constriction of the saphenous artery evoked both by NE and by readmission of CaCl2 (1.25 mmol.L-1). CONCLUSION: As compared with its effect on the saphenous artery, Dox selectively inhibited the basilar artery.     

Acute toxicity of dipfluzine and its effects on isolated vascular smooth muscle

Dipfluzine (Dip) is a new derivative of cinnarizine (Cin) first developed by Department of Chemistry, Beijing University. Dip showed a dose-dependently inhibitory effect on both KCl- and NE-induced contraction in the rabbit aortic rings. It was more effective in suppressing the contractile response evoked by KCl than that by NE. Dip also inhibited the KCl-induced contraction in porcine basilar, coronary and radial arteries. Their pD2' values were 5.7 +/- 0.6, 5.4 +/- 0.4 and 4.6 +/- 0.5 respectively. The selectivity of Dip for vasodilation was proved by higher pD2' value of the basilar artery than that of the coronary and radial arteries, and this selectivity of Dip was more significant than that of Cin. The acute iv LD50 of Dip and Cin in mice were 37 and 36 mg/kg, respectively.     

氯通道阻断剂对KCl、5-HT引起的兔脑椎基底动脉血管环收缩效应的影响

目的　探讨不同种类氯通道阻断剂在不同激动剂引起的脑血管平滑肌收缩反应中的作用。方法　记录离体兔脑椎基底动脉环收缩反应。结果　①氯通道阻断剂DIDS、Furosemide及NPPB均浓度依赖性抑制高K+ 及 5 HT引起血管环收缩反应 ,DIDS、Furosemide及NPPB对 5 HT引起收缩的抑制作用明显强于对KCl的作用 ;②在 5 HT引起血管收缩反应中 ,给予SK&F96 36 5引起血管最大舒张的基础上 ,DIDS、Furosemide及NPPB均可引起血管进一步舒张。结论　氯通道可能参与了由高K+ 去极化和 5 HT引起的兔脑椎基底动脉环收缩反应     

山楂水提取物对猪离体冠状动脉环的舒张作用研究

目的:研究山楂水提取物对猪离体冠状动脉环的舒张作用。方法:观察0.1、0.3、0.5mg·mL-1山楂水提取物对KC(l30mmol·L-1)诱发的猪离体冠状动脉环收缩的舒张作用。以Na+/Ca2+交换体阻滞剂KB-R7943(1×10-6mol·L-1)、电压依赖性钾通道(KV)阻滞剂四胺基吡啶(4-AP,1×10-3mol·L-1)、K+-ATP通道阻滞剂格列苯脲(Gli,1×10-5mol·L-1)、K+/Ca2+通道阻滞剂乙胺(TEA,1×10-2mol·L-1)、内向整流钾通道(KiR)阻滞剂氯化钡(BaCl2,1×10-3mol·L-1)预处理血管环,观察其对山楂水提取物舒血管作用的影响。结果:山楂水提取物对KCl预收缩的猪离体冠状动脉环产生浓度依赖性的舒张作用。用KB-R7943、4-AP、Gli预处理的血管环对山楂水提取物的舒张反应与未经处理时比较无显著性差异(P>0.05)。TEA和BaCl2预处理的血管环对山楂水提取物的舒张反应与未经处理时比较有显著性差异(P<0.01)。结论:山楂水提取物对KCl预收缩的猪离体冠状动脉环具有浓度依赖性的舒张作用,其舒张反应可能与K+/Ca2+通道和KiR通道有关,与Na+/Ca2+交换体、KV通道和K+-ATP通道无关。     

链佐星所致糖尿病大鼠主动脉内皮依据舒张反应损伤的特征

AIM: To study whether impaired endothelium-dependent relaxation (EDR) in early diabetic mellitus in response to different receptor-mediated and nonreceptor-mediated vasodilators ran parallel and its possible mechanism. METHODS: Isometric tension recording in aortic rings from streptozotocin (Str)-induced diabetic and age-matched nondiabetic rats. RESULTS: EDR induced by receptor agonist acetylcholine (ACh), histamine (His) or bradykinin (BK) were all significantly reduced in diabetic rings compared with control rings, whereas nonreceptor agonist calcimycin-induced EDR was well reserved in diabetic rings [IC50 control: (0.13 +/- 0.07) mumol.L-1 diabetic: (0.14 +/- 0.06) mumol.L-1, P > 0.05, n = 7]. Cyclopiazonic acid (CPA) which also is a nonreceptor mediated endothelium-dependent vasorelaxant and cells' capacitative Ca2+ entry stimulant, failed to trigger EDR in diabetic rings. Pretreatment with N omega-nitro-L-arginine methylester (L-NAME, 0.3 mmol.L-1) not only abolished all of the EDR elicited by above mentioned vasodilators in either of diabetic or control rings, but also leveled responses triggered by each of the agonists between diabetic and control rings. Upon the maximal EDR induced by ACh (1 mol.L-1) or CPA (3 mumol.L-1) in phenylephrine (1 mumol.L-1) precontracted rings, calcimycin (1 mumol.L-1) further relaxed diabetic rings, but contracted control preparations. When endothelium was denuded, relaxation evoked by sodium nitroprusside and contractions triggered by CPA or His were all identical between diabetic and control rings. CONCLUSION: Receptor agonists but not nonreceptor agonists-induced EDR are commonly impaired in 4-wk Str-induced diabetic rat aorta, and this defective effect is attributable to the low formation of EDRF/NO which is related to impaired capacitative Ca2+ entry pathway in endothelium.     

降钙素基因相关肽预适应对溶血磷脂酰胆碱抑制内皮依赖性舒张的…

目的：研究降钙素基因相关肽（ＣＧＲＰ）诱导预适应对溶血磷脂酰胆碱（Ｌｙｓ）抑制内皮依赖性舒张的作用。方法：用苯福林收缩兔与大鼠离体胸主动脉环，观察Ｌｙｓ对乙酰胆碱（ＡＣｈ）所致内皮依赖性舒张的影响。结果：ＣＧＲＰ预处理兔和大鼠离体胸主动脉环显著减轻Ｌｙｓ对ＡＣｈ舒血管效应的抑制，其作用可被蛋白激酶Ｃ（ＰＫＣ）抑制剂Ｈ－７所取消。结论：ＣＧＲＰ诱导预适应对所致内皮细胞损伤具有拮抗作用，此作用与激活Ｐ