Hypothesis that embolization is an important mechanism in the laser destruction of cutaneous vascular lesions

It is hypothesized that laser-induced red blood cell aggregations form emboli that assist in the therapeutic effect of lasers on vascular lesions.     

Arteriolar Dilation Produced by Venule Endothelium-Derived Nitric Oxide

Objective: We conducted bioassay experiments to determine whether nitric oxide produced by endothelial cells (endothelial-derived nitric oxide, or EDNO) within large venules could act to dilate arterioles. Methods: In these experiments, parallel segments of first-order arterioles and venules were isolated from skeletal muscle and were cannulated in series with a glass connecting tube (length: 300–500 μm). Arterioles were mechanically denuded of endothelium by a delicate yet abrasive rubbing technique. Venular endothelium remained intact. Endothelial denudation of arterioles was confirmed by the absence of dilation during exposure to acetylcholine (10^?6 mol/L). The cannulated vessels were pressurized to 30 cm H₂O and the arterioles preconstricted by approximately 50% with norepinephrine (10^?10 mol/L). Results: Topical applications of acetylcholine (10^?6 mol/L) or bradykinin (10^?9 mol/L) during luminal perfusion from venule to arteriole produced significant arteriolar dilation. In contrast, a slight arteriolar constriction was observed when the direction of flow was reversed (i.e., arteriole to venule) in the presence of either acetylcholine (10^?6 mol/L) or bradykinin (10^?9 mol/L). Inhibition of venular EDNO with; N^C-monomethyl-L-arginine (L-NMMA; 10^?5 mol/L; 1 hour) completely abolished the arteriolar dilation observed in response to acetylcholine or bradykinin during venule to arteriole perfusion. Conclusions: These results demonstrate that venular-derived EDNO can relax arteriolar vascular smooth muscle.     

不同年龄自发性高血压大鼠肾内小动脉的形态学重建

目的:探讨高血压大鼠年龄、高血压持续时间与肾内小动脉形态学重建的关系。方法:16,26,40和55周自发性高血压大鼠（SHR）,使肾内小动脉处于最大舒张状态后,在肾组织切片上用光镜配合计算机图像分析法观测肾内小动脉的几何形态。结果:与同龄正常血压大鼠(Wistar-Kyoto,WKY)相比,4个年龄组SHR肾内小动脉的壁厚、壁厚内径比都显著增大;外径在50-200 μm间的小动脉还伴有壁面积的增加;40和55周SHR外径在20-50 μm间的小动脉内径减小。肾内小动脉的形态学改变与年龄和高血压状态有关。结论:高血压是16-55周龄SHR肾内小动脉重建的主要因素,外径在50 μm以下的肾内小动脉的重建以中膜平滑肌细胞的重排为主,外径在50 μm以上的肾内小动脉的重建则存在中膜平滑肌细胞的增殖。     

犬肾动脉栓塞DSA成像技术的改进

本实验使用丝裂霉素c白芨胶行犬肾动脉栓塞，将30条犬随机分MMC白芨胶，MMC碘油，MMC白芨胶＋白芨、单纯白芨胶，MMC稀白芨胶、MMC溶液，对照7组。着重讨论大肾动脉栓塞前后DSA成像问题，指出了合理使用麻醉剂、安定、抑制肠蠕动等药物，以及犬腹部加压，选用DSA的TID程序，可望获得高质量的DSA图像。     

不同浓度丙泊酚通过缝隙连接通讯对舒张大鼠肠系膜动脉的影响

目的观察丙泊酚对SD大鼠肠系膜动脉的影响和对肠系膜动脉舒张作用是否与缝隙连接通讯相关。方法应用压力肌动图技术,在急性分离的SD大鼠肠系膜动脉2级血管上,观察1×10-7、3×10-7、1×10-6、3×10-6、1×10-5、3×10-5、1×10-4和3×10-4 mol/L丙泊酚对血管直径的影响,预孵育缝隙连接阻断剂18-β甘草次酸(18β-glycyrrhetinic acid,18β-GA)和2-aminoethoxydiphenylborate(2-APB)后,观察丙泊酚对血管直径的影响。结果给予1×10-7、3×10-7、1×10-6、3×10-6、1×10-5、3×10-5、1×10-4和3×10-4 mol/L的丙泊酚,使SD大鼠血管直径从(208.6±13.4)μm分别增加至(213.5±13.6)、(219.7±13.2)、(226.4±12.5)、(234.9±12.3)、(245.5±13.0)、(267.4±15.2)、(336.2±18.3)和(385.9±14.2)μm,1×10-4 mol/L的丙泊酚引起血管直径随着丙泊酚浓度增大而增加(P0.01)。分别预孵育18β-GA和2-APB后,1×10-4 mol/L的丙泊酚对大鼠肠系膜动脉舒张作用明显减弱(P0.01)。结论丙泊酚呈浓度依赖性舒张肠系膜动脉,其作用机制可能与缝隙连接通讯相关。     

视网膜动脉平滑肌细胞中大电导钙离子激活钾通道电流和钙离子浓度变化对糖尿病视网膜动脉收缩的影响

背景 糖尿病视网膜病变(DR)是常见的视网膜微血管并发症,视网膜血管平滑肌细胞大电导钙激活钾离子通道(BK)是调节血管舒缩和血液动力的主要因素.目前关于视网膜动脉平滑肌细胞(RASMCs)上BK通道的功能变化在DR形成中的作用鲜有研究报道. 目的 研究正常及糖尿病模型大鼠RASMCs中BK通道电流、钙离子浓度及不同钙离子浓度下BK通道开放概率(NP0)的变化,探讨DR早期的血管损伤机制. 方法 采用随机数字表法将50只SPF级8～12周龄SD大鼠随机分为正常对照组和糖尿病模型组,糖尿病模型组40只大鼠腹腔内注射60 mg/kg链脲佐菌素(STZ)法制作1型糖尿病模型,正常对照组大鼠10只同法注射枸橼酸钠溶液.采用酶消化法分离大鼠RASMCs,应用全细胞膜片钳技术记录大鼠RASMCs中BK通道电流;采用荧光探针法测定大鼠RASMCs内钙离子浓度;采用膜内向膜外型单通道膜片钳技术记录不同钙离子浓度条件下RASMCs中BK单通道NP0的变化.结果 36只大鼠糖尿病造模成功,造模成功率为90％.刺激电压大于60 mV时,糖尿病模型组大鼠RASMCs中BK通道电流密度明显下降,刺激电压为100 mV时,正常对照组和糖尿病模型组大鼠RASMCs BK通道电流分别为(100±23) PA/PF和(50±7) PA/PF,差异有统计学意义(t=19.80,P＜0.05).当加入BK通道特异性阻滞剂非洲蝎毒素100 nmol后,正常对照组的BK通道电流明显减弱,而糖尿病模型组BK通道电流无明显变化;正常对照组和糖尿病模型组大鼠RASMCs内钙离子浓度分别为(123±11)nmol/L和(255士10)nmol/L,差异有统计学意义(t=32.50,P＜0.05).在刺激电位为60 mV条件下,随着钙离子浓度增加,BK通道NP0增加,差异有统计学意义(F=15.28,P＜0.05).结论 糖尿病模型大鼠RASMCs中BK通道电流下降,细胞内钙离子浓度升高,BK单通道NP0下降.BK通道功能改变可能是导致糖尿病时视网膜动脉异常收缩的主要原因之一.