Regulatory role of endothelium in vascular contractility.

在生理和病理条件下，内皮细胞在调节血管张力方面起着重要的作用。前列腺素预缩窄的猪冠状动脉(Pg&lt；F2&Gt；)可被P物质以剂量依赖的方式松弛。这种松弛依赖于内皮的存在，当覆盖在内膜表面的内皮被故意摩擦超过50%时，这种松弛被显着抑制。在血液成分中，如血小板、白细胞、纤维蛋白原-纤维蛋白原产物和其他形成元素，包括红细胞，溶血物(HE)，特别是氧合血红蛋白(Hb)可强烈增强犬脑动脉的肌源性张力，这似乎也部分依赖于内皮。离体脑动脉螺旋段或环段的静态和动态拉伸，即制剂过度伸长至基础张力增加1.5g，以10厘米/秒的速度快速拉伸，或…当动脉圆柱段的腔内灌流压(IPP)从60 cm突然增加到100 cm时，会产生收缩。从自体血中提取少量HE(20-60 mg/dl，Hb)，引起基础张力轻微升高，不仅增强了牵张或IPP引起的收缩，而且增强了5-羟色胺、组胺、去甲肾上腺素和PG&lt；F_(2x)&Gt；产生的血管收缩，是对照组的2-3倍。硝苯地平-维拉帕米型钙拮抗剂可抑制HE所致的收缩和细胞外钙的回撤。他没有引起用皂苷化学剥皮和预加钙的大脑动脉肌束张力的明显增加。此外，去内皮可抑制HE所增强的收缩，而去内皮制剂与未去内皮的血管内膜接触时，可部分恢复这种收缩。用细胞内钙离子分析仪同时、连续地记录几种激动性刺激、高钾和氧合血红蛋白引起的脑血管收缩和钙瞬变，表明这些刺激引起的收缩增加伴随着钙瞬变的增加。这些结果表明，少量的HE可作为各种血管收缩刺激的钙依赖增强剂，其作用依赖于内皮。在本研究中，内皮在猪冠状动脉中起扩张作用，而在犬脑动脉中起收缩作用。血管内皮细胞释放血管扩张或收缩物质(S)似乎是可能的，这取决于所用的激动性刺激和血管组织。血管异质性意味着不仅内侧平滑肌及其周围组织如神经元件，而且内皮细胞在调节血管张力的结构和功能上也可能是不同的。较少

The endothelium has been known to play an important role in controlling vascular tone in physiological and pathological conditions. Isolated porcine coronary artery preconstricted with prostaglandin <F_2> (PG <F_2> ) relaxed by substance P in a dose-dependent manner. The relaxation was dependent on the presence of endothelium and was significantly inhibited when more than 50% of endothelium covered over the intimal surface was intentionally rubbed. Among blood components such as platelets, leucocytes, fibrin-fibrinogen products and other formed elements, includinig erythrocytes, hemolysate (HE), in particular oxyhemoglobin (Hb) strongly potentiated myogenic tone of canine cerebral artery, which also seems to be in part dependent on the endothelium. The static and dynamic stretch of isolated cerebral artery in form of helical or ring segment, i.e., excessive elongation of the preparation up to increase in basal tension of 1.5 g and quick stretch at a rate of 10 cm/sec, respectively, or … More sudden increase in the intraluminal perfusion pressure (IPP) of cylindrical segment of the artery from 60 to 100 cm <H_2> O produced contraction. A small amount of HE (20-60 mg/dl as Hb) obtained from autologous blood, inducing a slight increase in basal tension potentiated not only the stretch- or IPP-induced contraction but also vasoconstrictions produced by serotonin, histamine, norepinephrine and PG <F_(2X)> 2-3 times those of control. The contraction potentiated by HE was inhibited by Ca antagonists of nifedipine-verapamil type and withdrawal of wxtracellular Ca. HE did not produce any apparent increase in tension of muscle bundle of the cerebral artery which was chemically skinned by saponin and preloaded with Ca. Furthermore, the contraction potentiated by HE was inhibited by removal of endothelium, while the reduced contraction was partially restored when the endothelium-removed preparation was in contact with intimal surface of the endothelium-unrubbed one. Simultaneous and continuous recordings of contractions and Ca transients by use of intracellular Ca analyzer in the cerebral artery produced by several agonistic stimuli, high K and oxyhemoglobin indicated that the increase in contraction in response to these stimuli was concomitant with augmentation of ca transients. These results suggest that a small amount of HE acts as a Ca-dependent potentiator of various vasoconstrictor stimuli and that the effect is dependent on endothelium. In the study, endothelium acts dilative in porcine coronary artery, but constrictive in canine cerebral artery. It seems possible that the endothelium liberates vasodilative or constrictive substance(s), depending on the agonistic stimuli and vascular tissues used. Vascular heterogeneity implies that not only medial smooth muscles and their surrounding tissues such as nervous elements, but also the endothelium may be diverse in the structures and functins for regulation of vascular tone. Less