Regulatory role of endothelium in vascular contractility.

在生理和病理条件下，内皮在控制血管张力方面起着重要作用。前列腺素<F_2> (PG <F_2>)经P物质松弛后预缩离体猪冠状动脉呈剂量依赖性。松弛依赖于内皮细胞的存在，当有意摩擦覆盖在内膜表面的内皮细胞超过50%时，松弛被显著抑制。在血液成分中，如血小板、白细胞、纤维蛋白-纤维蛋白原产物和其他形成成分，包括红细胞、溶血物（HE），特别是氧合血红蛋白（Hb）强烈增强犬脑动脉的肌张力，这似乎也部分依赖于内皮。离体脑动脉静态和动态拉伸呈螺旋状或环状，即预备物的过度伸长分别达到基础张力增加1.5 g和以10 cm/sec的速度快速拉伸，或在60 ~ 100 cm的圆柱形动脉段内灌注压（IPP）突然升高<H_2>时产生收缩。从自体血液中获得少量HE (20-60 mg/dl，如Hb)，诱导基底张力轻微升高，不仅增强了拉伸或ipp诱导的收缩，而且增强了血清素、组胺、去甲肾上腺素和PG <F_(2X) bb0 2-3倍于对照的血管收缩。硝苯地平-维拉帕米型钙拮抗剂和脱细胞钙对HE增强的收缩作用有抑制作用。HE对经皂苷化学剥皮并预载钙的脑动脉肌束张力无明显增加作用，HE增强的收缩作用可通过去除内皮来抑制。而当去除内皮的制备物与未摩擦内皮的制备物的内膜表面接触时，减少的收缩部分恢复。利用细胞内钙分析仪同时连续记录脑动脉在多种激动性刺激、高钾和氧合血红蛋白作用下的收缩和钙瞬态，表明在这些刺激下收缩的增加伴随着钙瞬态的增强。这些结果表明，少量HE作为各种血管收缩刺激的钙依赖性增强剂，其作用依赖于内皮细胞。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。内皮细胞似乎有可能释放血管扩张或收缩物质，这取决于激动性刺激和使用的血管组织。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存在差异。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