Effect of bradykinin on platelet aggregation

The effect of bradykinin on ADP-induced aggregation of blood platelets was investigated in rabbits. Bradykinin reduced the degree of aggregation; maximal inhibition of aggregation was observed with the use of bradykinin in a concentration of 10–100 ng/ml. Higher concentrations of bradykinin were less effective. An essential condition for inhibition was a period of preincubation of bradykinin with the platelets. Inhibition of aggregation by bradykinin also was observed on canine platelets.Group for the Study of Mechanisms of Thrombosis, All-Union Cardiologic Scientific Center, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Sciences of the SSSR E. I. Chazov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 88, No. 8, pp. 139–141, August, 1979.     

Effect of high-density lipoproteins on ADP-induced platelet aggregation in plasma

Autooxidized high-density lipoproteins (HDL₂) inhibit ADP-induced platelet aggregation in platelet-rich plasma. Platelet aggregation in the presence of native HDL₂ and HDL₃ and autooxidized HDL₃ does not differ from the control (plasma with buffer). A conclusion is made on the important role of autooxidized HDL₂ as a thrombogenesis-inhibiting factor in atherosclerosis. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 126, No. 8, pp. 160–163, August, 1998     

中性粒细胞对洗涤血小板聚集功能的影响

目的:观察非激活或激活的中性粒细胞(PMN)对洗涤血小板聚集功能的影响。方法:采用Born方法测定血小板聚集功能。结果:非激活的PMN(5×10⁹cells/L)上清液对ADP和花生四烯酸(AA)诱导的血小板聚集具有显著抑制作用,阿司匹林可增强这种抑制作用;肉豆寇佛波醇(fMLP)及血小板活化因子(PAF)激活的PMN悬液或其上清液均能活化血小板聚集,且PMN悬液的诱聚作用比其上清液更强;阿司匹林对fMLP或PAF激活的PMN悬液或其上清液均无明显抑制作用。结论:不同状态(非激活或激活状态)的PMN对正常血小板的反应性表现出完全相反的作用,即非激活的PMN抑制血小板反应性,而激活的PMN则具有促血小板活化聚集作用。     

Effect of UV-modified fibrinogen on platelet aggregation in platelet-rich plasma

Oxidized UV-modified fibrinogen activates platelets in platelet-rich plasma. Kinetic turbidimetry showed that addition of oxidized fibrinogen to platelet-rich plasma led to platelet aggregation. Reversible aggregation is recorded starting from the 30th second and then constantly grows with the same rate. Nonoxidized fibrinogen produced no such effect. The relationship between aggregation intensity and rate and the degree of fibrinogen oxidation was described by a bell-shaped curve with a peak corresponding to 24% fibrinogen oxidation. The amplitude of aggregation increased with increasing the concentration of irradiated fibrinogen from 0.1 to 1.0 mg/ml and then plateaued. The rate of aggregation little depended on fibrinogen concentration.     

Dependence of platelet aggregation response on arginyl-glycyl-asparagine tripeptide

Laboratory of Biochemistry, Central Research Institute of Hematology and Blood Transfusion, Ministry of Health of the USSR. All-Union Cardiologic Scientific Center, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR A. I. Vorob'ev.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 107, No. 5, pp. 536–537, May, 1989.     

Difference between mechanisms of changes in platelet and erythrocyte aggregation in renal failure

Aggregation reactions of platelets and erythrocytes were studied in chronic renal failure. Differences in the mechanism of aggregation of platelets and erythrocytes are discussed on the basis of data showing opposite changes in the aggregation function of cells of the same subjects under similar conditions.Laboratory of Physiology of the Circulation, I. P. Pavlov Institute of Physiology, Academy of Sciences of the USSR. Department of Field Medicine, S. M. Kirov Military Medical Academy, Leningrad. (Presented by Academician of the Academy of Medical Sciences of the USSR V. N. Chernigovskii.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 89, No. 3, pp. 263–265, March, 1980.     

Effect of recent alcohol intake on acceptor properties of high-density lipoproteins and their interaction with liver cells

Institute of Therapy, Siberian Branch, Academy of Medical Sciences of the USSR, Novosibirsk. All-Union Preventive Medicine Research Center, Ministry of Health of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR Yu. P. Nikitin.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 110, No. 12, pp. 611–613, December, 1990.     

Investigation of the effect of some xanthine derivatives on platelet aggregation and other indices of hemostasis

Experiments on rabbits and in vitro showed the antiaggregation action of some new xanthine derivatives. It was shown that they also have anticoagulant activity and prevent thrombus formation.Department of Pharmacology, Moscow Medical Stomatological Institute. Laboratory of Pharmacology, S. Ordzhonikidze All-Union Pharmaceutical Chemical Research Institute, Moscow. Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 89, No. 2, pp. 181–182, February, 1980.     

Radio-isotopic platelet labeling with monoclonal antibody against membrane glycoprotein IIb–IIIa. Measurement of platelet adhesion/aggregation to the substrate

Institute of Experimental Cardiology, Cardiologic Scientific Center, Russian Academy of Medical Sciences, Moscow. Institute of Cardiology, Ministry of Health of the Uzbekistan Republic, Tashkent. (Presented by Academician of the Russian Academy of Medical Sciences V. N. Smirnov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 114, No. 11, pp. 529–532, November, 1992.     

Early stages in the mechanism of action of glucocorticoids on human platelets. Effect of hydrocortisone on platelet aggregation

Hydrocortisone (1–10 μM) has no effect on spontaneous platelet aggregation and induces a 5–10-sec latency after platelet activation with 1 μM ADP. Hydrocortisone inhibits collagen-induced platelet aggregation; this effect is blocked by excess of progesterone. Hydrocortisone potentiates the effect of adenosine on disaggregation: in the absence of the hormone IC₅₀ for adenosine is 2.5 μM, while in the presence of 3 and 10 μM hydrocortisone it drops to 1.7 and 0.4 μM, respectively. Translated fromByulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 123, No. 1, pp. 54–57, January, 1997     

高密度脂蛋白与血管内皮功能保护

高密度脂蛋白(HDL)由一系列结构和功能不同的脂蛋白家族组成,它通过与清道夫受体-B I(SR-B I)结合促进NO的生成,从而对血管内皮细胞依赖的血管活性具有直接的保护作用。SR-B I受体与内皮脂酶(EL)共同调节HDL的代谢而影响血管内皮功能。HDL的间接血管内皮功能保护作用-抗氧化作用与其携带的酶和转运的一些酶有关,如HDL抑制内皮细胞表达黏附分子而减轻炎症反应对内皮细胞的损伤;HDL包含的可溶性鞘内脂质调节血管内皮细胞的凋亡,抑制血管内皮细胞增殖。因此升高HDL有希望成为改善血管内皮细胞功能的临床治疗目标。     

Participation of IIb-IIIa glycoprotein in spontaneous platelet aggregation

In some patients with stable and unstable angina pectoris and in some donors without clinical manifestations of cardiovascular diseases and other pathologies, spontaneous platelet aggregation was completely suppressed by glycoprotein IIb-IIIa antagonists blocking the interaction of this glycoprotein with fibrinogen. Antibodies inhibiting binding of glycoprotein Ib with von Willebrand factor had no effect on the level and rate of spontaneous platelet aggregation. In the donor group, the level of spontaneous aggregation was almost 1.5-fold higher in persons with a certain genetic polymorphism (Leu-->Pro substitution in position 33 of glycoprotein IIIa). The level of spontaneous aggregation correlated with the amount of glycoprotein IIb-IIIa on the platelet surface (r = 0.41).