Effect of nicotine infusion in humans on platelet aggregation and urinary excretion of a major thromboxane metabolite

The objective of this study was to evaluate further a possible role of nicotine as a stimulator of platelet aggregability and platelet arachidonic acid metabolism in vivo. In six healthy, non-smoking males, platelet aggregability was assessed by filtragometry and impedance aggregometry before, during and after an intravenous infusion of nicotine at two different doses (0.25 and 0.5 μg kg^-1 min^-1) for 30 min. The aggregatory response was also measured after the addition of nicotine at final concentrations ranging from 10^-11 mol L^-1 to 10^-5 mol L^-1 directly to the aggregating blood. The synthesis of thromboxane A₂ (TxA₂) in platelets was estimated by quantitating the urinary excretion of 2,3-dinor-thromboxane B₂ (Tx-M). Despite the plasma concentrations of nicotine, cotinine and catecholamines in the range of those occurring during acute cigarette exposure, the excretion of Tx-M (204±36 pg mg^-1 creatinine) remained unaltered during nicotine infusion. Similarly, platelet aggregatory response to collagen was not influenced by nicotine when infused or added in vitro. However, an enhanced aggregability was detected by filtragometry during the infusion of nicotine at the higher dose employed. The results indicate that nicotine, infused at moderate doses, produces a weak platelet stimulation that is not accompanied by significant release of thromboxane A₂, as monitored by urinary excretion of Tx-M. Although a direct action of nicotine on platelets cannot be excluded, it appears more likely that the enhancement of platelet function is mediated by other, secondary mechanisms.     

Effects of adenosine on ex vivo filtragometry platelet aggregation in relation to plasma levels

The aim of the present study was to investigate the concentration effect of adenosine on unstimulated platelet aggregation in humans. Adenosine infusion was given intravenously to 12 volunteers in the antecubital vein with infusion rates increasing from 20 to 100 μg kg^?1 min^?1. Filtragometry measurements were obtained from the contralateral antecubital vein before and during 100 μg kg^?1 min^?1 or during maximal tolerable infusion rate. In another set of experiments with 10 volunteers, basal filtragometry measurements were obtained before and after infusion of various concentrations of adenosine into the filtragometer test unit. With intravenous infusion aggregation time tended to increase from 333±42 to 418±8 s (mean±SEM) and increased the venous plasma adenosine concentration from 0.42±0.09 μM to 1.52±0.38 μM . Adenosine infusion into the filtragometer tubing system dose-dependently inhibited aggregation (P<0.05). Adenosine was rapidly eliminated with a half-life of adenosine in the filtragometry tubing system calculated to be about 6 s. These data extend our knowledge from an in vitroto an ex vivo situation that adenosine dose-dependently has a platelet antiaggregatory effect.     

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.     

Synthetic polycations as activators of the endogenous mechanism of platelet aggregation

Synthetic nitrogenous cationic polymers possess the ability to aggregate platelets in citrated plasma in a concentration of 1.5–10 g/ml. The action of polycations on platelets leading to their aggregation is brought about, if the cells are in a functionally active state, through activation of the endogenous aggregation mechanism.Scientific-Research Institute of Medical Radiology, Academy of Medical Sciences of the USSR, Obninsk. (Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Fedorov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 83, No. 5, pp. 532–534, May, 1977.     

Effect of statins on platelet function in patients with hyperlipidemia

Introduction

It is generally assumed that cholesterol reduction by statins is the predominant therapeutic result underlying their beneficial effects in cardiovascular disease. However, the action of statins may be partially independent of their effects on plasma cholesterol levels, as they combine lipid lowering with positive effects on hemorheological conditions and endothelial function. We evaluated the impact of statin treatment on platelet adhesion to fibrinogen (spontaneous and ADP-activated), along with ADP, collagen or ristocetin-induced aggregation in type II hyperlipidemic patients.

Material and methods

The study group included 70 persons: 50 patients affected by type II hyperlipidemia without concomitant diseases and 20 healthy volunteers. The effects of 8-week statin treatment (atorvastatin 10 mg/day, simvastatin 20 mg/day, or pravastatin 20 mg/day) on platelet activation were evaluated.

Results

Regardless of the type of statin, a significant decrease in ADP-induced platelet aggregation was observed: for atorvastatin 50.6 ±12.8% vs. 41.1 ±15.8% (p < 0.05), for simvastatin 57.2 ±18.0% vs. 44.7 ±22.1% (p = 0.05), and for pravastatin 55.8 ±19.5% vs. 38.8 ±23.3% (p < 0.05). There was no significant effect of statins on collagen or ristocetin-induced platelet aggregation and adhesion.

Conclusions

Therapy with statins beneficially modifies ADP-induced platelet aggregation in patients with hyperlipidemia and does not affect spontaneous or ADP-induced platelet adhesion to fibrinogen and platelet aggregation induced by collagen or ristocetin.     

Effect of <Emphasis Type="Italic">n</Emphasis>-tyrosol on blood viscosity and platelet aggregation

Experiments on rats showed that n-tyrosol limited the increase in blood viscosity during thermal exposure at a shear rate of 5–300 sec⁻¹ and inhibited ADP-induced platelet aggregation. The effects of n-tyrosol are comparable to that of pentoxyphylline. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 143, No. 1, pp. 67–69, January, 2007     

Comparative study of vasaprostan and alprostan in spontaneous platelet aggregation test in mice

We propose a method for evaluation of spontaneous aggregation of mouse platelets based on routine clinical blood tests for humans. Comparative analysis of Vasaprostan and Alprostan drugs showed that this test can be used for testing of new drugs on animals.Translated from Byulleten Eksperimentalnoi Biologii i Meditsiny, Vol. 138, No. 10, pp. 475–476, October, 2004     

Comparative study of vasaprostan and alprostan in spontaneous platelet aggregation test in mice

We propose a method for evaluation of spontaneous aggregation of mouse platelets based on routine clinical blood tests for humans. Comparative analysis of Vasaprostan and Alprostan drugs showed that this test can be used for testing of new drugs on animals.Translated from Byulleten Eksperimentalnoi Biologii i Meditsiny, Vol. 138, No. 10, pp. 475–476, October, 2004     

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。