Aggregation of platelets and their role in the hypocoagulation syndrome was studied after in vitro irradiation of blood with a laser. Thromboelastography was performed in plateletrich and platelet-free plasma. Low-intensity laser radiation affected the coagulation system via platelets. It decreased platelet aggregation induced by ADP, collagen, epinephrine, ristocetin, platelet activating factor, and fibrinogen. Key Words: low intensity laser radiation; blood coagulation; blood plateletsLow-intensity laser radiation (LILR) improves rheological parameters of the blood and provokes hypocoagulation syndrome [6]. LILR affects blood coagulation system and fibrinolysis as evidenced by blood decreased blood coagulability and retards clot formation. This phenomenon is explained by inhibition of thromboplastin activation and delay of the prothrombin-thrombin conversion without any significant effect on fibrinogenesis [7]. There is evidence arguing these findings [10]. This discrepancy is probably related to different methods of LILR. Our data obtained in large-scale clinical studies show that irradiation of blood by a lowintensity laser light (L=630 nm, beam power 1 mW) decreases functional activity of platelets [9]. Our aim was to study the role of platelets in the hypocoagulation syndrome after irradiation of blood with a laser light. MATERIALS AND METHODSBlood was obtained from 10 donors. It was drawn from the cubital vein and stabilized with 3.8% sodium citrate, and irradiated in vitro for 15 min using

We have examined the effect of a low-intensity laser radiation (wavelength 630 nm, beam power 1 mW) on the aggregability of blood platelets, acidic tolerance of elythrocytes, and the structure of their membranes. Laser radiation suppressed platelet aggregability induced by ATP, epinephrine, collagen, platelet activating factor, and fibrinogen and enhanced the resistance of the erythrocytes. It decreased the lnicroviscosity of lipid bilayer and of the membrane protein-lipid contact regions and slowed down lipid peroxidation. These findings attest to a direct membranotropic effect of laser radiation, which is particularly strong in the protein-lipid contact regions.

Effects of laser radiation (wavelength 630 nm, power 1 roW) on platelet aggregation in human blood in vitro and in vivo and on platelet sensitivity to thromboxane A as well as on cyclooxygenase and thromboxane synthetase activities were studied. Changes in platelet functional activity were shown to be related to platelet transformation into inactive discoid form, suppression of their sensitivity to endogenous activators, and decreased activity of the arachidonic acid cascade enzymes. Key Words: blood; platelets; laser irradiationLow-intensity laser radiation produces a positive effect on microcirculation and on theological properties of the blood (suppression of the sludge phenomenon [7]) due to suppression of platelet function [1,8]. Platelet failure caused by laser rays results in the hypocoagulation syndrome [10]. All these factors increase the organic blood flow, in particular, in the case of vascular atherosclerotic lesions [5]. Modification of platelet function depends on the parameters of laser radiation [1]. Although the effects of laser radiation on platelet function have been thoroughly investigated, the mechanism of its action remains to be clarified.In the present work we studied mechanisms of the platelet function suppression produced by lowintensity laser radiation. MATERIALS AND METHODSBlood from 17 patients with nonspecific reactive hepatitis and 14 healthy volunteers was collected from the cubital vein in 3.8% sodium citrate. Donor's blood was permanently mixed and irradiated in vitro for 15 rain using an ALOK-1 laser (wavelength 630 nm, power 1 mW). In patients, in vivo blood irradiation in the cubital vein was performed through Department of Pharmacology and Department of Visceral Propedeutics, Volgogmd Medical Academy an intravenous light pipe. The same laser beam parameters were used. The 30-rain irradiations were repeated daily during a 5-day period. The blood was collected before and after the course of irradiation:Platelet-rich plasma was prepared according to [6]. Platelet aggregation was studied by the method [12] modified as in [2]. The kinetics of platelet aggregation was monitored with a 230LA dual-channel laser platelet aggregation analyzer (Biola Ltd., Russia). Platelets were activated with: ADP (5 gM, Serva), adrenaline hydrochloride (5 ~tM), platelet activating factor (0.01 gM, Sigma), collagen (4 ~tg/ml, Sigma), ristocetin (1.2 ~tg/ml, Sigma), and fibrinogen (3 g/l). The degree of platelet aggregation was expressed as percentage of light transmission. Aggregograms were analyzed suing an AGGR 2.20 (Biola) software [3]. Morphology and the number of platelets in aggregates were estimated with the Biola aggregation analyzer by the method [3].Platelet sensitivity to thromboxane A~ (Tx A2) , cyclooxygenase (COx) and thromboxane synthetase (TxS) activities were assessed indirectly in the tests with collagen (TxP h production inducer), aspirin (COx inhibitor), and imidasole (TxS inhibitor) by the method [4]. Platelet activity was assessed by changes in the mean size of aggregate.The resu...