Narcolepsy patients have antibodies that stain distinct cell populations in rat brain and influence sleep patterns.

Narcolepsy is a chronic sleep disorder, likely with an autoimmune component. During 2009 and 2010, a link between A(H1N1)pdm09 Pandemrix vaccination and onset of narcolepsy was suggested in Scandinavia. In this study, we searched for autoantibodies related to narcolepsy using a neuroanatomical array: rat brain sections were processed for immunohistochemistry/double labeling using patient sera/cerebrospinal fluid as primary antibodies. Sera from 89 narcoleptic patients, 52 patients with other sleep-related disorders (OSRDs), and 137 healthy controls were examined. Three distinct patterns of immunoreactivity were of particular interest: pattern A, hypothalamic melanin-concentrating hormone and proopiomelanocortin but not hypocretin/orexin neurons; pattern B, GABAergic cortical interneurons; and pattern C, mainly globus pallidus neurons. Altogether, 24 of 89 (27%) narcoleptics exhibited pattern A or B or C. None of the patterns were exclusive for narcolepsy but were also detected in the OSRD group at significantly lower numbers. Also, some healthy controls exhibited these patterns. The antigen of pattern A autoantibodies was identified as the common C-terminal epitope of neuropeptide glutamic acid-isoleucine/α-melanocyte-stimulating hormone (NEI/αMSH) peptides. Passive transfer experiments on rat showed significant effects of pattern A human IgGs on rapid eye movement and slow-wave sleep time parameters in the inactive phase and EEG θ-power in the active phase. We suggest that NEI/αMSH autoantibodies may interfere with the fine regulation of sleep, contributing to the complex pathogenesis of narcolepsy and OSRDs. Also, patterns B and C are potentially interesting, because recent data suggest a relevance of those brain regions/neuron populations in the regulation of sleep/arousal.

Effect of Sclerovit on endothelial dysfunction, hemorheological parameters, platelet aggregation, plasma concentration of homocysteine and progression of atherosclerosis in patients with vascular diseases.

In our prospective study the effect of Sclerovit (0.8 mg folic acid, 20 mug vitamin B12,5 mg vitamin B6,100 mg vitamin E) on inflammatory markers, hemorheological parameters, platelet aggregation, von Willebrand factor activity as a marker of endothelium dysfunction, plasma lipids, plasma levels of folic acid, vitamin B12 and homocysteine (hcy), flow mediated vasodilatation (FMD) and thickness of carotis intima-media after 1 and 6 months of treatment in patients with vascular diseases (10 patients took 1 capsule, 10 patients 2 capsules of Sclerovit and 10 patients placebo) was determined.Plasma level of vitamin B12, folic acid and elongation index of red blood cells (RBC) increased significantly (p<0.05-0.001), hcy and triglyceride concentrations decreased significantly (p<0.05-0.001) in patients taking Sclerovit. HDL-cholesterol, RBC count, hematocrit, plasma and whole blood viscosity increased significantly (p<0.05-0.001) both in patients taking placebo or vitamins. Fibrinogen and CRP showed a significant (p<0.05-0.01) increase in patients on placebo, but did not change in patients on Sclerovit therapy. FMD showed a significant (p<0.05) amelioration in patients on 1 capsule of Sclerovit.Beside the favorable effects of Sclerovit on some of the measured parameters, the observed deterioration in hemorheological parameters can correlate with the contradictory results of large prospective studies with vitamins.

Effect of parenteral or oral vinpocetine on the hemorheological parameters of patients with chronic cerebrovascular diseases.

INTRODUCTION: Hemorheological factors play an important role in the pathomechanism of ischemic cerebrovascular disorders. Abnormal rheological conditions in patients with chronic cerebrovascular disease predispose for recurrent strokes. Vinpocetine (VP), a synthetic ethyl esther of apovincamine, has successfully been used in the treatment of cerebrovascular diseases, in part because of its favourable rheological effects. PATIENTS AND METHODS: The study investigates the hemorheological changes in 40 patients in the chronic stage of ischemic cardiovascular disease after administration of vinpocetine. All patients received a high dose of intravenous VP in doses gradually increased to l mg/kg/day. In addition, 20 patients (mean age: 61+/-8 years) received 30 mg VP orally for 3 months. The other 20 patients (mean age: 59+/-6 years), who received placebo tablets, served as controls. Hemorheological parameters (hematocrit, plasma fibrinogen, whole blood viscosity, red blood cell aggregation and deformability) were evaluated at 1 and 3 months. RESULTS: The high-dose parenteral VP significantly decreased red blood cell aggregation, plasma and whole blood viscosity (p < 0.05) compared to the initial values. In patients with additional oral treatment, plasma and whole blood viscosities were significantly lower compared to the placebo patients at 3 months (p < 0.05). CONCLUSION: Our results confirmed the beneficial rheological effects of high-dose parenteral VP (partially caused by hemodilution) observed previously, and also warrant its long-term oral admission to maintain the beneficial rheological changes.

[Effect of atorvastatin treatment on the hemorheologic and hemostatic parameters in chronic cerebrovascular patients]. / Az atorvastatinkezelés haemorrheologiai és haemostaseologiai hatásai krónikus agyérbetegekben.

UNLABELLED: Hemorheologic and hemostatic parameters are known to be altered in cerebrovascular diseases. Statin therapy is an effective treatment in the prevention of ischemic stroke, the beneficial effects may also involve lipid-independent mechanisms. AIMS: In their publication the authors review the references based on the effect of atorvastatin on stroke prevention, hemorheologic and hemostatic parameters, referred to in their previous study, investigating the short-term effect of low-dose atorvastatin on hemorheologic parameters, and endothelial dysfunction, platelet aggregation. METHODS: 27 chronic cerebrovascular patients (mean age: 61 +/- 8 years) with hyperlipidemia were investigated for serum lipid levels, hemorheologic parameters (hematocrit, plasma fibrinogen level, plasma and whole blood viscosity, red blood cell aggregation and deformability) and platelet aggregation at baseline, and after one and three months treatment with 10 mg atorvastatin daily. Endothelial dysfunction, characterized by von Willebrand factor activity was measured before and after 1-month treatment. RESULTS: The mean decrease of plasma total cholesterol level was 28% both after 1 and 3 months ( p < 0.001), that of LDL-cholesterol was 40% and 38% ( p < 0.001) compared to baseline values. Atorvastatin significantly improved whole blood viscosity after 3-month treatment and red blood cell deformability even after 1-month treatment ( p < 0.05). Collagen induced platelet aggregation provided a significant ( p < 0.001) decrease compared to that of baseline values beside unaltered antiplatelet therapy. Von Willebrand factor activity was also improved significantly ( p < 0.05) after 1-month treatment. CONCLUSIONS: Data of the literature and findings of the authors show that the beneficial effects of atorvastatin are complex. Besides lipid lowering, atorvastatin can improve hemorheologic parameters, platelet aggregation and endothelial dysfunction after short-term and low-dose therapy.

Relation of platelet aggregation and fibrinogen levels to advancing age in aspirin- and thienopyridine-treated patients.

In our present study we investigated the association between platelet aggregation in patients treated with the most widely used antiplatelet agents (100 and 300-325 mg acetylsalicylic acid (ASA), 75 mg clopidogrel, 500 mg ticlopidine and the combination of 100 mg aspirin and 75 mg clopidogrel), fibrinogen levels and aging. Between 2001 and 2005 we measured in vitro platelet aggregation in 5026 vascular patients according to the method of Born. Platelet aggregation was tested with 5 and 10 microM adenosine-diphosphate, 2 microg/ml collagen and 10 microM epinephrine stimulants. Fibrinogen level was simultaneously measured in a subgroup of 3243 patients. The subjects were divided by age into decades. Platelet aggregation increased significantly with advancing age in the case of 100 and 300-325 mg ASA-treated patients (p<0.001). In aspirin-treated patients also fibrinogen levels increased with aging (p<0.001). There was no association between platelet aggregation or fibrinogen levels and aging either in patients treated with 75 mg clopidogrel or with 500 mg ticlopidine. Thienopyridine-treated patients exhibited significantly lower fibrinogen levels than ASA-treated individuals (p<0.001). Our results suggest that advancing age is associated with elevated platelet aggregability in widely used antiplatelet regimens that might contribute to higher risk of cardiovascular events in the elderly.

Does glycoprotein IIIa gene (Pl(A)) polymorphism influence clopidogrel resistance? : a study in older patients.

BACKGROUND: Clopidogrel is a potent antiplatelet drug used for secondary prevention after ischaemic cardiovascular or cerebrovascular events. In patients with aspirin (acetylsalicylic acid) intolerance or resistance, it is used as monotherapy. Recent data report that Pl(A) polymorphism of the glycoprotein IIIa gene may account for differences in aspirin-induced antiplatelet effects. An increased degree of platelet reactivity was also reported in Pl(A2) carriers compared with Pl(A1/A1) patients after administration of a clopidogrel 300mg loading dose. OBJECTIVES: The aim of this study was to assess the modulatory effect of the Pl(A2) allele on platelet aggregation in patients taking long-term clopidogrel. M ETHODS: The prevalence of the Pl(A2) allele was assessed in 38 (21 males, 17 females; mean age 63 +/- 13 years) clopidogrel-resistant and 59 (26 males, 33 females; mean age 63 +/- 11 years) clopidogrel-responsive patients. The polymerase chain reaction-restriction fragment length polymorphism method was utilised to evaluate Pl(A) polymorphism. A Carat TX4 optical platelet aggregometer (Carat Diagnostics Ltd, Budapest, Hungary) was used to measure 5 and 10 micromol/L adenosine diphosphate-induced platelet aggregation. RESULTS: Significantly more patients were taking combination antiplatelet therapy in the clopidogrel-resistant group than in the clopidogrel-responsive group (50% vs 30%, respectively). The prevalence of the Pl(A2) allele did not differ significantly between the two groups (0.09 vs 0.13), even after adjustment for combination therapy and various risk factors. CONCLUSIONS: Our results show that carriers of the Pl(A2) allele do not have an increased risk of clopidogrel resistance. These findings and data from our previous studies suggest that patients with a Pl(A2) allele homozygosity may benefit from antiplatelet therapy based on clopidogrel rather than aspirin.

Viscosity, hemostasis and inflammation in atherosclerotic heart diseases.

BACKGROUND: In atherosclerotic diseases vascular reserve is impaired and pressure gradient is decreased, therefore the reduced blood fluidity can lead to tissue ischemia more rapidly. In previous investigations we demonstrated the deterioration of plasma and whole blood viscosities in patients with acute ischemic coronary syndromes, chronic coronary artery disease, and percutaneous transluminal coronary angioplasty. METHODS: Hemorheological variables (plasma and whole blood viscosities, hematocrit, red blood cell aggregation), hemostaseological parameters (plasma fibrinogen and von Willebrand factor (vWf)), and platelet aggregation were detected in more recent studies in cardio- and cerebrovascular diseases, and diabetes mellitus. Common risk factors (lipid profile, smoking, glucose level, previous diseases) and medication were also recorded. RESULTS: High portion of vascular patients were demonstrated to have poor ex vivo platelet inhibition. Effective antiplatelet treatment detected by aggregometry was related to lower plasma fibrinogen concentration and red blood cell aggregation and was also associated with less recurrent vascular events during the follow-up (p < 0.001). Beside the impaired hemorheological characteristics, the diabetic patients showed elevated vWf activity, which turned to correlate with hemoglobin A1c concentration (p < 0.01) rather than the fasting glucose. SUMMARY: Our studies indicate the active role and interaction of hemorheological and hemostaseological factors in atherosclerotic heart diseases.

Glycoprotein IIIA gene (PlA) polymorphism and aspirin resistance: is there any correlation?

BACKGROUND: Platelet glycoprotein (GP) IIb/IIIa receptors play an inevitable role in platelet aggregation. The GP IIIa gene is polymorphic (PlA1/PlA2) and the presence of a PlA2 allele might be associated with an increased risk for acute coronary syndrome (ACS). OBJECTIVE: To examine the prevalence of the PlA2 allele in patients with ACS and in subjects with or without aspirin resistance. METHODS: The prevalence of the PlA2 allele was assessed in 158 patients with ACS and PlA2 compared with its prevalence in 199 healthy volunteers. The antiplatelet efficacy of aspirin was examined in all patients with ACS, as well as in 69 individuals who had suffered ischemic stroke and in 58 high-risk subjects without any known ischemic vascular events. RESULTS: PlA2 prevalence was significantly higher in patients with ACS (59/158) than in the control group (51/199; p < 0.05). Carriers of the PlA2 allele had a significantly higher risk of developing ACS, even after an adjustment to the risk factors (OR 5.74; 95% CI 1.75 to 18.8; p = 0.004). The occurrence of the PlA2 allele was significantly higher among patients with aspirin resistance than in subjects who demonstrated an appropriate response to the drug (allele frequencies, 0.21 vs 0.14; p < 0.05). All patients homozygous for the PlA2 allele had an inadequate platelet response to aspirin. CONCLUSIONS: Our results support the hypothesis that carriers of the PlA2 allele might have an increased risk for ACS. PlA2 homozygosity was associated with an inadequate response to aspirin therapy. Our data further suggest that patients with PlA2 allele homozygosity might benefit from antiplatelet therapy based on adenosine diphosphate antagonists throughout secondary treatment for prevention of ACS.

Hemorheological methods in drug research.

Development of new drugs is a sophisticated process that requires several, different methods. In our experiments we have applied two rheological models to study experimental and clinically used drugs. The antioxidant properties of several agents were estimated by erythrocyte filtration technique. The known antioxidant compound vitamin E was used to validate our measurements. An experimental cardioprotective agent, H-2545 provided significant protection against oxidative changes in red blood cell filterability (p<0.001). Although some of the examined, known cardiovascular drugs also showed significant antioxidant effect, they were less efficient than H-2545 and the scavenger effect of this novel agent exceeded the antioxidant properties of vitamin E. Modification of mexiletine with a pyrroline ring improved significantly its antioxidant capacity suggesting this molecular segment to be responsible for the antioxidant effect. In our second model the antiplatelet effect of experimental poly(ADP-ribose) polymerase (PARP) inhibitors was evaluated. Two widely used antiplatelet agents: acetyl salicylic acid and eptifibatide served as controls in the validation of the measurements. PARP inhibitors reduced ADP-induced platelet aggregation in a dose-dependent manner (p<0.05). However, their hindrance on platelet aggregation waned as the concentration of ADP rose. Regarding the platelets' role in the development of ischemic vascular diseases, the antiaggregating property of PARP inhibitors may exert additional beneficial effects on tissue blood supply under conditions of compromised vascular flow.

Inhibition of ADP-evoked platelet aggregation by selected poly(ADP-ribose) polymerase inhibitors.

Pathologic platelet activation has been implicated in the pathogenesis of ischemic heart disease. Since cardiomyocytes can be protected from ischemia-reoxygenation injury by poly(ADP-ribose) polymerase (PARP) inhibitors mimicking the adenine/ADP part of NAD, their structural resemblance to ADP may also enable the blockade of platelet aggregation via binding to ADP receptors. Blood samples drawn from healthy volunteers were pre-incubated with different concentrations of PARP inhibitors: 4-hydroxyquinazoline, 2-mercapto-4(3 H)-quinazolinone, or HO-3089. ADP-, collagen- and epinephrine-induced platelet aggregation was evaluated according to the method described by Born. The effect of PARP inhibitors on thrombocyte aggregation was also examined when platelets were sensitized by heparin and in the presence of incremental concentrations of ADP. All examined PARP inhibitors reduced the ADP-induced platelet aggregation in a dose-dependent manner (significant inhibition at 20 microM for HO-3089 and at 500 microM for the other agents; P < 0.05), even if platelets were sensitized with heparin. However, their hindrance on platelet aggregation waned as the concentration of ADP rose (no effect at 40 microM ADP). PARP inhibitors had minimal effect on both collagen- and epinephrine-induced platelet aggregation. Our study first demonstrates the feasibility of a design for PARP inhibitors that does not only protect against ischemia-reperfusion-induced cardiac damage but may also prevent thrombotic events.

Short-term effect of low-dose atorvastatin on haemorrheological parameters, platelet aggregation and endothelial function in patients with cerebrovascular disease and hyperlipidaemia.

INTRODUCTION AND OBJECTIVE: Haemorrheological parameters and endothelial function are known to be altered in vascular diseases, including stroke. Treatment with HMG-CoA reductase inhibitors ('statins') improves cerebrovascular (and cardiovascular) morbidity and mortality in patients with atherosclerosis; the beneficial effects may involve lipid-independent mechanisms. The aim of this study was to assess the short-term effect of low-dose atorvastatin on haemorrheological parameters, platelet aggregation and endothelial dysfunction in patients with chronic cerebrovascular disease and hyperlipidaemia. PATIENTS AND METHODS: Twenty-seven patients (mean age 61 +/- 8 years) with chronic cerebrovascular disease and hyperlipidaemia were included in the study. Serum lipid levels, haemorrheological parameters (haematocrit, plasma fibrinogen levels, plasma and whole blood viscosity [WBV] and red blood cell [RBC] aggregation and deformability) and platelet aggregation were assessed at baseline and after 1 and 3 months of treatment with atorvastatin (Sortis) 10 mg/day. von Willebrand factor (vWF) activity (a measure of endothelial function) was measured at baseline and after 1 month of treatment. Adverse events were recorded at each visit. Physical examinations, haematological assessments and serum and urine chemistry assays were performed during the study. RESULTS: Plasma total cholesterol levels were reduced by a mean of 27% compared with baseline after both 1 and 3 months of treatment (p < 0.001). Low density lipoprotein-cholesterol levels were reduced by a mean of 40% and 38% (p < 0.001), respectively, after 1 and 3 months of treatment, compared with baseline values. Triglyceride levels decreased by 20% at 1 month and by 10% after 3 months (p < 0.001). Atorvastatin significantly improved WBV after 3 months of treatment and RBC deformability after 1 month and 3 months of treatment (p < 0.05). Collagen-induced platelet aggregation was significantly decreased at 1 (p < 0.05) and 3 months (p < 0.001) compared with baseline values, despite unaltered antiplatelet therapy. vWF activity was also improved significantly (p < 0.05) after 1 month of treatment. CONCLUSIONS: Our findings show that the beneficial effects of atorvastatin are complex. Besides lipid lowering, atorvastatin can improve haemorrheological parameters, platelet aggregation and endothelial dysfunction after short-term and low-dose therapy. Whether such early laboratory changes translate into clinical utility for secondary stroke prevention awaits the results of endpoint trials.

Measurement of von Willebrand factor as the marker of endothelial dysfunction in vascular diseases.

BACKGROUND: von Willebrand factor is a blood glycoprotein that is required for normal hemostasis. Its level can be increased by endothelial cell damage. HYPOTHESIS: von Willebrand factor is a suitable marker of endothelial dysfunction. METHODS: von Willebrand factor activity was determined by ELISA in patients with acute coronary syndromes, acute stroke and chronic vascular diseases, and was compared with the values of healthy controls. RESULTS: von Willebrand factor activity of patients in each group was significantly higher (P<0.001) than that of the control group. The values of patients with acute coronary syndrome and acute stroke were significantly higher (P<0.05 and P<0.01, respectively) than those of patients with chronic vascular diseases. von Willebrand factor activity was significantly higher in patients with acute coronary syndrome and acute stroke (P<0.05 and P<0.01, respectively) on the sixth day than on admission. CONCLUSIONS: By measuring von Willebrand factor activity, a considerable, significant difference could be found between healthy people and chronic and acute vascular patients. The routine measurement of von Willebrand factor activity in vascular patients as an index of endothelial dysfunction may have clinical importance, because detection of this marker can be a noninvasive way of assisting diagnosis and indicating disease progression.

[Effect of vinpocetin on the hemorheologic parameters in patients with chronic cerebrovascular disease]. / Vinpocetin hatása krónikus agyérbetegségben szenvedók hemoreológiai viszonyaira.

INTRODUCTION: Data collected from large number of multicenter, randomized trials in acute and chronic stroke patients provide evidence, that incidence and high mortality of cerebrovascular disorders can be decreased mainly by prevention and that the effectiveness of acute stroke treatment is limited. The terminology of "chronic cerebrovascular diseases" involves many pathologic entities and often atypical clinical symptoms refer to the focal or global hypoperfusion of the brain. However, hemorheological disturbances seem to be important factors of the complex pathomechanism. Vinpocetine has successfully been used in the treatment of cerebrovascular diseases, the part of the mechanism of action are the favourable rheological effects demonstrated after oral administration in more previous studies. AIMS AND METHODS: In this study the hemorheological changes after administration of small (30 mg/day) and high dose (increased to 70 mg/day) intravenous vinpocetine for 7 days in 30 patients in chronic phase of ischemic cerebrovascular disease were investigated. RESULTS: High dose parenteral vinpocetine treatment significantly (p < 0.05-0.005) decreased the hematocrit, the whole blood and plasma viscosity and red blood cell aggregation compared to the values before the treatment. Only red blood cell aggregation was improved significantly (p < 0.05) by small dose treatment. CONCLUSION: This study and other hemorheological studies in cerebrovascular patients demonstrated persistent rheological abnormalities despite the preventive therapy. The beneficial rheological effect of high dose parenteral vinpocetine indicates the use of this drug in the treatment of chronic cerebrovascular diseases.

[Effects of cardiovascular risk factors on hemorheologic parameters in cerebrovascular patients]. / A kardiovaszkuláris rizikófaktorok hatása az agyérbetegek hemoreológiai viszonyaira.

INTRODUCTION: Hemorheological factors are of significance in the determination of flow characteristics of blood and play an important role in the pathogenesis of cerebrovascular diseases. AIMS AND METHODS: In this study the changes of rheological factors--hematocrit (Hct), plasma fibrinogen concentration (PFC), whole blood (WBV) and plasma viscosity (PV), red blood cell aggregation (AI) and deformability and the association between these parameters and cardiovascular risk factors were investigated in 297 patients (173 males, 124 females, mean age: 60 11 years) with chronic phase (3 months after onset) ischemic cerebrovascular diseases, and in 68 healthy volunteers (30 males, 38 females, mean age: 36 6 years). RESULTS: All investigated hemorheological factors were significantly (p < 0.05-0.0001) elevated in cerebrovascular patients compared to normal controls, the rise in Hct, WBV and PV are some of the most prominent findings. In the group of hypertensive, hyperlipidemic patients, smokers and alcoholics Hct, PFC, WBV, PV and AI were significantly (p < 0.05-0.0001) higher compared to healthy controls, the same factors except plasma fibrinogen concentration showed association with diabetic history. Comparing cerebrovascular patients with or without risk factors, the most severe hemorheological deficit was observed in patients with hyperlipidemia and smoking habits. CONCLUSIONS: In this study the authors proved in chronic ischemic cerebrovascular patients that hemorheological abnormalities persist in most cases for a long time after an acute stroke, significant correlation could be seen between blood rheology and cardiovascular risk factors. Examination of rheological parameters can support to choose the optimal medical treatment in the secondary prevention of stroke, correction of hemorheological disturbances can reduce the risk of recurrent stroke.

[Investigation of von Willebrand-factor as a marker of endothelial dysfunction in atherosclerotic patients]. / A von Willebrand-faktornak, mint az endothelium diszfunkció markerének vizsgálata érbetegekben.

OBJECTIVE: To determine von Willebrand-factor activity as the marker of endothelium dysfunction in vascular diseases and to compare it to healthy controls. METHODS: von Willebrand-factor activity was determined by enzyme-linked immunosorbant assay (ELISA) in patients with acute coronary syndromes (29 patients, 67 +/- 13 years), acute stroke (15 pts, 67 +/- 12 years) on admission, 2nd and 6th day; and chronic vascular diseases (56 pts, 67 +/- 10 years) and was compared to the values of healthy controls (23 persons, 36 +/- 12 years). RESULTS: von Willebrand-factor activity was significantly (p < 0.001) higher in all the measured vascular patients than in the control group. The values of acute patients were significantly (p < 0.05-0.001) higher than those of patients with chronic vascular diseases. In the hospital phase von Willebrand-factor activity in acute patients increased continuously and on day 6 was significantly (p < 0.05-0.01) higher than on admission. von Willebrand-factor activity was significantly (p < 0.05) higher in troponin positive patients with acute coronary syndromes compared to the troponin negative subjects. CONCLUSIONS: von Willebrand-factor was found to be a suitable marker of endothelial dysfunction. The higher von Willebrand-factor activity in patients with vascular diseases compared to the control group can be caused by the endothelial dysfunction and extensive atherosclerosis. The significantly higher von Willebrand-factor activity in acute disorders suggests the more severe endothelium dysfunction and could be related to the development of acute event through increased platelet adhesion and aggregation.

In vitro antioxidant properties of pentoxifylline, piracetam, and vinpocetine.

Oxygen-free radicals play an important role in several physiologic and pathophysiologic processes. In pathologic circumstances, they can modify and damage biologic systems. Because oxygen-free radicals are involved in a wide range of diseases (cerebrovascular, cardiovascular, etc.), scavenging these radicals should be considered as an important therapeutic approach. In our in vitro study, we investigated the antioxidant capacity of three drugs: pentoxiphylline (Sigma Aldrich, St. Louis, MO, USA) piracetam (Sigma Aldrich), and vinpocetine (Richter Gedeon RT, Budapest, Hungary). Phenazine methosulphate was applied to generate free radicals, increasing red blood cell rigidity. Filtration technique and potassium leaking were used to detect the cellular damage and the scavenging effect of the examined drugs. According to our results, at human therapeutic serum concentration, only vinpocetine (Richter Gedeon RT) had significant (p < 0.01) scavenging activity with a protective effect that increased further at higher concentrations. Pentoxiphylline (Sigma Aldrich) and piracetam (Sigma Aldrich) did not have significant antioxidant capacity at therapeutic concentrations, but increasing their concentrations (pentoxiphylline at 100-times, and piracetam at 10-times higher concentrations) led to a significant (p < 0.01) scavenger effect. Our findings suggest that this pronounced antioxidant effect of vinpocetine and even the milder scavenging capacity of pentoxiphylline and piracetam may be of value in the treatment of patients with cerebrovascular disorders, but merits further investigations.