High Glucose, But Not Testosterone, Increases Platelet Aggregation Mediated by Endothelial Cells

Endothelial cells inhibit platelet aggregation by releasing thromboregulators, such as prostacyclin and nitric oxide. Male subject is a traditional risk factor for cardiovascular diseases. Platelet hyperreactivity has been frequently found in patient with diabetes mellitus. To examine whether testosterone and high glucose modify platelet aggregation through endothelial cells, we did an in vitro study using endothelial cells culture from human umbilical vein (HUVEC). Treatments were performed in HUVEC sub culture as either normoglucose (5.6 mM) or high glucose (22.4 mM) medium, with or without testosterone (0, 1, 10, 100 nM), for 24 hours. HUVEC were trypsinized, resuspended, and then incubated with platelet rich plasma from healthy male donors with ratio 1:104 for 3 minutes. Platelet aggregation measured by turbidimetry methode. This study showed that testosterone did not significantly influence platelet aggregation through endothelial cells in normoglucose (p = 0.144) or high glucose (p = 0.916) medium. There was no main effect of testosterone (p = 0.73) as well as no interaction between testosterone and glucose (p = 0.69), but there was a main effect of glucose (p = 0.004), to platelet aggregation through endothelial cells. In conclusion, high glucose, but not testosterone, inhibits platelet aggregation mediated by endothelial cells

Effects of High Flavanol Dark Chocolate on Cardiovascular Function and Platelet Aggregation.

Regular consumption of chocolate and cocoa products has been linked to reduced cardiovascular mortality. This study compared the effects of high flavanol dark chocolate (HFDC; 1064mg flavanols/day for 6 weeks) and low flavanol dark chocolate (LFDC; 88mg flavanols/day for 6 weeks) on blood pressure, heart rate, vascular function and platelet aggregation in men with pre-hypertension or mild hypertension. Vascular function was assessed by pulse wave analysis using radial artery applanation tonometry in combination with inhaled salbutamol (0.4 mg) to assess changes due to endothelium-dependent vasodilatation. HFDC did not significantly reduce blood pressure compared to baseline or LFDC. Heart rate was increased by LFDC compared to baseline, but not by HFDC. Vascular responses to salbutamol tended to be greater after HFDC. Platelet aggregation induced by collagen or the thromboxane analogue U46619 was unchanged after LFDC or HFDC, whereas both chocolates reduced responses to ADP and the thrombin receptor activator peptide, SFLLRNamide (TRAP6), relative to baseline. Pre-incubation of platelets with theobromine also attenuated platelet aggregation induced by ADP or TRAP6. We conclude that consumption of HFDC confers modest improvements in cardiovascular function. Platelet aggregation is modulated by a flavanol-independent mechanism that is likely due to theobromine.This study was supported by a grant (to R. Corder) from Barry Callebaut Belgium N

The Effect of Paraprotein on Platelet Aggregation

Background Some patients with paraproteinemia have platelet aggregation disorders and the aim of this study was to examine disturbance of platelet aggregation in healthy blood donors by isolated paraprotein in vitro. Methods Using Rivanol, paraprotein was separated from the serum of ten patients with paraproteinemia, who had decreased platelet aggregation with several inducers. Platelet aggregation in ten healthy donors was measured with and without addition of the isolated induced paraprotein. The test was repeated with added human immunoglobulins for intravenous use. Results Average of maximal levels of platelet aggregation has been significantly decreased in plasma rich in platelets (PRP) of healthy donors after addition of paraprotein when inducers are used: adenosine diphosphate (ADP) (P = 0.007), collagen (COL) (P = 0.008), ristocetin (RIS) (P = 0.001), and epinephrine (EPI) (P = 0.002). Average of latent time of platelet aggregation was significantly prolonged in healthy donors after addition of paraprotein with inducers: COL (P = 0.008), RIS (P = 0.008) and EPI (P = 0.006) while addition of human immunoglobulins caused no change in platelet aggregation. In comparison, when human immunoglobulins were added, maximal platelet aggregation and latent time did not change significantly. Paraprotein isolated from patients with paraproteinamia, who had decrease platelet aggregation, had significantly decreased platelet aggregation when added to PRP of healthy donors, in vitro. Conclusion Platelet aggregation was not significantly changed was confirmed with addition of human immunoglobulins

PLATELET AGGREGATION PROFILE AND CARDIOVASCULAR EVENT IN CORONARY HEART DISEASE PATIENTS WITH DUAL ANTIPLATELET

Platelet aggregation plays an important role in atherosclerosis process in Coronary Heart Disease (CHD) patients. Antiplatelet acts to prevent platelet aggregation and thrombus subsequently. Thrombus will block artery coronaries. Antiplatelet responsiveness can be seen by aggregation platelet profile. Based on the background, the aim of this research was to review platelet aggregation and cardiovascular event profile in CHD patients with dual antiplatelet. Prospective study was used in this study. CHD patients with dual antiplatelet therapy, willing to follow this research, and compliance with therapy were recruited into this study. Blood samples from patients were collected for platelet aggregation test. Platelet aggregation was analyzed by Light Aggregometry which used three platelet inducer (ADP, Collagen, Epinephrine). Cardiovascular event was defined by ischemic attack that CHD patients got in 3 months. 12 patients were recruited for this research. From the 12 patients, 5 patients occured ischemic attack within follow up. Platelet aggregation for that 5 patients which had ischemic attack, was normal and under normal platelet aggregation. Platelet activation is contributor subsequent atherothrombosis in patients with high inflammatory regulations in artery wall and systemic circulation. Platelet aggregation profile can be reflected as antiplatelet activity. Statistical analysis was done for aggregation profile and cardiovascular event. P-values > 0.05 which means there’s no correlation between platelet aggregation and cardiovascular event. Platelet aggregation in this research showed in normal and unde

An investigation of the antiplatelet effects of succinobucol (AGI-1067)

Succinobucol is a phenolic antioxidant with anti-inflammatory and antiplatelet effects. Given the importance of oxidant stress in modulating platelet–platelet and platelet–vessel wall interactions, the aim of this study was to establish if antioxidant activity was responsible for the antiplatelet activity of succinobucol. Platelet aggregation in response to collagen and adenosine diphosphate (ADP) was studied in rabbit whole blood and platelet-rich plasma using impedance aggregometry. The effect of oxidant stress on aggregation, platelet lipid peroxides, and vascular tone was studied by incubating platelets, washed platelets or preconstricted rabbit iliac artery rings respectively with a combination of xanthine and xanthine oxidase (X/XO). To study the effect of succinobucol in vivo, anaesthetized rats were injected with up to 150 mg/kg succinobucol and aggregation measured in blood removed 15 mins later. Succinobucol (10−5–10−4 M) significantly attenuated platelet aggregation to collagen and ADP in whole blood and platelet-rich plasma. X/XO significantly increased aggregation to collagen and platelet lipid peroxides and this was reversed by succinobucol. Addition of X/XO to denuded rabbit iliac arteries caused a dose-dependent relaxation which was significantly inhibited by succinobucol. In vivo administration up to 150 mg/kg had no effect on heart rate or mean arterial blood pressure but significantly inhibited platelet aggregation to collagen ex vivo. In conclusion, succinobucol displays anti-platelet activity in rabbit and rat blood and reverses the increase in platelet aggregation in response to oxidant stress

HUBUNGAN MEROKOK DENGAN AGREGASI TROMBOSIT PADA MAHASISWA DI LINGKUNGAN UNIVERSITAS DIPONEGORO

Background : Smoking is a risk factor for several diseases. One of the important mechanisms involved is an atherothrombosis process. This process can be initiated by platelet aggregation. Nicotine and other oxidants contained in cigarette smoke may induce excretion of thromboxane’s metabolites and inhibit release of nitric oxide, which have important roles to increase platelet activity. Aim : to prove the correlation between duration of smoking and platelet aggregation, and the correlation between amount of cigarette per day and platelet aggregation in college students at Diponegoro University. Methods : This study was an analytic observasional with cross sectional design. Subject of the study was 22 male smokers among college students at Diponegoro University. The sampling method of this study was consecutive sampling. Platelet aggregation test was conducted using method of peripheral blood smear. Blood sampling was performed after 12 hours of fasting. Data analysis using Pearson test and Spearman test. Results : A total of 22 healthy male smokers of mean age 21±2 years were included. The subjects had smoked an average of 10±6 cigarettes a day for 54±32 months. The mean platelet aggregation was 68±8% which was interpreted as normoaggregation. Analysis result of Pearson test showed no significant correlation between duration of smoking and platelet aggregation (p=0,189, p>0,05). Analysis result of Spearman test showed no significant correlation between amount of cigarette per day and platelet aggregation (p=0,439, p>0,05). Conclusions : There was no significant correlation between duration of smoking and platelet aggregation, and there was no significant correlation between amount of cigarette per day and platelet aggregation. Keywords : Smoking, platelet, aggregatio

Correlation Between P-Selectin Level and Platelet Aggregation in Cerebral Venous Sinus Thrombosis Patients

One of the causes of cerebral venous sinus thrombosis (CVST) is platelet hyperactivity. Adhesion and secretion are the beginning of platelet activation, which is indicated by a change in the Platelet-selectin (P-selectin) level. The end result of platelet activation is platelet aggregation. However, it is unknown whether the beginning of platelet activation ends with platelet aggregation. This study aimed to discover the correlation between P-selectin level and platelet aggregation in CVST. This study used a cross-sectional escriptive observational correlative approach. Subjects were the CVST outpatients visiting the Neurology Department of Dr. Hasan Sadikin General Hospital, Bandung, Indonesia, from July to September 2021. A total of 49 subjects met the inclusion and exclusion criteria. This study used citrate plasma samples for platelet aggregation and serum for P-selectin assessment. Platelet aggregation were assessed using the light transmission platelet aggregation method while P-selectin was assessed using Enzyme-linked immunosorbent assay (ELISA). Platelet aggregation median was 10.6% (range 0.2–82.4%), which reflected normoaggregation. Platelet hyperaggregation were seen in 9 samples (8.4%). Median of P-selectin was 2.4 ng/mL (range 0.1–10.1 ng/mL) which were normal. High P-selectin level was observed in 16 (32.7%) with 4/16 (25%) experiencing platelet hyperaggregation. Statistical analysis showed a weak negative correlation between P-selectin and platelet aggregation (r=-0.012; p=0.467). In conclusion, no correlation is seen between P-selectin and platelet aggregation, which may be due to the fact that platelets are influenced by many factors that are not examined in this study

Novel aspects of platelet aggregation

The platelet aggregation is an important process, which is critical for the hemostatic plug formation and thrombosis. Recent studies have shown that the platelet aggregation is more complex and dynamic than it was previously thought. There are several mechanisms that can initiate the platelet aggregation and each of them operates under specific conditions in vivo. At the same time, the influence of certain plasma proteins on this process should be considered. This review intends to summarize the recent data concerning the adhesive molecules and their receptors, which provide the platelet aggregation under different conditions

CYP2C19*17 Polymorphisms And Platelet Aggregation In Coronary Artery Disease Patients With Clopidgrel

Background: Clopidogrel is the alternative therapy for patients with Coronary Artery Disease (CAD) that couldn’t use Aspirin as antiplatelet. There’s some factors that contribute to clopidogrel effectiveness, such as obesity, Diabetes Mellitus, Smoking, and genetic polymorphisms. Objective: The aim of this study is to analyze the CYP2C19*17 polymorphism related with platelet aggregation as marker of Clopidogrel effectiveness. Methods: Cross sectional study was used. Some criteria were used for patient recruitment such as: compliance with drug therapy (measured by Morisky Medication Adherence Scale), without diabetes mellitus, no obese and no smoking. Patients used clopidogrel for 3 months. Blood sample was collected for genetic polymorphism analysis and platelet aggregation. Genetic polymorphisms would analyze by Polymerase Chain Reaction and Platelet Aggregation with Light Transmission Aggregometry. Result 20 CAD patients used for this study. 30% patients have polymorphisms in CYP2C19*17. 80% patients have hipoaggregation and 20% have normoaggregation. In this study, 30% patients that have CYP2C19*17 polymorphisms still have a normal platelet aggregation. None of them have a high level of platelet aggregation. Conclusion: Patients with CYP2C19*17 polymorphisms have a normal and low level of platelet aggregation

Evaluation of Anti-Platelet Aggregation Effect of Some Allium Species

Epidemiologic studies show that the cardiovascular diseases are associated with multiple factors such as raised serum total cholesterol, increased LDL, increased platelet aggregation, hypertension and smoking. In-vitro studies have confirmed the ability of some plants of Allium species to reduce these parameters. Therefore, we evaluated anti-platelet aggregation effect of some Allium species (Allium ampeloprasum, A. hirtifolium, A. haemanthoides, A. vavillovi, A. atroviolaceum, A. jesdianum, A. shelkovnikovii) using arachidonic acid (AA) and adenosine diphosphate (ADP) as platelet aggregation inducers. The screening results for methanolic extract of Allium species showed that the maximum effect of anti-platelet aggregation was related to A. atroviolaceum. This extract inhibited the in-vitro platelet aggregation induced by AA and ADP with IC50 values of 0.4881 (0.4826-0.4937) mg/ml and 0.4945 (0.4137-0.5911) mg/ml respectively. These results support the hypothesis that the dietary intake of Allium could be beneficial for prevention of cardiovascular diseases