scholarly journals Inhibitory effect of Fruitflow on platelet function: a randomized placebo-controlled trial in elderly subjects

2020 ◽  
Author(s):  
Huilian Chen ◽  
Shenghao Zhang ◽  
Hui Wang ◽  
Yun Jiang ◽  
Li Bao ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Controlled Trial ◽  
Adenosine Diphosphate ◽  
The Elderly ◽  
Inhibitory Effect ◽  
Water Soluble ◽  
Elderly Subjects ◽  
Platelet Factor ◽  
Prostaglandin F

Abstract Background: The elderly have a high risk of cardiovascular disease, which is often accompanied by platelet hyperactivity. Tomato extracts can inhibit platelet activation and have beneficial health effects. We aimed to investigate the effect of Fruitflow (FF), a water-soluble tomato extract, on platelet function in elderly subjects.Methods: This randomized group study was conducted with people over 50 years old. The participants were randomly divided into four groups: placebo (150 mg/day), FF (150 mg/day), acetylsalicylic acid (ASA; 100 mg/day), and FF (150 mg/day) + ASA (100 mg/day). These groups received the respective supplements after dinner daily for 7 days. Fasting blood was collected from the participants on days 0 and 8 to analyze platelet aggregation and the content of thromboxane B2 (TXB2), 6-keto-prostaglandin F1α, and platelet factor 4 (PF4). Results: One hundred ninety elderly subjects were recruited and completed this clinical trial. The results showed that the FF intervention for 7 days decreased platelet aggregation by 7.7% in adenosine diphosphate-stimulated platelets, which was similar to the effect of ASA, which decreased platelet aggregation by 9.4%. Fruitflow reduced platelet aggregation by 10.2% in collagen-stimulated platelets, and ASA reduced platelet aggregation by 38.3% in collagen-activated platelets. This suggests that ASA exerts a stronger inhibitory effect than FF on collagen-stimulated platelet aggregation. The combination of FF + ASA did not exert a synergistic inhibitory effect on platelet aggregation. Treatment with FF significantly decreased plasma TXB2, 6-keto-PGF1α, and PF4 levels, and its effects were similar to ASA. Conclusion: Fruitflow suppressed platelet aggregation and decreased TXB2, 6-keto-PGF1α, and PF4 levels in elderly subjects. These findings indicate that FF might reduce the risk of thrombosis in cardiovascular diseases.Trial registration code: ChiCTR2000034647 at www.clinicaltrials.gov.

scholarly journals Inhibitory effect of Fruitflow on platelet function: a randomized placebo-controlled trial in elderly subjects

2021 ◽  
Author(s):  
Huilian Chen ◽  
Shenghao Zhang ◽  
Hui Wang ◽  
Yun Jiang ◽  
Li Bao ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Controlled Trial ◽  
Adenosine Diphosphate ◽  
The Elderly ◽  
Inhibitory Effect ◽  
Water Soluble ◽  
Elderly Subjects ◽  
Platelet Factor ◽  
Prostaglandin F

Abstract Background: The elderly has a high risk of cardiovascular disease, which is often accompanied by platelet hyperactivity. Tomato extracts can inhibit platelet activation and have beneficial health effects. We aimed to investigate the effect of Fruitflow® (FF), a water-soluble tomato extract, on platelet function in elderly participants.Methods: This randomized group study was conducted with people over 50 years old. The participants were randomly divided into four groups: placebo (150 mg/day), FF (150 mg/day), acetylsalicylic acid (ASA; 100 mg/day), and FF (150 mg/day) + ASA (100 mg/day). These groups received the respective supplements after dinner daily for 7 days. Fasting blood was collected from the participants on days 0 and 8 to analyze platelet aggregation and the content of thromboxane B2 (TXB2), 6-keto-prostaglandin F1α, and platelet factor 4 (PF4). Results: One hundred ninety elderly participants were recruited and completed this clinical trial. The results showed that the FF intervention for 7 days decreased platelet aggregation by 7.7% in adenosine diphosphate-stimulated platelets, which was similar to the effect of ASA, which decreased platelet aggregation by 9.4%. FF reduced platelet aggregation by 10.2% in collagen-stimulated platelets, and ASA reduced platelet aggregation by 38.3% in collagen-activated platelets. This suggests that ASA exerts a stronger inhibitory effect than FF on collagen-stimulated platelet aggregation. The combination of FF + ASA did not exert a synergistic inhibitory effect on platelet aggregation. Treatment with FF significantly decreased plasma TXB2, 6-keto-PGF1α, and PF4 levels, and its effects were similar to ASA. Conclusion: Fruitflow® suppressed platelet aggregation and decreased TXB2, 6-keto-PGF1α, and PF4 levels in elderly participants. These findings indicate that FF might reduce the risk of thrombosis in cardiovascular diseases.Trial registration code: ChiCTR2000034647 at www.clinicaltrials.gov.

Inhibition of Platelet Function by Antiarrhythmic Drugs, Verapamil and Disopyramide

1982 ◽  
Vol 47 (02) ◽  
pp. 150-153 ◽  
Author(s):  
P Han ◽  
C Boatwright ◽  
N G Ardlie
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Antiarrhythmic Drugs ◽  
Adenosine Diphosphate ◽  
Inhibitory Effect ◽  
Second Phase ◽  
Ionophore A23187 ◽  
High Concentrations ◽  
Artery Disease

SummaryVarious cardiovascular drugs such as nitrates and propranolol, used in the treatment of coronary artery disease have been shown to have an antiplatelet effect. We have studied the in vitro effects of two antiarrhythmic drugs, verapamil and disopyramide, and have shown their inhibitory effect on platelet function. Verapamil, a calcium channel blocker, inhibited the second phase of platelet aggregation induced by adenosine diphosphate (ADP) and inhibited aggregation induced by collagen. Disopyramide similarly inhibited the second phase of platelet aggregation caused by ADP and aggregation induced by collagen. Either drug in synergism with propranolol inhibited ADP or collagen-induced platelet aggregation. Disopyramide at high concentrations inhibited arachidonic add whereas verapamil was without effect. Verapamil, but not disopyramide, inhibited aggregation induced by the ionophore A23187.

Effects of Ticlopidine of Platelet Function in Men with Stable Angina Pectoris

1985 ◽  
Vol 54 (04) ◽  
pp. 808-812 ◽  
Author(s):  
Ulf Berglund ◽  
Henning von Schenck ◽  
Lars Wallentin
Keyword(s):  
Platelet Aggregation ◽  
Angina Pectoris ◽  
Platelet Function ◽  
Plasma Levels ◽  
Platelet Reactivity ◽  
Inhibitory Effect ◽  
Controlled Study ◽  
Double Blind ◽  
Platelet Factor

SummaryThe effects of ticlopidine (T) (500 mg daily) on platelet function were investigated in a double-blind placebo-controlled study in 38 middle-aged men with stable incapacitating angina pectoris. The in vitro platelet reactivity to aggregating agents, the platelet sensitivity to prostacyclin and the plasma levels of platelet specific proteins and fibrinogen were determined before and after 4 and 8 weeks of treatment. T exerted a potent inhibitory effect on ADP- and collagen-induced platelet aggregation. The effect of T was proportional to the pretreatment reactivity to ADP and collagen. The inhibitory effect of T on the epinephrine response was less pronounced. The plasma levels of beta-thromboglobulin, platelet factor 4 and fibrinogen were not influenced by T. The platelet inhibition of prostacyclin was potentiated by T, and it was demonstrated that T and prostacyclin had synergistic inhibitory effects on platelet aggregation.

Effects of N-(2-Diethylaminoethyl)-N-(2-hydroxy- 2-phenylethyl)-2,5-dichloroaniline (AN 162) on Platelet Function and Blood Coagulation

1971 ◽  
Vol 26 (03) ◽  
pp. 576-587
Author(s):  
R. D Mac Kenzie ◽  
T. R Blohm
Keyword(s):  
Platelet Aggregation ◽  
Blood Clotting ◽  
Platelet Rich Plasma ◽  
Adenosine Diphosphate ◽  
Inhibitory Effect ◽  
Clotting Time ◽  
Clotting Factors ◽  
Platelet Factor ◽  
Inhibition Of Platelet Aggregation

SummaryWhen AN 162 was added to human citrated platelet-rich plasma at 30-300 µg/ml, it inhibited platelet aggregation induced by adenosine diphosphate, collagen, and thrombin. When AN 162 was given orally to guinea pigs at 30 to 100 mg/kg, an in vivo inhibitory effect on platelet aggregability was found. Though it activated platelet factor 3, the concentration of AN 162 required for substantial activation was greater than that for inhibition of platelet aggregation. No effect on plasma clotting factors was found at or below 300 µg/ml. Slight prolongation of whole blood clotting time was found in the rat and monkey.

The Inhibition of Platelet Aggregation by an Aorta Intima Extract

1974 ◽  
Vol 32 (02/03) ◽  
pp. 417-431 ◽  
Author(s):  
A. du P Heyns ◽  
D. J van den Berg ◽  
G. M Potgieter ◽  
F. P Retief
Keyword(s):  
Platelet Aggregation ◽  
Degradation Products ◽  
Adenosine Diphosphate ◽  
Inhibitory Effect ◽  
Protective Role ◽  
Vascular Trauma ◽  
Wear And Tear ◽  
Sequential Addition ◽  
Aggregation Activity

SummaryThe platelet aggregating activity of extracts of different layers of the arterial wall was compared to that of Achilles tendon. Arterial media and tendon extracts, adjusted to equivalent protein content as an index of concentration, aggregated platelets to the same extent but an arterial intima extract did not aggregate platelets. Platelet aggregation induced by collagen could be inhibited by mixing with intima extract, but only to a maximum of about 80%. Pre-mixing adenosine diphosphate (ADP) with intima extracts diminished the platelet aggregation activity of the ADP. Depending on the relationship between ADP and intima extract concentrations aggregating activity could either be completely inhibited or inhibition abolished. Incubation of ADP with intima extract and subsequent separation of degradation products by paper chromatography, demonstrated a time-dependent breakdown of ADP with AMP, adenosine, inosine and hypoxanthine as metabolic products; ADP removal was complete. Collagen, thrombin and adrenaline aggregate platelets mainly by endogenous ADP of the release reaction. Results of experiments comparing inhibition of aggregation caused by premixing aggregating agent with intima extract, before exposure to platelets, and the sequential addition of first the intima extract and then aggregating agent to platelets, suggest that the inhibitory effect of intima extract results from ADP breakdown. It is suggested that this ADP degradation by intima extract may play a protective role in vivo by limiting the size of platelet aggregates forming at the site of minimal “wear and tear” vascular trauma.

The Effect of Dimethyl Sulfoxide on In Vitro Platelet Function

1976 ◽  
Vol 36 (01) ◽  
pp. 221-229 ◽  
Author(s):  
Charles A. Schiffer ◽  
Caroline L. Whitaker ◽  
Morton Schmukler ◽  
Joseph Aisner ◽  
Steven L. Hilbert
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Dimethyl Sulfoxide ◽  
Platelet Function ◽  
Platelet Volume ◽  
Short Term ◽  
Platelet Factor ◽  
Short Term Exposure ◽  
Structural Abnormalities

SummaryAlthough dimethyl sulfoxide (DMSO) has been used extensively as a cryopreservative for platelets there are few studies dealing with the effect of DMSO on platelet function. Using techniques similar to those employed in platelet cryopreservation platelets were incubated with final concentrations of 2-10% DMSO at 25° C. After exposure to 5 and 10% DMSO platelets remained discoid and electron micrographs revealed no structural abnormalities. There was no significant change in platelet count. In terms of injury to platelet membranes, there was no increased availability of platelet factor-3 or leakage of nucleotides, 5 hydroxytryptamine (5HT) or glycosidases with final DMSO concentrations of 2.5, 5 and 10% DMSO. Thrombin stimulated nucleotide and 5HT release was reduced by 10% DMSO. Impairment of thrombin induced glycosidase release was noted at lower DMSO concentrations and was dose related. Similarly, aggregation to ADP was progressively impaired at DMSO concentrations from 1-5% and was dose related. After the platelets exposed to DMSO were washed, however, aggregation and release returned to control values. Platelet aggregation by epinephrine was also inhibited by DMSO and this could not be corrected by washing the platelets. DMSO-plasma solutions are hypertonic but only minimal increases in platelet volume (at 10% DMSO) could be detected. Shrinkage of platelets was seen with hypertonic solutions of sodium chloride or sucrose suggesting that the rapid transmembrane passage of DMSO prevented significant shifts of water. These studies demonstrate that there are minimal irreversible alterations in in vitro platelet function after short-term exposure to DMSO.

Adenosine Diphosphate (ADP) Breakdown in Human Plasma with Reference to Platelet Aggregation and Uraemia

1968 ◽  
Vol 19 (03/04) ◽  
pp. 438-450
Author(s):  
I. E. T Gan ◽  
B. G Firkin
Keyword(s):  
Platelet Aggregation ◽  
Human Plasma ◽  
Platelet Function ◽  
Adenosine Diphosphate ◽  
Plasma Enzyme ◽  
Aggregation Of Platelets ◽  
Plasma Activity

Summary1. A correlation between platelet aggregation and the plasma enzyme(s) ability to degrade Adenosine Diphosphate (ADP) has been confirmed.2. This plasma activity has been shown to be reduced in 6 patients with uraemia in whom platelet aggregation was demonstrably impaired but not in two whose platelet function was normal. The incorporation of 14C labelled ADP-8-14C was also only reduced in uraemic patients with abnormal platelet aggregation.3. These findings are discussed with particular reference to possible implication in mechanism involved in ADP aggregation of platelets.

The Effect of Barbituric Acid Derivatives on Platelet Function in Vitro and in Vivo

1973 ◽  
Vol 30 (02) ◽  
pp. 315-326
Author(s):  
J. Heinz Joist ◽  
Jean-Pierre Cazenave ◽  
J. Fraser Mustard
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Barbituric Acid ◽  
Platelet Rich Plasma ◽  
Inhibitory Effect ◽  
Primary Response ◽  
Sodium Pentobarbital ◽  
Barbituric Acid Derivatives

SummarySodium pentobarbital (SPB) and three other barbituric acid derivatives were found to inhibit platelet function in vitro. SPB had no effect on the primary response to ADP of platelets in platelet-rich plasma (PRP) or washed platelets but inhibited secondary aggregation induced by ADP in human PRP. The drug inhibited both phases of aggregation induced by epinephrine. SPB suppressed aggregation and the release reaction induced by collagen or low concentrations of thrombin, and platelet adherence to collagen-coated glass tubes. The inhibition by SPB of platelet aggregation was readily reversible and isotopically labeled SPB did not become firmly bound to platelets. No inhibitory effect on platelet aggregation induced by ADP, collagen, or thrombin could be detected in PRP obtained from rabbits after induction of SPB-anesthesia.

The Effect of Collagen Mediated Platelet Release on Plasma Prekallikrein Activation

1984 ◽  
Vol 51 (01) ◽  
pp. 037-041 ◽  
Author(s):  
K M Weerasinghe ◽  
M F Scully ◽  
V V Kakkar
Keyword(s):  
Platelet Aggregation ◽  
Healthy Volunteers ◽  
Platelet Rich Plasma ◽  
Age Groups ◽  
Inhibitory Effect ◽  
Age Group ◽  
Platelet Factor ◽  
Activated Platelets ◽  
Platelet Release ◽  
Collagen Treatment

SummaryCollagen mediated platelet aggregation caused -5.6 ± 6.7% inhibition and +39.1 ± 15.2% potentiation of prekallikrein activation in plasma from normal healthy volunteers between 20–40 and 50–65 years of age, respectively (n = 15, p <0.01). The amouns of platelet factor-four (PF4) released in the two groups were not significantly different. Collagen treatment in the presence of indomethacin caused +11.5 ± 3.6% and +59.6 ± 19.5% potentiation in the 20–40 and 50–65 age groups respectively (p <0.02). Adrenaline mediated platelet aggregation caused -55.2 ± 7.1% and -35.2 ± 8.3% inhibition in the 20–40 and 50–65 age groups, respectively. Collagen treatment of platelet-deficient-plasma and platelet-rich-plasma in EDTA also caused potentiation of prekallikrein activation.The results indicate that the observed degree of prekallikrein activation after platelet aggregation is a net result of the inhibitory effect of PF4 and the potentiatory effect of activated platelets. The potentiatory effect was greater after collagen treatment as compared to adrenaline treatment, and in the 50–65 age group as compared to the 20–40 age group.

Opposite Effect of Lysine on Platelet Aggregation Induced by Arachidonate and by Other Aggregants

1982 ◽  
Vol 48 (01) ◽  
pp. 078-083 ◽  
Author(s):  
C Ts'ao ◽  
S J Hart ◽  
D V Krajewski ◽  
P G Sorensen
Keyword(s):  
Platelet Aggregation ◽  
Secondary Phase ◽  
Aminocaproic Acid ◽  
Adenosine Diphosphate ◽  
Inhibitory Effect ◽  
Human Platelets ◽  
Primary Phase ◽  
High Doses ◽  
The Many ◽  
Induced Aggregation

SummaryEarlier, we found that ε-aminocaproic acid (EACA) inhibited human platelet aggregation induced by adenosine diphosphate (ADP) and collagen, but not aggregation by arachidonic acid (AA). Since EACA is structurally similar to lysine, yet these two agents exhibit vast difference in their antifibrinolytic activities, we chose to study the effect of lysine on platelet aggregation. We used L-lysine-HCl in these studies because of its high solubility in aqueous solutions while causing no change in pH when added to human plasma. With lysine, we repeatedly found inhibition of ADP-, collagen- and ristocetin-induced aggregation, but potentiation of AA-induced aggregation. Both the inhibitory and potentiation effects were dose-dependent. Low doses of lysine inhibited the secondary phase of aggregation; high doses of it also inhibited the primary phase of aggregation. Potentiation of AA-induced aggregation was accompanied by increased release of serotonin and formation of malondialdehyde. These effects were not confined to human platelets; rat platelets were similarly affected. Platelets, exposed to lysine and then washed and resuspended in an artificial medium not containing lysine, remained hypersensitive to AA, but no longer showed decreased aggregation by collagen. Comparing the effects of lysine with equimolar concentrations of sucrose, EACA, and α-amino-n-butyric acid, we attribute the potent inhibitory effect of lysine to either the excess positive charge or H+ and C1− ions. The -NH2 group on the α-carbon on lysine appears to be the determining factor for the potentiation effect; the effect seems to be exerted on the cyclooxygenase level of AA metabolism. Lysine and other chemicals with platelet-affecting properties similar to lysine may be used as a tool for the study of the many aspects of a platelet aggregation reaction.

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