scholarly journals Effects of Juglans regia Root Bark Extract on Platelet Aggregation, Bleeding Time, and Plasmatic Coagulation: In Vitro and Ex Vivo Experiments

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
A. Amirou ◽  
M. Bnouham ◽  
A. Legssyer ◽  
A. Ziyyat ◽  
M. Aziz ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Bleeding Time ◽  
Ex Vivo ◽  
Juglans Regia ◽  
Anticoagulant Effect ◽  
Bark Extract ◽  
Root Bark ◽  
Thrombin Time ◽  
Induced Aggregation

Platelets have an important role in thrombosis and haemostasis. Hyperactivity of the platelets has been associated with thromboembolic diseases and represents the main cause of complications of cardiovascular diseases. Crude aqueous extract (CAE) of Juglans regia root bark was evaluated for bleeding time, antiaggregant activity by using agonists, thrombin, ADP, collagen, or arachidonic acid (in vitro and ex vivo), and anticoagulant activity by measuring the clotting parameters: activated partial thromboplastin time, prothrombin time, thrombin time, and fibrinogen dosage (in vitro and ex vivo). The result of this study reported that the strongest antiaggregant effect of CAE in vitro was observed on the ADP-induced aggregation with inhibitions up to 90 %, while, in ex vivo experiments, the inhibition (more than 80 %) was observed with all agonists. Anticoagulant effect of CAE significantly prolonged the TT and decreased the fibrinogen level in vitro and ex vivo without interfering with APTT and PT. The bleeding time in mice and rats was significantly increased by CAE. The antiplatelet and anticoagulant effect observed in this study suggest that Juglans regia could have antithrombotic and/or thrombolytic activities and provide an alternative therapy against thrombotic complications related to cardiovascular diseases.

ORALLY ADMINISTERED VITAMIN B PROLONGS THE BLEEDING TIME AND INHIBITS PLATELET AGGREGATION IN HUMAN VOLUNTEERS.

1987 ◽  
Author(s):  
A M Randi ◽  
E Sacchi ◽  
M Cattaneo
Keyword(s):  
Platelet Aggregation ◽  
Vitamin B6 ◽  
Bleeding Time ◽  
Ex Vivo ◽  
Vitamin B ◽  
Thrombin Time ◽  
Fibrin Formation ◽  
Primary Hemostasis ◽  
Coagulation Tests

It is known that mM concentrations of vitamin B6 inhibit human platelet aggregation and fibrin formation in vitro. There are very few and controversial data on the ex vivo effects of vitamin B6 on hemostatic parameters. We evaluated the effects of oral administration of vitamin B6 on bleeding time (BT), fibrin formation, platelet aggregation (PA) and the release reaction (RR). Vitamin B6 300 mg/day p.o., was given to 18 healthy volunteers (8 M, 10 F, aged 23-35) for 8 days. BT was measured before the first dose (Baseline), 2 hr after the first (Day 1) and the last dose (Day 8). In 7 subjects BT was measured also 7 days after the suspension of the drug (Day 15). Before and 2 hr after the first dose, prothrombin time (PT), partial thromboplastin time (PTT), thrombin time (TT), PA and the RR induced by different concentrations of ADP, PAF-acether, collagen (coll), epinephrine (epi), arachidonate (AA) were studied. BT was significantly prolonged after vitamin B6 administration, and returned to baseline values 7 days after suspension of the drug. PA and the RR induced by 1 uM ADP, 1 ug/ml coll or 5 uM epi were significantly inhibited 2 hours after vitamin B6 administration. Vitamin B6, however, did not affect PA or the RR induced by 0.2-2 uM PAF-acether, 2 uM ADP, 1 mM AA, 2 ug/ml coll, nor did it affect PT, PTT or TT. These data show that orally administered vitamin B impairs primary hemostasis, but does not affect fibrin 6 formation, as measured with standard coagulation tests.

Augmentation of the Anticoagulant Effects of Heparin By a Tri-Block Polymer MST-188

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 5080-5080
Author(s):  
Daniel Dansdill ◽  
Jae Cho ◽  
Daneyal Syed ◽  
Jawed Fareed ◽  
Martin Emanuele
Keyword(s):  
Blood Vessel ◽  
Bleeding Time ◽  
Jugular Vein ◽  
Ex Vivo ◽  
Rat Plasma ◽  
Acute Limb Ischemia ◽  
Thrombin Time ◽  
Blood Samples

Abstract Introduction: MST-188 (purified poloxamer 188) is a tri-block co-polymer with high affinity to hydrophobic cellular surfaces that inhibits hydrophobic adhesive interactions in the circulation. It also facilitates blood flow by reducing blood viscosity and reportedly exhibits anti-adhesion and anti-inflammatory properties. Currently, this agent is under study in with patients experiencingsickle cell crisis and in patients with acute limb ischemia. Since MST-188 may be administered with other anti-coagulant agents such as heparin its potential interaction to modulate the anti-coagulant effects of this drug require experimental validation. These studies are designed to investigate the potential interactions between heparin and MST-188 in a rat model of tail transection bleeding and jugular vein clamping induced thrombosis model. Materials and Methods: The in vitro interactions between MST-188 were investigated by supplementing this agent to normal rat plasma (NRP) and heparinized rat plasma at a fixed concentrations of 1.25 and 2.50 mg/mL. The concentration of heparin was kept at 1.25 and 2.50 μg/mL. In the in vivo studies individual groups of rats (n=6-8) were administered with saline as a control, heparin in the dosage range of 125-500 ug/kg intravenously and MST-188 at 25 mg/kg IV followed by heparin at the 125-500 ug/kg dosages. Rat tail resection time was measured 5 minutes after administration of heparin and clot occlusion index was measured as number of jugular vein clamping required to occlude the blood vessel. After the completion of the procedure blood samples were obtained through cardiac puncture and used for ex vivo analysis of PT, aPTT, heptest and thrombin time. Results: In the in vitro studies heparin produced a concentration dependent prolongation of the aPTT, heptest and thrombin time. MST-188 did not produce any effects on the aPTT and heptest time, however it decreased the thrombin time. MST-188 at a higher concentration of 2.5 and 5.0 mg/ml produced a shorting of heparins anticoagulant responses, as measured by aPTT and thrombin time. Heparin produced a dose dependent increase in both the bleeding time (p<0.0001) and number of jugular vein clamps to occlude the blood vessel (p<0.0001). MST-188 at dosages of 25 mg/kg produced a significant increase on both bleeding time (p <0.05) and number of clampings required to occlude the blood vessel (p<0.0001). When MST-188 was administered simultaneously with heparin it augmented the bleeding time (p < 0.05) and increased the number of jugular vein clamps required to occlude the blood vessel (p < 0.05). The ex vivo analysis of blood samples collected from rats treated in different regimens did not exhibit any anti-coagulant effects as measured by PT, aPTT, heptest and thrombin time. Conclusion: These studies suggest a differential response of MST-188. While in vitro it exhibits a prohemostatic response as evident by shortening of thrombin time, in the in vivo setting it enhances the anticoagulant effects of heparin as evident by increased bleeding time and increased number of jugular vein clamps required to occlude the vessel. Thus, both of these mechanisms are involved in the mediation of the beneficial effects observed with this agent in vaso-occlusive and thrombotic processes. Disclosures Emanuele: Mast Therapeutics: Employment.

Comparative Arterial Antithrombotic Activity of Clopidogrel and Acetyl Salicylic Acid in the Pig

1992 ◽  
Vol 68 (05) ◽  
pp. 500-505 ◽  
Author(s):  
Ch M Samama ◽  
Ph Bonnin ◽  
M Bonneau ◽  
G Pignaud ◽  
E Mazoyer ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Femoral Artery ◽  
Bleeding Time ◽  
Ex Vivo ◽  
Flow Reduction ◽  
Cyclic Flow ◽  
Left Femoral Artery ◽  
Before And After ◽  
The Right ◽  
Induced Aggregation

SummaryWe investigated the comparative antithrombotic properties of clopidogrel, an analogue of ticlopidine, and aspirin, using the Folts' model on femoral arteries in 22 pigs. On each animal, clopidogrel or aspirin were used to treat the thrombotic process on the left femoral artery and to prevent this process on the right femoral artery. Sequentially: an injury and stenosis were carried out on the left femoral artery; the thrombotic process was monitored with a Doppler during a 30-min observation period for cyclic flow reductions or permanent cessation of flow; after the first cyclic flow reduction occurred, clopidogrel (5 mg kg-1) or aspirin (2.5, 5, 100 mg kg-1) were injected intravenously; if cyclic flow reductions were abolished, epinephrine (0.4 µg kg-1 min-1) was injected to try to restore cyclic flow reductions and/or permanent cessation of flow; then injury and stenosis were applied on the right femoral artery. Before and after injection of clopidogrel or aspirin, ear immersion bleeding times and ex-vivo platelet aggregation were performed. Clopidogrel (n = 7) abolished cyclic flow reductions in all animals and epinephrine did not restore any cyclic flow reduction. On the right femoral artery, cyclic flow reductions were efficiently prevented, even for two injuries. Basal bleeding time (5 min 28) was lengthened (>15 min, 30 min after clopidogrel and remained prolonged even after 24 h). ADP-induced platelet aggregation was inhibited (more than 78%). Comparatively, aspirin had a moderate and no dose-dependent effect. Aspirin 2.5 mg kg-1 (n = 6) abolished cyclic flow reductions in 2 animals, CFR reoccurred spontaneously in one animal and epinephrine restored it in a second animal. Aspirin 5 mg kg-1 (n = 6) abolished cyclic flow reductions in only 3 animals and epinephrine always restored it. Aspirin 100 mg kg-1 (n = 3) was unable to abolish cyclic flow reductions. On the right femoral artery, aspirin did not significantly prevent cyclic flow reductions which occurred in all animals after one (n = 14) or two injuries (n = 1), except for one animal. Basal bleeding time was lengthened but it shortened rapidly, reaching its basal value after 24 h. ADP-induced aggregation was not significantly inhibited, whereas arachidonic acid induced aggregation was always inhibited. Clopidogrel appears as a more potent antithrombotic drug than aspirin in this model, in treating and preventing spontaneous or epinephrine-induced cyclic flow reductions and lengthening bleeding time.

The d-Enantiomer Form of Indobufen Totally Accounts for the Anti-Cyclooxygenase and Antiplatelet Activity Ex Vivo and for the Increase in Bleeding Time by Indobufen in Man

1992 ◽  
Vol 67 (02) ◽  
pp. 258-263 ◽  
Author(s):  
Raffaele De Caterina ◽  
Rosa Sicari ◽  
An Yan ◽  
Walter Bernini ◽  
Daniela Giannessi ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Plasma Levels ◽  
Bleeding Time ◽  
Ex Vivo ◽  
Random Sequence ◽  
Antiplatelet Agent ◽  
Antiplatelet Drug ◽  
Double Blind

SummaryIndobufen is an antiplatelet drug able to inhibit thromboxane production and cyclooxygenase-dependent platelet aggregation by a reversible inhibition of cyclooxygenase. Indobufen exists in two enantiomeric forms, of which only d-indobufen is active in vitro in inhibiting cyclooxygenase. In order to verify that also inhibition of platelet function is totally accounted for by d-indobufen, ten patients with proven coronary artery disease (8 male, 2 female, age, mean ± S.D., 58.7 ± 7.5 years) were given, in random sequence, both 100 mg d-indobufen and 200 mg dl-indobufen as single administrations in a double-blind crossover design study with a washout period between treatments of 72 h. In all patients thromboxane (TX) B2 generation after spontaneous clotting (at 0, 1, 2, 4, 6, 8, 12, 24 h), drug plasma levels (at the same times), platelet aggregation in response to ADP, adrenaline, arachidonic acid, collagen, PAF, and bleeding time (at 0, 2, 12 h) were evaluated after each treatment. Both treatments determined peak inhibition of TXB2 production at 2 h from administration, with no statistical difference between the two treatments (97 ±3% for both treatments). At 12 h inhibition was 87 ± 6% for d-indobufen and 88 ± 6% for dl-indobufen (p = NS). Inhibition of TXB2 production correlated significantly with plasma levels of the drugs. Maximum inhibitory effect on aggregation was seen in response to collagen 1.5 pg/ml (63 ± 44% for d-indobufen and 81 ± 22% for dl-indobufen) and arachidonic acid 0.5-2 mM (78 ± 34% for d-indobufen and 88 ± 24% for dl-indobufen) at 2 h after each administration. An effect of both treatments on platelet aggregation after 12 h was present only for adrenaline 2 μM (55 ± 41% for d-indobufen and 37 ± 54% for dl-indobufen), collagen 1.5 pg/ml (69 ± 30% for d-indobufen and 51 ± 61% for dl-indobufen), arachidonic acid 0.5-2 mM (56 ± 48% for d-indobufen and 35 ± 49% for dl-indobufen). The extent of inhibition of TX production and the extent of residual platelet aggregation were never significantly different between treatments. Bleeding time prolongation was similar in the two treatment groups without showing a pronounced and long lasting effect (from 7.0 ± 2.0 min to 10.0 ± 3.0 min at 2 h and 8.0 ± 2.0 min at 12 h for d-indobufen; from 6.0 ±1.0 min to 8.5 ± 2.0 min at 2 h and 8.0 ± 1.0 min at 12 h for dl-indobufen). These results demonstrate that the biological activity of dl-indobufen as an antiplatelet agent in vivo is totally accounted for by d-indobufen.

Dipyridamole Inhibits Platelet Aggregation in Whole Blood

1983 ◽  
Vol 50 (04) ◽  
pp. 852-856 ◽  
Author(s):  
P Gresele ◽  
C Zoja ◽  
H Deckmyn ◽  
J Arnout ◽  
J Vermylen ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Whole Blood ◽  
Ex Vivo ◽  
Platelet Rich Plasma ◽  
Significant Negative Correlation ◽  
Significant Inhibition ◽  
Oral Drug ◽  
Human Blood Samples ◽  
Induced Aggregation

SummaryDipyridamole possesses antithrombotic properties in the animal and in man but it does not inhibit platelet aggregation in plasma. We evaluated the effect of dipyridamole ex vivo and in vitro on platelet aggregation induced by collagen and adenosine- 5’-diphosphate (ADP) in human whole blood with an impedance aggregometer. Two hundred mg dipyridamole induced a significant inhibition of both ADP- and collagen-induced aggregation in human blood samples taken 2 hr after oral drug intake. Administration of the drug for four days, 400 mg/day, further increased the antiplatelet effect. A significant negative correlation was found between collagen-induced platelet aggregation in whole blood and dipyridamole levels in plasma (p <0.001). A statistically significant inhibition of both collagen (p <0.0025) and ADP-induced (p <0.005) platelet aggregation was also obtained by incubating whole blood in vitro for 2 min at 37° C with dipyridamole (3.9 μM). No such effects were seen in platelet-rich plasma, even after enrichment with leukocytes. Low-dose adenosine enhanced in vitro inhibition in whole blood.Our results demonstrate that dipyridamole impedes platelet aggregation in whole blood by an interaction with red blood cells, probably involving adenosine.

scholarly journals In vitro and in vivo evaluation of antibacterial activity of Bridelia ferruginea extracts on some clinical isolates

2018 ◽  
Vol 7 (4) ◽  
pp. 392-398
Author(s):  
B.T Yunana ◽  
◽  
B. B Bukar ◽  
J. C Aguiyi ◽  
◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Staphylococcus Aureus ◽  
Antibacterial Activity ◽  
Bark Extract ◽  
Root Extract ◽  
Root Bark ◽  
Zone Of Inhibition ◽  
Bridelia Ferruginea

The ethanol extracts of root, bark and leaf of Bridelia ferruginea was investigated for antibacterial activity against clinical isolate of Staphylococcus aureus and Escherichia coli. The extracts had significant antibacterial activity in vitro at concentration of 25 mg/ml, 50 mg/ml, 100 mg/ml and 200 mg/ml and in vivo at dose of 50 mg/kg and 100 mg/kg. The root extract in vitro had the highest zone of inhibition, followed by the bark extract for both Staphylococcus aureus and Escherichia coli. The concentration of 200 mg/ml had the highest zone of inhibition in vitro. The minimum inhibitory concentration (MIC) showed a decreasing inhibitory effect of the plant extracts for both Staphylococcus aureus and Escherichia coli as the concentration decreases with root having 3.125 mg/ml, bark having 6.25 mg/ml and leaf having 25 mg/ml for Staphylococcus aureus and Escherichia coli. Likewise, the minimum bactericidal concentration (MBC) showed decreasing bactericide effects with decrease concentration with root having 12.5 mg/ml, bark having 12.5 mg/ml and leaf having 25 mg/ml for Escherichia coli while root had 6.25mg/ml, bark had 12.5mg/ml and leaf had 25mg/ml for Staphylococcus aureus. The in vivo investigation showed that the root and bark extract exhibited antibacterial activity on both Staphylococcus aureus and Escherichia coli at doses of 100mg/kg and 50mg/kg; the root extract had higher activity than the bark and root/bark combined. The dose of 100 mg/kg had the highest colonies reduction for Staphylococcus aureus and Escherichia coli in vivo. Preliminary phytochemical screening of root, bark and leaves of Bridelia ferruginea revealed the presence of tannins, flavonoids, carbohydrates, cardiac glycoside (root, bark and leaves), saponins (root and bark). The presence of tannins, saponins, flavonoid, cardiac glycoside and carbohydrate in the bark and root extracts of the plant indicates that the bark and root extracts were pharmacological importance

In vitro antioxidant and anti-arthritic effect of the aqueous and ethanolic leaf and root bark extract of Alafia barteri

2021 ◽  
Vol 10 (1) ◽  
pp. 10-14
Author(s):  
Ikeoluwapo Olanike Kolawole ◽  
◽  
Osareti Albert Taiwo Ebuehi ◽  
Esther Ayomide Awoyera ◽  
◽  
...  
Keyword(s):  
Protein Denaturation ◽  
Reducing Power ◽  
Assay Method ◽  
Bark Extract ◽  
Root Extract ◽  
Root Bark ◽  
Eye Infections ◽  
Root Extracts ◽  
Ethanol Extracts

Alafia barteri (Apocynaceae) is a climbing shrub having white or pink flowers. Traditionally, it has been used to treat diseases like malaria, sickle cell anemia, and eye infections. This research is focused on investigating the antioxidant and anti-arthritic activities of the aqueous and ethanol leaf and root extract of Alafia barteri plant in vitro. In-vitro antioxidant methods used were 2, 2 -diphenyl-1-picrylhydrazyl assay, reducing power activity and hydrogen peroxide scavenging assay while the anti-arthritic activity was studied using the assay method of protein denaturation. Results revealed that aqueous and ethanol root extracts scavenge free radicals, thus inhibiting damage caused by oxidative stress in arthritis while the ethanol extracts of both the leaf and roots had good anti-arthritic activities as seen in its ability to decrease protein denaturation.

Effects Of Pentoxifylline, Penbutolol, Prenylamine, Clofibric Acid And Nicotinic Acid On The Release Of Prostacyclin-(PGI2-) Like Activity From Rat Aorta In Vivo And In Vitro

1981 ◽  
Author(s):  
K U Weithmann ◽  
A G Hoechst
Keyword(s):  
Cyclic Amp ◽  
Nicotinic Acid ◽  
Ex Vivo ◽  
Synergistic Effects ◽  
Rat Aorta ◽  
Clofibric Acid ◽  
Vessel Walls ◽  
Induced Aggregation

Aortas from rats, treated with 5-20 mg/kg of pentoxifylline (pof), penbutolol, prenylamine, clofibric acid or nicotinic acid showed, ex vivo, a significantly higher release of acid labile PGI2-like anti-aggregatory activity compared to controls. This activity could be suppressed by pre-treatment with 2 mg/kg Indomethacin. When incubated with rat aortas in vitro, pof showed a similar stimulatory effect on PGI2-like release, whereas clofibric-and nicotinic acid had no significant effect in this system. Pof and all other drugs mentioned above in therapeutical concentrations had virtually no effect on induced aggregation of human platelets in vitro. However, in the presence of small amounts PGI2 in vitro, inhibition of aggregation and platelet cyclic AMP are enhanced synergistically above the effects of PGI2 and pof individually.We conclude from these experiments that therapeutic doses of all drugs in our study stimulate in vivo the release of PGI2-like activity from vessel walls, thus inhibiting platelet aggregation in vivo. The primary site of action of pof seems to be the vessel wall, whereas the effect of clofibric acid and nicotinic acid on the vessel walls seem to be secondary. The elevation of platelet cyclic AMP levels which generally parallels PGI2-induced inhibition of aggregation might be further enhanced by pof known as an inhibitor of platelet cyclic AMP phosphodiesterase, thus explaining the observed synergistic effects between PGI2 and pof.

Sex-Associated Differences On The Effect Of Asa Or Flurbiprofen On Platelet Function Ex Vivo

1981 ◽  
Author(s):  
E E Nishizawa ◽  
B A Molony ◽  
M M Meinzinger ◽  
D J Williams
Keyword(s):  
Arachidonic Acid ◽  
Platelet Function ◽  
Bleeding Time ◽  
Ex Vivo ◽  
Normal Male ◽  
Normal Response ◽  
Beneficial Effects ◽  
Acid Pathway ◽  
Induced Aggregation ◽  
Arachidonic Acid Pathway

It has been reported that although ASA may have some beneficial effects in males, no differences from placebo was detected in females in clinical trials on venous thrombosis, TIA and stroke. Since ASA inhibits platelet function and because the end-points measured in the above clinical studies may be related to platelet function, we measured bleeding time and platelet aggregation induced by collagen or arachidonic acid following oral administration of ASA (650 mg) or flurbiprofen (100 mg) in normal male and female volunteers (10 per group, total of 40 subjects) between the age of 50 and 70.No sex-associated differences in response with either drug were observed in bleeding time or platelet function. Thus, we were unable to confirm that the observation of beneficial effect of ASA in males was due to its effect on platelets. However, more interestingly there was a statistically shorter bleeding time in males (p = 0.026) before administration of drug. It was also found that despite the normal response to collagen, PRP prepared from pre-drug blood samples from 6 individuals (15%) did not aggregate when stimulated with arachidonic acid at concentrations as high as 1 mM. These results suggest that, at least in some individuals, collagen-induced aggregation may proceed by a pathway independent of the arachidonic acid pathway.

scholarly journals Effects of Sodium Nitroprusside on Platelet Adhesion, Subsequent Aggregation and Vasoconstriction

1977 ◽  
Author(s):  
H.R. Baumgartner
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Sodium Nitroprusside ◽  
Platelet Adhesion ◽  
Ex Vivo ◽  
Balloon Catheter ◽  
Strong Inhibitor ◽  
Induced Aggregation

Sodium nitroprusside (SNP), a potent vasodilator, has shown beneficial effects in acute myocardial infarction. Since platelets may play an important role in the pathogenesis of myocardial infarction, the effect of SNP on their interaction with rabbit aorta subendothelium was investigated in vivo and under controlled blood flow conditions ex vivo and in vitro.One iliac artery and the abdominal aorta were denuded of endothelium by balloon catheter injury during infusion of glucose, SNP at 6 or 12 μg/kg/min in groups of 12, 6 and 7 rabbits respectively. The aorta and their branches were perfuse-fixed under controlled pressure 10 min after denudation. Morphometric evaluation showed dose-dependent and significant (2p < 0.01 or 0.001) inhibition of platelet spreading, adhesion and aggregation. The latter was abolished at the higher dose of SNP. Denudation and subsequent platelet adhesion caused strong vasoconstriction (2p < 0.001) which was inhibited by SNP (2p < 0.01).By exposure of subendothelium to either citrated blood or native blood in a flow chamber (2000 sec-1 shear rate) strong inhibition of spreading and adhesion-induced aggregation was again demonstrated at 6 and 12 μg/kg/min SNP. In vitro, adhesion-induced aggregation was completely abolished after the addition of SNP to rabbit (at 20 μg/ml) or human blood (2 μg/ml). 1 μg/ml PGE1 was needed to induce a similar inhibitory effect.Thus SNP is a strong inhibitor of platelet function and of injury + platelet induced vasoconstriction. These findings may explain its beneficial effect in acute myocardial infarction.

Sign in / Sign up

Export Citation Format

Share Document