Effect of capsaicin and dihydrocapsaicin on in vitro blood coagulation and platelet aggregation

2009 ◽  
Vol 124 (6) ◽  
pp. 721-723 ◽  
Author(s):  
Murray J. Adams ◽  
Kiran D.K. Ahuja ◽  
Dominic P. Geraghty
Keyword(s):  
Platelet Aggregation ◽  
Blood Coagulation

scholarly journals The effects of fructose diphosphate on routine coagulation tests in vitro

2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Tongqing Chen ◽  
Duan Chen ◽  
Lu Chen ◽  
Zhengxu Chen ◽  
Baolong Wang ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Blood Coagulation ◽  
Detection System ◽  
Coagulation System ◽  
Thrombin Time ◽  
Aggregation Rate ◽  
Coagulation Testing ◽  
Coagulation Tests ◽  
Routine Coagulation

AbstractTo evaluate the effects of fructose diphosphate (FDP) on routine coagulation tests in vitro, we added FDP into the mixed normal plasma to obtain the final concentration of 0, 1, 2, 3, 4, 5, 6, 10, 15, 20, 25, 30 and 35 mg/mL of drug. Prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen (FBG) and thrombin time (TT) of samples were analyzed with blood coagulation analyzers from four different manufacturers(Sysmex, Stago, SEKISUI and Werfen) and their corresponding reagents, respectively. Before the experiment, we also observed whether there were significant differences in coagulation test results of different lots of reagents produced by each manufacturer. At the same time as the four routine clotting tests, the Sysmex blood coagulation analyzer and its proprietary analysis software were used to detect the change of maximum platelet aggregation rate in platelet-rich plasma after adding FDP (0, 1, 2, 3, 4, 5 and 6 mg/mL). The results of PT, aPTT and TT showed a FDP (0–35 mg/mL) concentration-dependent increase and a FBG concentration-dependent decrease. The degree of change (increase or decrease) varied depending on the assay system, with PT and aPTT being more affected by the Sysmex blood coagulation testing instrument reagent system and less affected by CEKISUI, TT less affected by CEKISUI and more affected by Stago, and FBG less affected by Stago and more affected by Sysmex. The results of PT, aPTT and TT were statistically positively correlated with their FDP concentrations, while FBG was negatively correlated. The correlation coefficients between FDP and the coagulation testing systems of Sysmex, Stago, Werfen and SEKISUI were 0.975, 0.988, 0.967, 0.986 for PT, and 0.993, 0.989, 0.990 and 0.962 for aPTT, 0.994, 0.960, 0.977 and 0.982 for TT, − 0.990, − 0.983, − 0.989 and − 0.954 for FBG, respectively. Different concentrations of FDP (0, 1, 2, 3, 4, 5 and 6 mg/mL) had different effects on the maximum aggregation rate of platelet induced by the agonists of adenosine diphosphate (ADP, 5 µmol/L), arachidonic acid (Ara, 1 mmol/L), collagen (Col, 2.5 µg/mL) and epinephrine (Epi,10 µmol/L), but the overall downward trend was consistent, that is, with the increase of FDP concentration, the platelet aggregation rate decreased significantly. Our experimental study demonstrated a possible effect of FDP on the assays of coagulation and Platelet aggregation, which may arise because the drug interferes with the coagulation and platelet aggregation detection system, or it may affect our in vivo coagulation system and Platelet aggregation function, the real mechanism of which remains to be further verified and studied.

scholarly journals Glycocalyx components affect platelet function, whole blood coagulation, and fibrinolysis: an in vitro study suggesting a link to trauma-induced coagulopathy

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Martin W. Britten ◽  
Laura Lümers ◽  
Kenji Tominaga ◽  
Jürgen Peters ◽  
Daniel Dirkmann
Keyword(s):  
Platelet Aggregation ◽  
Heparan Sulfate ◽  
Chondroitin Sulfate ◽  
Blood Coagulation ◽  
Platelet Function ◽  
Whole Blood ◽  
Dependent Manner ◽  
Trauma Induced Coagulopathy ◽  
Coagulation And Fibrinolysis

Abstract Background The mechanisms of trauma induced coagulopathy (TIC) are considered multifactorial. Amongst others, however, shedding of the endothelial glycocalyx resulting in increased concentrations of glycocalyx fragments in plasma might also play a role. Thus, we hypothesized that shedded glycocalyx components affect coagulation and may act as humoral mediators of TIC. Methods To investigate effects of heparan sulfate, chondroitin sulfate, syndecan-1, versican, and thrombomodulin we added these fragments to in vitro assays of whole blood from healthy volunteers to yield concentrations observed in trauma patients. Platelet function, whole blood coagulation, and fibrinolysis were measured by standard coagulation tests, impedance aggregometry (IA), and viscoelastic tests (VET). To assess dose-response relationships, we performed IA with increasing concentrations of versican and VET with increasing concentrations of thrombomodulin. Results Intrinsically activated clotting times (i.e., activated partial thromboplastin time and intrinsically activated VET with and without heparinase) were unaffected by any glycocalyx fragment. Thrombomodulin, however, significantly and dose-dependently diminished fibrinolysis as assessed by VET with exogenously added rt-PA, and increased rt-PA-induced lysis Indices after 30 (up to 108% of control, p <  0,0001), 45 (up to 368% of control, p <  0,0001), and 60 min (up to 950% of control, p <  0,0001) in VET. Versican impaired platelet aggregation in response to arachidonic acid (up to − 37,6%, p <  0,0001), ADP (up to − 14,5%, p <  0,0001), and collagen (up to − 31,8%, p <  0,0001) in a dose-dependent manner, but did not affect TRAP-6 induced platelet aggregation. Clotting time in extrinsically activated VET was shortened by heparan sulfate (− 7,2%, p = 0,024), chondroitin sulfate (− 11,6%, p = 0,016), versican (− 13%, p = 0,012%), and when combined (− 7,2%, p = 0,007). Conclusions Glycocalyx components exert distinct inhibitory effects on platelet function, coagulation, and fibrinolysis. These data do not support a ‘heparin-like auto-anticoagulation’ by shed glycosaminoglycans but suggest a possible role of versican in trauma-induced thrombocytopathy and of thrombomodulin in trauma-associated impairment of endogenous fibrinolysis.

scholarly journals The Antithrombotic Potential of Dihomo-γ-Linolenic Acid

1977 ◽  
Author(s):  
P.B.A. Kernoff ◽  
J.A. Davies ◽  
G.P. McNicol ◽  
A.L. Willis ◽  
K.J. Stone
Keyword(s):  
Platelet Aggregation ◽  
Blood Coagulation ◽  
Linolenic Acid ◽  
Blood Viscosity ◽  
Ex Vivo ◽  
Normal Subjects ◽  
Antithrombotic Agent ◽  
Patients With Diabetes ◽  
Favourable Change

Dihomo-γ-linolenic acid (DHLA; Ro 12–1989, Roche), a natural precursor of prostaglandin E1, has been evaluated as a potential antithrombotic agent by studying its effects on platelet function, blood coagulation and blood viscosity. In vitro investigations were performed on blood obtained from 10 normal subjects and 10 patients with diabetes mellitus, 8 of whom had evidence of severe microangiopathy. Prior incubation of normal platelets with DHLA caused a marked and dose-related inhibition of : platelet aggregation in response to stimulation with ADP, collagen, epinephrine, thrombin and ristocetin; platelet glass-bead retention; release of serotonin and platelet factors 3 and 4. Effects on diabetic platelets were less marked but still highly significant. DHLA also reversed platelet aggregation and inhibited the adhesion of porcine platelets to collagen-coated glass. No significant effects were found on whole-blood viscosity or tests of blood coagulation apart from a slight shortening of the one-stage prothrombin time. Ex vivo studies were performed on 3 normal volunteers after oral administration of single doses of DHLA. Increased plasma DHLA/arachidonic acid ratios resulted in all instances (Stone et al, this meeting). No adverse effects were noted but consistent evidence of a favourable change in haemostatic tests was not obtained. The spectrum of in vitro inhibitory activity of DHLA on platelets is wider than that reported for other potential anti-thrombotic agents and our results suggest that DHLA shows considerable promise in this respect.

Abstract 140: Magnesium Lithospermate B Inhibits Blood Coagulation and Platelet Aggregation: Novel Mechanism of a Traditional Drug for Cardiovascular Diseases

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Yiming Wang ◽  
Dan Zhang ◽  
Xiaohong Xu ◽  
Xi Lei ◽  
Yiping Wang ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Blood Plasma ◽  
Blood Coagulation ◽  
Salvia Miltiorrhiza ◽  
Low Cost ◽  
Coagulation Factors ◽  
Coagulation Cascade ◽  
Network Pharmacology ◽  
Magnesium Lithospermate B

Magnesium lithospermate B (MLB) is one of the major components of Salvia miltiorrhiza root (Danshen). Danshen extracts have been used to control cardiovascular disease for centuries. In 2005, intravenous injection of Danshen depside salt was approved in China for treatment of chronic angina. Although clinical observations have suggested that Danshen extracts inhibited thrombosis, the exact mechanism has not been adequately explored. Using an in vitro whole blood clotting assay, we observed that MLB (250 μM) significantly reduced clot size. Both the clot wet and dry weights were decreased following treatment (108.3 mg vs. 63.5 mg, and 32.8 mg vs. 18.5 mg, p<0.05, respectively). Using thromboelastography, we found that MLB markedly decreased the mechanical strength of the clot and modestly delayed initiation of coagulation in cell-free blood plasma prepared by centrifugation (10,000 хg, 10 min). Under confocal microscopy, we further observed that MLB significantly reduced the density of the fibrin network formed in plasma following thrombin treatment, suggesting that MLB targets coagulation factors to inhibit coagulation. Recent network pharmacology analyses predict that MLB may interact with VWF, factor XIII (FXIII), or thrombin in the coagulation cascade. We found that MLB did not inhibit VWF-dependent platelet agglutination induced by botrocetin. ELISA revealed that MLB also did not significantly alter the binding of activated FXIII (FXIIIa) to fibrinogen. However, when native FXIII from blood plasma was used for the same assay, MLB significantly reduced the binding of FXIIIa to fibrinogen. Since generation of FXIIIa from FXIII is thrombin-dependent, these data suggest that MLB inhibits thrombin activity or thrombin generation. Indeed, we found that MLB markedly inhibited thrombin-induced gel-filtered human and mouse platelet aggregation. These data demonstrated a novel role for MLB in the inhibition of blood coagulation and platelet aggregation, likely through direct inhibition of thrombin function, although we cannot exclude its additional anti-thrombotic activities. Thus, purified MLB may represent an efficient, low-cost agent for treatment of artery and deep vein thrombosis.

Effect of Aspirin Infusions on Platelet Function in Humans

1990 ◽  
Vol 79 (1) ◽  
pp. 37-42 ◽  
Author(s):  
K. M. Wilson ◽  
D. M. Siebert ◽  
E. M. Duncan ◽  
A. A. Somogyi ◽  
J. V. Lloyd ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Blood Coagulation ◽  
Platelet Function ◽  
Whole Blood ◽  
Dependent Manner ◽  
Inhibitory Effects ◽  
Concentration Dependent Manner ◽  
Infusion Period

1. The inhibitory effects of aspirin on platelet function in vitro have been shown to be both time (over 3 h) and concentration (1–10 μmol/l) dependent. 2. To determine if these effects occurred in vivo, four volunteers received intravenous infusions on four occasions, to give constant plasma aspirin concentrations of 0, 1, 2 and 4 μmol/l over 3 h. Infusions were performed at intervals of at least 2 weeks. 3. Before and during the infusions, blood was taken for assay of aspirin concentrations, and measurements of platelet aggregation in response to collagen, adenosine 5′-pyrophosphate and arachidonate. Thromboxane generation after stimulated platelet aggregation and whole-blood coagulation was also measured. 4. At each aspirin concentration, both platelet aggregation and thromboxane generation in response to collagen and arachidonate were inhibited progressively over the 3 h infusion period. Greatest inhibition was seen during the 4 μmol/l infusion, which produced maximal or near-maximal inhibition by the third hour. 5. Thromboxane generated during whole-blood coagulation was similarly inhibited in both a time- and concentration-dependent manner throughout all aspirin infusions. 6. The progressive nature of the inhibition of platelet function with these low aspirin concentrations may be due to either slow aspirin transport across the platelet membrane or delayed interaction with cyclo-oxygenase.

scholarly journals A Comparative Study of Rutin and Rutin Glycoside: Antioxidant Activity, Anti-Inflammatory Effect, Effect on Platelet Aggregation and Blood Coagulation

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1696
Author(s):  
Sung-Sook Choi ◽  
Hye-Ryung Park ◽  
Kyung-Ae Lee
Keyword(s):  
Antioxidant Activity ◽  
Platelet Aggregation ◽  
Blood Coagulation ◽  
Prostaglandin E ◽  
Coagulation Test ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Blood Coagulation Test

The effects of rutin and rutin glycoside with different solubility were compared on antioxidant activity and anti-inflammatory effects in vitro and the effects on platelet aggregation and blood coagulation in vitro and in vivo. Rutin glycoside (consisting of rutin mono-glucoside and rutin di-glucoside) was prepared via enzymatic transglycosylation from rutin. Rutin glycoside showed a higher effect than rutin on radical scavenging activity in antioxidant assays. Rutin showed a higher toxicity than rutin glycoside in murine macrophage RAW264.7 cells. They had similar effects on the levels of nitric oxide (NO), prostaglandin E (PGE) 2 and pro-inflammatory cytokines (such as tumor necrosis factor (TNF)-α, and interleukin (IL)-6) in the cells. Both rutin and rutin glycosides similarly reduced the rate of platelet aggregation compared to controls in vitro. They also similarly delayed prothrombin time (PT) and activated partial thromboplastin time (APTT) in an in vitro blood coagulation test. The effect of repeated administration of rutin and rutin glycoside was evaluated in vivo using SD rats. The platelet aggregation rate of rutin and the rutin glycoside administered group was significantly decreased compared to that of the control group. On the other hand, PT and APTT of rutin and rutin glycoside group were not significantly delayed in vivo blood coagulation test. In conclusion, rutin and rutin glycoside showed differences in antioxidant activities in vitro, while they were similar in the reduction of NO, PGE2, TNF-α and IL-6 in vitro. Rutin and rutin glycoside also showed similar platelet aggregation rates, and blood coagulation both in vitro and in vivo condition. Comparing in vitro and in vivo, rutin and rutin glycoside were effective on platelet aggregation both in vitro and in vivo, but only in vitro on blood coagulation.

The effects of tetrahydrocurcumin compared to curcuminoids on human platelet aggregation and blood coagulation in vitro

2019 ◽  
Vol 179 ◽  
pp. 28-30 ◽  
Author(s):  
Kent Chapman ◽  
Fiona E. Scorgie ◽  
Anita Ariyarajah ◽  
Eleanor Stephens ◽  
Anoop K. Enjeti ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Blood Coagulation ◽  
Human Platelet ◽  
Human Platelet Aggregation

Effect of Temperature on ADP-Induced Platelet Aggregation

1973 ◽  
Vol 29 (01) ◽  
pp. 183-189
Author(s):  
C. A Praga ◽  
E. M Pogliani
Keyword(s):  
Platelet Aggregation ◽  
Incubation Period ◽  
Room Temperature ◽  
Important Variable ◽  
Practical Significance ◽  
Effect Of Temperature ◽  
Induce Platelet Aggregation ◽  
Cuvette Holder ◽  
Exact Temperature

SummaryTemperature represents a very important variable in ADP-induced platelet aggregation.When low doses of ADP ( < 1 (μM) are used to induce platelet aggregation, the length of the incubation period of PRP in the cuvette holder of the aggregometer, thermostatted at 37° C, is very critical. Samples of the same PRP previously kept at room temperature, were incubated for increasing periods of time in the cuvette of the aggregometer before adding ADP, and a significant decrease of aggregation, proportional to the length of incubation, was observed. Stirring of the PRP during the incubation period made these changes more evident.To measure the exact temperature of the PRP during incubation in the aggre- gometer, a thermocouple device was used. While the temperature of the cuvette holder was stable at 37° C, the PRP temperature itself increased exponentially, taking about ten minutes from the beginning of the incubation to reach the value of 37° C. The above results have a practical significance in the reproducibility of the platelet aggregation test in vitro and acquire particular value when the effect of inhibitors of ADP induced platelet aggregation is studied.Experiments carried out with three anti-aggregating agents (acetyl salicyclic acid, dipyridamole and metergoline) have shown that the incubation conditions which influence both the effect of the drugs on platelets and the ADP breakdown in plasma must be strictly controlled.

Enhancement of ADP-induced Platelet Aggregation by Adrenaline in Vivo and Its Prevention

1973 ◽  
Vol 29 (02) ◽  
pp. 490-498 ◽  
Author(s):  
Hiroh Yamazaki ◽  
Itsuro Kobayashi ◽  
Tadahiro Sano ◽  
Takio Shimamoto
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
The Other ◽  
Endothelial Surface ◽  
Important Interaction ◽  
Blood Coagulability ◽  
The Difference

SummaryThe authors previously reported a transient decrease in adhesive platelet count and an enhancement of blood coagulability after administration of a small amount of adrenaline (0.1-1 µg per Kg, i. v.) in man and rabbit. In such circumstances, the sensitivity of platelets to aggregation induced by ADP was studied by an optical density method. Five minutes after i. v. injection of 1 µg per Kg of adrenaline in 10 rabbits, intensity of platelet aggregation increased to 115.1 ± 4.9% (mean ± S. E.) by 10∼5 molar, 121.8 ± 7.8% by 3 × 10-6 molar and 129.4 ± 12.8% of the value before the injection by 10”6 molar ADP. The difference was statistically significant (P<0.01-0.05). The above change was not observed in each group of rabbits injected with saline, 1 µg per Kg of 1-noradrenaline or 0.1 and 10 µg per Kg of adrenaline. Also, it was prevented by oral administration of 10 mg per Kg of phenoxybenzamine or propranolol or aspirin or pyridinolcarbamate 3 hours before the challenge. On the other hand, the enhancement of ADP-induced platelet aggregation was not observed in vitro, when 10-5 or 3 × 10-6 molar and 129.4 ± 12.8% of the value before 10∼6 molar ADP was added to citrated platelet rich plasma (CPRP) of rabbit after incubation at 37°C for 30 second with 0.01, 0.1, 1, 10 or 100 µg per ml of adrenaline or noradrenaline. These results suggest an important interaction between endothelial surface and platelets in connection with the enhancement of ADP-induced platelet aggregation by adrenaline in vivo.

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