scholarly journals Comparison of effect of aloe Vera gel with aspirin and celecoxib on platelet aggregation.

2020 ◽  
Vol 27 (05) ◽  
pp. 973-978
Author(s):  
Sidra Mushtaq ◽  
Zobia Mushtaq ◽  
Javeria Arif ◽  
Mufakhara Fatima ◽  
Sadida Bahawal ◽  
...  

Objective: This study was designed to compare the effect of Aloe vera gel with aspirin and celecoxib on platelet aggregation. Study Design: Comparative Study. Setting: Post graduate Medical Institute Lahore, Children Hospital, Lahore. Period: September 2015 to September 2016. Material & Methods: Blood was withdrawn from anti-cubital vein, complete blood count was checked, platelet rich plasma was prepared by centrifuging citrated whole blood and then incubated with  Aloe vera low (AVL), Aloe vera high (AVH), aspirin and celecoxib for 30 minutes at 37C. After adding the agonist arachidonic acid, reading was then taken for 3 minutes and percentage aggregation was recorded. Results: Platelet aggregation with aspirin, AVH and AVL was statistically significantly lower as compared to control and celecoxib groups. Conclusion: This study has demonstrateda dose dependentanti-platelet effect of Aloe vera gel which is comparable to aspirin.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4018-4018
Author(s):  
Anna M. Dyszkiewicz-Korpanty ◽  
Anne Kim ◽  
James D. Burner ◽  
Eugene P. Frenkel ◽  
Ravindra Sarode

Abstract The reported incidence of aspirin (ASA) resistance ranges from 5 to 30%. Various platelet function assays have been employed to detect aspirin resistance in patients with cardio- and cerebrovascular disease. Such a high proposed incidence of ASA resistance poses a critical need for a rapid point-of -care (POC) platelet function test. Unfortunately, no uniformly accepted definition of ASA resistance exists. Platelet aggregation studies that have been used to define ASA resistance are time consuming and require special technical expertise. The Ultegra Rapid Platelet Function -ASA (RPFA-ASA) has been developed as a POC test that is performed without sample processing. This optical method measures agglutination of fibrinogen-coated beads upon platelet activation with arachidonic acid. In the presence of aspirin effect, however, the agglutination of the beads is inhibited. The described cutoff of ≥ 550 Aspirin Reaction Units (ARU) is termed non-responsiveness to ASA based on a preclinical study and subsequent correlation with epinephrine-induced platelet aggregation in platelet rich plasma. Since RPFA-ASA uses whole blood, we validated its performance characteristics against a classic whole blood platelet aggregation assay (WBA). We studied 50 healthy volunteers, aged 25–75 (24 men, 26 women) with normal CBC, who had not ingested anti-platelet drugs for 14 days prior to the study. Baseline studies included WBA (dual channel aggregometer, Chrono-log Inc., Havertown, PA) using both arachidonic acid (AA -0.5; 0.25 mM) and collagen (1; 2 μg/mL) as well as an RPFA-ASA assay (Accumetrics Inc., San Diego, CA). These studies were repeated after 3 days of ASA (325 mg/d) intake. Based on a review of the literature, we defined an adequate ASA response as a completely inhibited AA-induced platelet aggregation and at least 30% inhibition of collagen-induced aggregation (both concentrations of the agonist). Thus, those with < 30% inhibition of aggregation response to collagen were considered ASA resistant. Eleven subjects were ASA resistant by WBA (20%; 8 females and 3 males (aged 25–63). In contrast, since all 50 subjects achieved ARU values of < 550 ARU, none were recognized as an ASA non-responder by the RPFA-ASA. While the current cutoff of < 550 ARU posed by the Ultegra RPFA-ASA does identify those who have taken ASA, the assay is unable to recognize ASA non-responders. Thus, based on these data, the appropriate cutoff for the recognition of ASA resistance by the RPFA-ASA should be re-adjusted to a significantly lower level to ensure appropriate assay results.


2018 ◽  
Vol 25 (03) ◽  
pp. 448-453
Author(s):  
Sidra Mushtaq ◽  
Mufakhara Fatima ◽  
Zobia Mushtaq ◽  
Roohi Manzoor Khan ◽  
Muhammad Naeem Iqbal ◽  
...  

The herbal use for medical purposes is increasing world over. Aloe vera is onesuch herb with established anti-inflammatory action. It has great prospect in terms of replacingtraditional NSAIDS due to better side effect profile on gastrointestinal tract but its effect onplatelet aggregation is what needs to be determined. Objectives: This study was designed tosee the concentration dependent action of Aloe vera gel on platelet aggregation. Study Design:Comparative study. Setting: Post Graduate Medical Institute Lahore, Children Hospital Lahore.Duration of Study: One Year. Methodology: This study was conducted on healthy volunteersselected from staff and students of Ameer-ud-din Medical College. After determining baselineHb and platelet counts, PRP was prepared and then incubated with 2 different concentrationsof Aloe vera low (AVL) and Aloe vera high (AVH) for 30 minutes. Aggregation was stimulatedby adding the agonist arachidonic acid. Light transmission aggregometer was used to recordplatelet aggregation activity graphically for 3 minutes. Results: The data was analyzed usingSPSS version 20. Kruskal Wallis H test was performed to compare the platelet aggregation,which revealed that platelet aggregation with AVL and AVH were statistically significantly lower,amounting to 25.89% and 16.72% respectively as compared to 88.28% observed with control.Conclusion: This study has established in vitro anti-platelet effect of Aloe vera which is dosedependent.


Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 2622-2622
Author(s):  
Zafar Siddiqui ◽  
Omer Iqbal ◽  
Debra Hoppensteadt ◽  
Mary Lewis ◽  
Rohan Rege ◽  
...  

Abstract Introduction: Idarucizumab is a humanized monoclonal antibody fragment which is capable of neutralizing Dabigatran and is currently clinically available for the control of bleeding associated with Dabigatran. Although this antibody is capable of neutralizing the anticoagulant effects of Dabigatran, its effect on the blood coagulation and platelet activation profile are not completely understood. There is limited data on the effect of Idarucizumab on the blood coagulation and platelet activation profile. The purpose of this study is to determine the effect of this antibody on blood coagulation and platelet activation profile. Materials: Idarucizumab was purchased from Brigham and Women's Hospital (Boston, MA) and was provided as a 50 mg/mL solution. Dabigatran was of synthetic origin and obtained from Sellec Chemical (Houston, TX). Whole blood from healthy volunteers was collected in plastic syringes using a sterile method for the TEG and ACT analysis. Citrated whole blood was used for the preparation of platelet rich plasma which was used in platelet aggregation studies. Such agonists as arachidonic acid, ADP, epinephrine, thrombin, and collagen were used. Methods: The TEG studies were carried on a Haemoscope 500 instrument. Native whole blood was supplemented with Idarucizumab in a concentration range of 0-10 mg/mL. Saline was used as a control. The TEG profile was measured for 15-30 minutes. Such parameters as R time, K time, angle, and max amplitude were recorded. The ACT studies were carried out in celite tubes in a concentration of 0-5 mg/mL. The agonist-induced platelet aggregation profile was studied by pre incubating platelet rich plasma with Idarucizumab at a fixed concentration of 1.0 mg/mL and studying its effect on the aggregation profile of such agonists as arachidonic acid, ADP, epinephrine, thrombin, and collagen. Both the slope and percent aggregation were measured. The effect of Idarucizumab on HIT antibodies mediated platelet aggregation was studied by pre incubating platelets with Idarucizumab and determining its effect on the HIT antibody mediated aggregation of platelets. Pooled plasma from symptomatic HIT patients was pre incubated with Idarucizumab at 1.0 mg/mL followed by the addition of HIT antibody pool in a 1:10 dilution. The aggregation profile was noted for up to an hour. Results: Idarucizumab produced a dose-dependent hypercoagulable effect in the TEG profile of native whole blood resulting in a reduction in R time and max amplitude at 35% and 45% respectively. At high concentrations, Idarucizumab produced a marked effect on the clot retraction. In the ACT studies, Idarucizumab produced a mild shortening of the ACT at a 5 mg/mL at 6%. Idarucizumab produced variable augmentation of different agonists mediated platelet aggregation. In the HIT mediated aggregation studies, Idarucizumab produced a strong augmentation of HIT antibody mediated platelet aggregation. At 1.0 ug/mL, Idarucizumab produced almost a 20% increase in platelet aggregation. Conclusions: These studies indicate that Idarucizumab produces mild procoagulant effects on whole blood coagulation process as studied by TEG and ACT. This agent also produces the augmentation of the platelet aggregation profile by various agonists including Anti-heparin platelet factor IV antibodies. These procoagulant effects of Idarucizumab may contribute to the potential hypercoagulable/prothrombotic events associated with its use. Disclosures No relevant conflicts of interest to declare.


1981 ◽  
Vol 45 (03) ◽  
pp. 204-207 ◽  
Author(s):  
Wolfgang Siess ◽  
Peter Roth ◽  
Peter C Weber

SummaryPlatelets have been implicated in the development of atherosclerotic and thrombotic vascular diseases. Evaluation of platelet aggregation in relation to endogenously formed compounds which affect platelet function may provide information of clinical and pharmacological relevance. We describe a method in which thromboxane B2 (TXB2) formation was analyzed following stimulation of platelet-rich plasma (PRP) with ADP, 1-epinephrine, collagen, and arachidonic acid. In addition, we determined platelet sensitivity to prostacyclin following ADP- and collagen-induced platelet aggregation. The parameters under study were found to depend on the platelet count in PRP, on the type and dose of the aggregating agent used, and on the test time after blood sampling. By standardization of these variables, a reliable method was established which can be used in clinical and pharmacological trials.


1981 ◽  
Vol 46 (02) ◽  
pp. 538-542 ◽  
Author(s):  
R Pilo ◽  
D Aharony ◽  
A Raz

SummaryThe role of arachidonic acid oxygenated products in human platelet aggregation induced by the ionophore A23187 was investigated. The ionophore produced an increased release of both saturated and unsaturated fatty acids and a concomitant increased formation of TxA2 and other arachidonate products. TxA2 (and possibly other cyclo oxygenase products) appears to have a significant role in ionophore-induced aggregation only when low concentrations (<1 μM) of the ionophore are employed.Testosterone added to rat or human platelet-rich plasma (PRP) was shown previously to potentiate platelet aggregation induced by ADP, adrenaline, collagen and arachidonic acid (1, 2). We show that testosterone also potentiates ionophore induced aggregation in washed platelets and in PRP. This potentiation was dose and time dependent and resulted from increased lipolysis and concomitant generation of TxA2 and other prostaglandin products. The testosterone potentiating effect was abolished by preincubation of the platelets with indomethacin.


1983 ◽  
Vol 50 (04) ◽  
pp. 852-856 ◽  
Author(s):  
P Gresele ◽  
C Zoja ◽  
H Deckmyn ◽  
J Arnout ◽  
J Vermylen ◽  
...  

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.


1979 ◽  
Author(s):  
K.E. Sarji ◽  
J. Gonzalez ◽  
H. Hempling ◽  
J.A. Colwell

To determine whether Vitamin C might relate to the increased platelet sensitivity in the diabetic, we have measured levels of platelet Vitamin C and studied the effects of Vitamin C on platelet aggregation. Ascorbic acid levels in washed platelets from diabetics were significantly lower than from normals (4s.2±3 μg/1010 platelets vs. 2s.s±2 μg/1010 platelets, p<.001). The effects of ascorbic acid on platelet aggregation in vitro were studied by adding ascorbic acid in buffered solution (pH 7.35) prior to-aggregating agents. Ascorbic acid in platelet-rich plasma consistently inhibited platelet aggregation with threshold concentrations of ADP, epinephrine, and collagen. With washed platelets, ascorbic acid inhibited arachidonic, acid-induced aggregation. When platelets were incubated at 37°C for 10 minutes with varying concentrations of ascorbic acid, rewashed, and aggregation with arachidonic acid tested, aggregation was inhibited in a linear dose-dependent fashion. Oral ingestion of ascorbic acid (2 gm/day) for seven days by normal non-smoking males produced a marked inhibition of aggregation. In a similar study, platelets from an insulin-dependent diabetic showed no change in aggregation. These results suggest that platelet levels of ascorbic acid may relate to the hyperaggregat ion of platelets from diabetics.


1988 ◽  
Vol 59 (03) ◽  
pp. 383-387 ◽  
Author(s):  
Margaret L Rand ◽  
Marian A Packham ◽  
Raelene L Kinlough-Rathbone ◽  
J Fraser Mustard

SummaryEthanol, at physiologically tolerable concentrations, did not affect the primary phase of ADP-induced aggregation of human or rabbit platelets, which is not associated with the secretion of granule contents. Potentiation by epinephrine of the primary phase of ADP-induced aggregation of rabbit platelets was also not inhibited by ethanol. However, ethanol did inhibit the secondary phase of ADP-induced aggregation which occurs with human platelets in citrated platelet-rich plasma and is dependent on the formation of thromboxane A2. Inhibition by ethanol of thromboxane production by stimulated platelets is likely due to inhibition of the mobilization of arachidonic acid from membrane phospholipids, as ethanol had little or no effect on aggregation and secretion induced by arachidonic acid or the thromboxane mimetic U46619. Rabbit platelet aggregation and secretion in response to low concentrations of collagen, thrombin, or PAF were inhibited by ethanol. Inhibition of the effects of thrombin and PAF was also observed with aspirin-treated platelets. Thus, in addition to inhibiting the mobilization of arachidonate for thromboxane formation that occurs with most agonists, ethanol can also inhibit aggregation and secretion through other effects on platelet responses.


2007 ◽  
Vol 98 (12) ◽  
pp. 1266-1275 ◽  
Author(s):  
Ruben Xavier ◽  
Ann White ◽  
Susan Fox ◽  
Robert Wilcox ◽  
Stan Heptinstall

SummaryThe effects on platelet function of temperatures attained during hypothermia used in cardiac surgery are controversial. Here we have performed studies on platelet aggregation in whole blood and platelet-rich plasma after stimulation with a range of concentrations of ADP, TRAP, U46619 and PAF at both 28°C and 37°C. Spontaneous aggregation was also measured after addition of saline alone. In citrated blood, spontaneous aggregation was markedly enhanced at 28°C compared with 37°C. Aggregation induced by ADP was also enhanced. Similar results were obtained in hirudinised blood. There was no spontaneous aggregation in PRP but ADP-induced aggregation was enhanced at 28°C. The P2Y12 antagonist AR-C69931 inhibited all spontaneous aggregation at 28°C and reduced all ADP-induced aggregation responses to small, reversible responses. Aspirin had no effect. Aggregation was also enhanced at 28°C compared with 37°C with low but not high concentrations of TRAP and U46619. PAF-induced aggregation was maximal at all concentrations when measured at 28°C, but reversal of aggregation was seen at 37°C. Baseline levels of platelet CD62P and CD63 were significantly enhanced at 28°C compared with 37°C. Expression was significantly increased at 28°C after stimulation with ADP, PAF and TRAP but not after stimulation with U46619. Overall, our results demonstrate an enhancement of platelet function at 28°C compared with 37°C, particularly in the presence of ADP.


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