• Journal of Chest Surgery
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• v.21 no.1
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• pp.26-35
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• 1988

The effect of cardiopulmonary bypass on platelet count, platelet function, and bleeding time was studied in 60 patients. Platelet count was significantly reduced during and after cardiopulmonary bypass. Platelet function also had a reduced aggregation response to adenosine diphosphate. Bleeding time was prolonged to over 30 minutes during cardiopulmonary bypass and not returned to normal level until postbypass 1 hour. The amount of postoperative bleeding was proportional to the degree of decrease in platelet count and function, degree of decrease in platelet count and function. There was no significant correlation between duration of cardiopulmonary bypass and platelet count, platelet function, bleeding time, or amount of postoperative bleeding. Patients with cyanotic congenital heart disease showed a larger amount of postoperative bleeding than patients with acyanotic congenital heart disease [P<0.01], and this difference was due to the fact that platelet function was more significantly affected by cardiopulmonary bypass in cyanotic group. Patients using membrane oxygenator showed a less amount of postoperative bleeding than patients using bubble oxygenator [p<0.005] reflecting better preservation of platelet count and function by membrane oxygenator.

• Journal of Veterinary Clinics
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• v.40 no.5
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• pp.330-335
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• 2023

Platelet function evaluation by PFA-100 or -200 has been known to be objective and sensitive for assessing platelet function and dysfunction of Von Willebrand Factor in humans and dogs. However, using the C/EPI cartridge in dogs is controversial. This study aimed to establish a reference range for PFA closure time in healthy small breed dogs (body weight < 10 kg) and to evaluate the effectiveness of both C/ADP and C/EPI cartridges for these dogs. Citrated blood samples were collected from 50 clinically healthy small breed dogs that were admitted for presurgical procedures or health checkups, and closure times were measured using the PFA-200. Reference ranges were determined as 42-144 s (median 67 s, mean 71.2 s, SD ± 21.2 s, 95% RI 43-140 s) , for CT-C/ADP and 41-200 s (median 87, mean 91.2 s, SD ± 31.8 s, 95% RI 44-195 s) for CT-C/EPI. The present study demonstrated that the reference ranges for PFA closure times in small breed dogs are in line with existing reference ranges. The utilization of C/ADP cartridges is the preferred choice for evaluating platelet function in small breed dogs. However, due to variable responses of epinephrine to platelet aggregation in dogs, caution should be exercised when using C/EPI cartridges.

• Journal of Interdisciplinary Genomics
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• v.3 no.2
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• pp.41-46
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• 2021

Inherited platelet function disorders (IPFDs) are a disease group of heterogeneous bleeding disorders associated with congenital defects of platelet functions. Normal platelets essential role for primary hemostasis by adhesion, activation, secretion of granules, aggregation, and procoagulant activity of platelets. The accurate diagnosis of IPFDs is challenging due to unavailability of important testing methods, including light transmission aggregometry and flow cytometry, in several medical centers in Korea. Among several IPFDs, Glanzmann thrombasthenia (GT) is a most representative IPFD and is relatively frequently found compare to the other types of rarer IPFDs. GT is an autosomal recessive disorder caused by mutations of ITGA2B or ITGB3. There are quantitative or qualitative defects of the GPIIb/IIIa complex in platelet, which is the binding receptor for fibrinogen, von Willbrand factor, and fibronectin in GT patients. Therefore, patients with GT have normal platelet count and normal platelet morphology, but they have severely decreased platelet aggregation. Thus, GT patients have a very severe hemorrhagic phenotypes that begins at a very early age and persists throughout life. In this article, the general contents about platelet functions and respective IPFDs, the overall contents of GT, and the current status of genetic diagnosis of GT in Korea will be reviewed.

• Korean Journal of Clinical Laboratory Science
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• v.41 no.1
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• pp.1-5
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• 2009

The Platelet Function Analyzer (PFA)$^{(R)}$-100 measures the ability of platelets activated in a high-shear environment to occlude an aperture in a membrane treated with collagen and epinephrine (CEPI) or collagen and ADP (CADP). The time taken for the flow across the membrane to stop (closure time, CT) is recorded. The aim of this study was to assess the potential of the PFA$^{(R)}$-100 as a primary clinical screening tool using the wide spectrum of clinical samples assessed for platelet function as well as to perform the optimal algorithm for the use of PFA$^{(R)}$-100. We established the reference interval in 460 hospital inpatients defined as having normal platelet function based on classical laboratory tests. The reference interval by using the range $5^{th}$ and $95^{th}$ percentile was 84~251 seconds for males CEPI-CT and 85~249 seconds for females CEPI-CT. A total of 1,200 inpatients were enrolled to identify impaired hemostasis before surgical interventions. The abnormal group showing prolonged CEPI-CT was 303 cases (18.9%). Only 3 cases had both abnormal CEPI-CT and CADP-CT. Several factors including sample errors, drugs, hematologic abnoralities were contributed to unexpected prolonged CEPI-CT for screening test. The von Willebrand factor (vWF:Ag) assay was performed only in one patient to verify the algorithm for the use of PFA$^{(R)}$-100. The PFA$^{(R)}$-100 was sensitive and rapid method for primary screening test of platelet dysfunction, so we can substitute it for the bleeding time in routine clinical practice.

• Biomedical Science Letters
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• v.19 no.3
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• pp.233-238
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• 2013

Aspirin is still the mainstay of antiplatelet therapy in the cardiovascular and cerebrovascular disease. However, some patients are not responsive to the antithrombotic action of aspirin. The aim of this study was to assess the prevalence and clinical characteristics of aspirin resistance in patients with cerebral infarction. We tested platelet function in 557 patients who had been treated with aspirin in J general hospital. Platelet function was tested using the multiple electrode platelet aggregometry (MEA). Platelet reactivity was expressed as area under the aggregation curve (AUC, U) and >30 AUC was defined as aspirin resistance. Aspirin resistance was detected in 16.2% patients. There was not any significant differences in age, gender between aspirin resistance and aspirin sensitive patients. WBC was significantly higher in patients with aspirin resistance (P < .05). HDL-cholesterol was significantly higher in patients with aspirin sensitive (P < .05). Aspirin resistance was positive correlation with platelet count (r =.314, P =.003). The prevalence of aspirin resistance in cerebral infarction was 16.2%, and platelet count were related with aspirin resistance.

• Journal of Applied Biological Chemistry
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• v.63 no.4
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• pp.339-345
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• 2020

Euchrestaflavanone A (EFA) is a flavonoid found in the root bark of Cudrania tricuspidata. C. tricuspidata extract, widely used throughout Asia in traditional medicine, has been investigated phytochemically and biologically and is known to have anti-obesity, anti-inflammatory, and anti-tumor effects. It has been reported that C. tricuspidata extract also possesses anti-platelet effects; however, the mechanism of its anti-platelet and anti-thrombotic activities is yet to be elucidated. In this study, we investigated the effects of EFA on the modulation of platelet function using collagen-induced human platelets. Our results showed that EFA markedly inhibited platelet aggregation. Furthermore, it downregulated glycoprotein IIb/IIIa (αIIb/β3)-mediated signaling events, including platelet adhesion, granule secretion, thromboxane A2 production, and clot retraction, but upregulated the cyclic adenosine monophosphate-dependent pathway. Taken together, EFA possesses strong anti-platelet and anti-thrombotic properties and is a potential therapeutic drug candidate to prevent platelet-related thrombosis and cardiovascular disease.

• Journal of Korean Neurosurgical Society
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• v.62 no.1
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• pp.3-9
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• 2019

As more intracranial aneurysms and other cerebrovascular pathologies are treated with neurointervention procedure, thromboembolic events that frequently lead to serious neurological deficit or fatal outcomes are increasing. In order to prevent the thromboembolic events, antiplatelet therapy is used in most procedures including coil embolization, stenting, and flow diversion. However, because of variable individual pharmacodynamics responses to antiplatelet drugs, especially clopidogrel, it is difficult for clinicians to select the adequate antiplatelet regimen and its optimal dose. This article reviews the neurointervention literature related to antiplatelet therapy and suggests a strategy for tailoring antiplatelet therapy in individual patients undergoing neurointervention based on the results of platelet function testing.

• Journal of Chest Surgery
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• v.25 no.5
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• pp.526-532
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• 1992

The effect of cardiopulmonary bypass on platelet count and function was studied in 20 patients who underwent cardiac operation from April 1991 to August 1991 at the Department of thoracic and Cardiovascular Surgery, School of Medicine, Keimyung University. Ten patients were perfused with a bubble oxygenator, 10 with a membrane oxygenator. During and after bypass, platelet counts decreased in both groups and significantly reduced in those perfused with a bubble oxygenator. All 20 patients studied for platelet functions had an abnormal postoperative aggregation response to collagen and epinephrine, but no significant difference in both groups. One hour after bypass, bleeding times increased in both groups but did not differ significantly between groups. Postoperative 24 hour blood losses were significantly higher in patients perfused with a membrane oxygenator. Platelet damage and postoperative blood loss are less severe after cardiopulmonary bypass performed with a membrane oxygenator than with a bubble oxygenator.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1996.11a
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• pp.75-84
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• 1996

Platelets from a patient with a mild inherited bleeding disorder and abnormal platelet aggregation and secretion show reduced generation of inositol 1,4,5-trisphosphate (IP$_3$), mobilization of intracellular Ca$\^$2+/, and phosphorylation of pleckstrin in response to several G protein mediated agonists, suggesting a possible defect at the level of phospholipase C (PLC) activation. A procedure was developed that allows quantitation of platelet PLC isozymes. After fractionation of platelet extracts by high-performance liquid chromatography, seven, out often known PLC isoforms were detected by immunoblot analysis. The amount of these isoforms in normal platelets decreased in the order PLC-${\gamma}$2 > PLC-${\beta}$2 > PLC-${\beta}$3 > PLC-${\beta}$l > PLC-${\gamma}$ > PLC-$\delta$1 > PLC-${\beta}$4. Compared with normal platelets, platelets from the patient contained approximately one-third the amount of PLC-${\beta}$2, whereas PLC-${\beta}$4 was increased threefold. These results suggest that the impaired platelet function in the patient in response to multiple G protein mediated agonists is attributable to a deficiency of PLC-${\beta}$2. They document for the first time a specific PLC isozyme deficiency in human platelets and provide an unique opportunity to understand the role of different PLC isozymes in normal platelet function.

• Korean Journal of Clinical Pharmacy
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• v.2 no.1
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• pp.1-9
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• 1992

Protective effect of urokinase on reperfusion were studied followed by global ischemia in the isolated perfused rat heart. Separately, anti-platelet aggregation effect of urokinase also investigated. Urokinase exhibited positive effect for the protection of rat heart function by increasing the LV dp/dt, coronary flow(CF) and the Tate pressure product(RPP), and by decreasing the LVEDP on reperfusion. Urokinase also decreased arrhythmia by $74.7\%(P<0.05) induced by global ischemia in the rat heart. In the platelet aggregation study, urokinase did not show the inhibitory effect of ADP or collagen induced platelet aggregation inviuo and exvivo.