Screen Filtration Pressure Method Research Articles

Ethanol-Induced Inhibition of Platelet Aggregation in Whole Blood from Healthy Donors

Ethanol is known to inhibit platelet aggregation. In order to examine effects of ethanol on platelet aggregation, isolated platelet-rich plasma and platelet suspension are often used. However, it remains to be clarified whether and how ethanol affects platelet aggregation in whole blood. In this concise study, we examined effects of ethanol on platelet aggregation induced by different stimulants in whole blood by using the screen filtration pressure method. Thapsigargin and 1-oleoyl-2-acetyl-sn-glycerol (OAG), which cause Ca2+ entry into platelets through the storeoperated Ca2+ channels and the diacylglycerol-dependent Ca2+ channels, respectively, were used for inducing platelet aggregation. Thapsigargin-induced platelet aggregation was markedly inhibited by ethanol at 0.25% or higher, and OAG-induced platelet aggregation was significantly inhibited by ethanol at 1% or higher. These results indicate that inhibitory effect of ethanol was more prominent on thapsigargin-induced aggregation than on OAGinduced aggregation. Thus, ethanol inhibits thapsigargin- and OAG-induced platelet aggregation in whole blood, and the effect of ethanol on platelet aggregation through the store-operated Ca2+ channels is thought to be stronger than that on aggregation through the diacylglycerol-dependent Ca2+ channels.

Keishibukuryogan, a Traditional Japanese Medicine, Inhibits Platelet Aggregation in Guinea Pig Whole Blood.

Effects of keishibukuryogan (KBG) on platelet aggregation were investigated. To ensure the specificity of KBG, tokishakuyakusan (TSS) and kamisyoyosan (KSS), which are known to have platelet aggregation-inhibiting effects, and rikkunshito (RKT) and shakuyakukanzoto (SKT), which are considered to be devoid of such effects, were used for comparison. The platelet aggregation of each test drug was measured by the screen filtration pressure method using whole blood of guinea pigs and expressed as a collagen-induced pressure rate (%) or a collagen concentration required for 50% increase in the pressure rate (PATI value). KBG suppressed the collagen-induced whole blood pressure rate increase and increased the PATI value, like TSS and KSS. Neither RKT nor SKT showed these effects. The Moutan cortex and Cinnamomi cortex, the constituent crude drugs of KBG, showed KBG-like pressure rate suppression and PATI-increasing effects. Furthermore, paeonol, a representative component of Moutan cortex, and aspirin which is known to have platelet aggregation-inhibiting activity (COX-1 inhibitor) also showed similar effects. These results suggest that the platelet aggregation-inhibiting activity of the constituent crude drugs Moutan cortex and Cinnamomi cortex is involved in the improving effects of KBG on impaired microcirculation and that paeonol plays a role in these effects.

Impact of Platelet Reactivity to Adenosine Diphosphate Before Implantation of Drug-Eluting Stents on Subsequent Adverse Cardiac Events in Patients With Stable Angina

Diverse pharmacological effects of anti-platelet thienopyridines due to individual differences in metabolism have been reported. However, an association between on-treatment platelet reactivity and adverse ischemic events after drug-eluting stent (DES) implantation in Japanese patients has not been fully elucidated. A total of 450 consecutive patients on dual anti-platelet therapy (aspirin and ticlopidine) with stable angina who underwent DES implantation were enrolled. Adenosine diphosphate (ADP)-induced platelet aggregation was measured before DES implantation using the screen filtration pressure method. The ADP concentration necessary for 50% aggregation was designated as the platelet aggregation threshold index (PATI). A composite primary endpoint of cardiac death, myocardial infarction, target lesion revascularization (TLR), and stent thrombosis occurring within 1 year after stenting, was evaluated. A PATI value <4.8 µmol/L was defined as high on-treatment reactivity to ADP. The composite primary endpoint occurred in 55 patients (12.2%) in the 1-year-period after DES implantation, and the prevalence was 19.0% and 5.1% in groups with high and low on-treatment reactivity to ADP, respectively, showing a significantly higher prevalence in the high reactivity group (P<0.001). The main event was TLR (18.1% vs. 5.1%, P<0.001). These data suggested that high on-treatment platelet reactivity to ADP and subsequent occurrence of adverse ischemic events (particularly TLR) were correlated in patients with stable angina who underwent DES implantation.

Impact of concomitant use of proton-pump inhibitors and thienopyridine derivatives on the antiplatelet effects

Although there has been an intense debate whether concomitant use of proton-pump inhibitors (PPIs) attenuates the antiplatelet effects of thienopyridine derivatives, the drug-drug interaction remains unclear in Japanese patients with coronary artery disease. Platelet function test was performed in 461 patients who were scheduled for or had undergone stent implantation, treated with 100mg/day of aspirin and a thienopyridine (200mg/day of ticlopidine or 75 mg/day of clopidogrel) for at least 14 days. Adenosine diphosphate-induced platelet aggregation was evaluated with screen filtration pressure method, and the upper quartile of high platelet reactivity was defined as high on-treatment platelet reactivity (HPR). PPI use was at physician's discretion. Patients taking a thienopyridine plus a PPI (n=166) were older and had a higher incidence of acute coronary syndromes on admission compared with patients taking a thienopyridine without a PPI (n=295). The rate of HPR was higher in patients taking a thienopyridine plus a PPI than in patients taking a thienopyridine without a PPI (31% vs 21%, p=0.01). On multivariate logistic regression analysis, independent predictors of HPR were concomitant PPI use [odds ratio (OR): 1.66, 95% confidence interval (CI): 1.03-2.68], diabetes mellitus (OR: 1.76, CI: 1.11-2.81), and calcium channel blockers use (OR: 1.93, CI: 1.18-3.18). However, there was no significant difference in the rate of extremely high platelet reactivity [58 patients (12.5%) with PATI<4.0 μM] between patients treated with a thienopyridine plus a PPI and those without a PPI (14% vs 11%, NS). HPR was frequently observed in Japanese patients treated with thienopyridines plus PPIs compared to those without PPIs. Further prospective studies are needed to estimate the risk of adverse cardiovascular events associated with concomitant use of PPIs and thienopyridines.

Evaluation of Clopidogrel Resistance in Ischemic Stroke Patients

Clopidogrel has potent antiplatelet effects, but recent interest has focused on clopidogrel resistance, in which platelet function is not inhibited despite taking the drug. This study evaluated clopidogrel resistance in ischemic stroke patients. After taking oral clopidogrel 75 mg/day for ≥1 week, platelet aggregometry was performed by turbidimetry in all patients, and by a screen filtration pressure method using whole blood in 37 patients. Using turbidimetry, resistance was defined as platelet maximum aggregation rate ≥34% with aggregation-inducing agent ADP 1 µmol/L, or ≥66% with ADP 4 µmol/L. Using the screen filtration pressure method, resistance was defined as a minimum concentration of ≤3 µmol/L ADP to induce secondary aggregation of platelets. This study was conducted in 72 patients (52 men, 20 women; mean age, 69 ± 8 years; range, 50-84 years) with non-cardiogenic ischemic cerebrovascular disease. Based on turbidimetry, the rate of clopidogrel resistance was 8.3% with ADP 1 µmol/L and 18.1% with 4 µmol/L. Based on the screen filtration pressure, the rate of clopidogrel resistance was 8.1%. The differences between turbidimetry and screen filtration pressure methods, regarding the measurement of the presence of resistance in the same patient, were observed. Clopidogrel resistance varies greatly depending on the method of measuring platelet aggregation and the definition of resistance. Rates of 8-18% were obtained using our methods and criteria.

Measuring Platelet Aggregation in Dialysis Patients With a Whole Blood Aggregometer by the Screen Filtration Pressure Method

A semi-automatic, whole-blood aggregometer based on the screen filtration pressure (SFP) method is now widely used clinically and in research, but has not been used with hemodialysis (HD) patients. We measured whole-blood platelet aggregation in HD patients by the SFP method. This retrospective cross-sectional study included 62 HD patients, of whom 47 were non-diabetic and 15 were diabetic; we also included a control group of healthy, non-uremic subjects. With the t-test, we examined differences in the platelet aggregation threshold index (PATI) in meaningful sub-groupings of the HD patients, depending on whether or not they had diabetes, and whether or not they had been given antiplatelet agents. Considering the non-diabetic HD patients first, their PATI values were significantly higher than those values in the control subjects (3.1 [1.0-5.2] vs. 1.8 [1.3-2.3] µM, P<0.001). The non-diabetic HD patients taking antiplatelet agents showed significantly (1.9 times) higher PATI values than the non-diabetic HD patients without antiplatelet agents (4.4 [1.8-7.0] vs. 2.3 [1.3-3.3] µM, P=0.003). We observed similar trends among diabetic HD patients. Whole-blood analysis by the SPF method seems to be a promising way of monitoring platelet function for HD patients.

Platelet Function Measured Using a Whole Blood Aggregometer Can Predict Bleeding Events

We hypothesized that excessive suppression of platelet function due to antiplatelet therapy can increase the incidence of bleeding complications. The aim of the present study was to find whether we could predict bleeding events by measuring platelet function. We enrolled 743 subjects whose platelet function was measured using a whole blood aggregometer based on a screen filtration pressure method. Of these subjects, 551 (74.2%) were treated with some type of antiplatelet agent. The endpoints were bleeding or ischemic events requiring hospitalization or extension of hospital stay. We prospectively compared the platelet function of subjects with and without bleeding or ischemic events. During 556 ± 207 days of follow-up, 52 (7.0%) bleeding events and 20 (2.7%) ischemic events were observed. Kaplan-Meier analysis using the log-rank test revealed that an aggregation rate of < 20% induced by 8 µ M adenosine diphosphate (ADP) was significantly associated with a greater number of bleeding events (11.9% vs. 5.2%; p = 0.0007). Cox proportional hazards model showed that age > 75 years (hazard ratio [HR], 1.78; 95% confidence interval [CI], 1.03-3.10; p = 0.039), estimated glomerular filtration rate < 60 ml/min/1.73 m(2) (HR, 1.82; 95% CI, 1.06-3.18; p = 0.031) and aggregation rate < 20% induced by 8 µ M ADP (HR, 2.18; 95% CI, 1.24-3.80; p = 0.0071) were independent predictors of bleeding events. Low platelet function demonstrated using a whole blood aggregometer was an independent predictor of bleeding complications.

Sensitivity of thrombin-induced platelet aggregation to inhibition by ethanol

Background The purpose of this study was to determine the concentration of ethanol required for inhibition of thrombin-induced aggregation of human platelets in vitro. Methods Three methods, light transmission method, particle counting method using light scattering and screen filtration pressure method using whole blood, were used for evaluation of platelet aggregation. Results Thrombin (0.2 U/ml)-induced platelet aggregation was significantly inhibited by ethanol, and the threshold ethanol concentrations for inhibition determined by measurements using the light transmission method, particle counting method and screen filtration pressure method were 0.5%, 0.125% and 2%, respectively. Platelet aggregation induced by a lower concentration (0.05 U/ml) of thrombin was detected by the screen filtration pressure method but not by the light transmission method or particle counting method. The threshold ethanol concentration for the inhibition of thrombin (0.05 U/ml)-induced platelet aggregation was 0.125% according to results obtained by using the screen filtration pressure method. Conclusions Sensitivities for detection of thrombin-induced platelet aggregation and for detection of inhibition of platelet aggregation by ethanol were high in the screen filtration pressure method and the particle counting method, respectively. The threshold concentration of ethanol to inhibit thrombin-induced platelet aggregation is about 0.125% (approximately 21 mmol/l), which is easily attainable after drinking alcohol.

Action of Aspirin on Whole Blood-Aggregation Evaluated by the Screen Filtration Pressure Method

There are few monitoring systems widely used in clinical practice for evaluating the effectiveness of aspirin therapy, so in the present study aspirin's antiplatelet effects we investigated with a whole blood aggregometer using a screen filtration pressure (SFP) method. Thirty-five healthy male volunteers took 100 mg/day aspirin for 14 days. Whole-blood aggregation was analyzed at baseline and on days 7 and 14, using collagen and adenosine diphosphate as the stimuli, and compared with the platelet-rich plasma (PRP) aggregation measured by optical aggregometer. The platelet-aggregation threshold index (PATI) for both methods, which was defined as the putative agonist-concentration giving half-maximal aggregation, and the PRP-maximal aggregation rate were analyzed. The maximal aggregation rate induced by 1.6 mg/L collagen decreased from 85.5% (80.8-92.8) [median (interquartile range)] at baseline to 51.5% (39-63.8) on day 14 (p<0.0001). The PRP-PATI and whole-blood PATI for collagen increased from 0.32 (0.28-0.70) to 1.82 mg/L (1.25-2.89) (p<0.0001) and from 0.28 (0.22-0.3) to 1.06 mg/L (1.01-1.29) (p<0.0001) respectively. The whole-blood PATI and PRP-PATI for collagen, as well as the maximal PRP aggregation rate, clearly distinguish platelet aggregability before and after aspirin intake. However, whole-blood analysis by the SFP-method is easier to perform, and is a promising method of monitoring aspirin's effects.

Characterization of platelet aggregation in whole blood of laboratory animals by a screen filtration pressure method

The characteristics of platelet aggregation of laboratory animals were investigated with whole blood and platelet-rich plasma (PRP). We measured the platelet aggregation threshold index (PATI) of whole blood and PRP aggregations induced by ADP or collagen, using a novel whole blood aggregometer, the WBA analyzer, with a screen filtration pressure (SFP) method. At 60 min after blood collection, PATI values of guinea pig, mouse, rat, dog and rabbit were 0.83, 1.78, 46.48, 49.85 and 53.42 μM for ADP-induced whole blood aggregation, respectively, whereas their PATI values for ADP-induced PRP aggregation were 1.16, 2.77, 2.65, 10.81 and 18.77 μM, respectively. These suggest that ADP-induced platelet aggregations of rat, dog and rabbit are suppressed in whole blood. PATI values of guinea pig, mouse, rat, dog and rabbit were 1.84, 0.62, 11.90, 2.34, 12.32 μg/ml for the collagen-induced whole blood aggregation, respectively, whereas their PATI values for the collagen-induced PRP aggregation were 4.21, 1.50, 5.36, 11.31, 13.30 μg/ml, respectively. Collagen-induced aggregation activity of the guinea pig, mouse and dog was significantly higher in whole blood than in the PRP. These results demonstrated that species differences in laboratory animals exist for whole blood aggregation, and that the SFP aggregometer may be useful to evaluate platelet function in various animal species.

Evaluation of Whole Blood Aggregation with a New Type of Aggregometer by a Screen Filtration Pressure Method

Evaluation of Whole Blood Aggregation with a New Type of Aggregometer by a Screen Filtration Pressure Method

Estimation of anti-platelet drugs on human platelet aggregation with a novel whole blood aggregometer by a screen filtration pressure method.

1. The effects of anti-platelet drugs on human whole blood aggregation were evaluated using a novel whole blood aggregometer by a screen filtration pressure (SFP) method. 2. The SFP whole blood aggregometer was found to successfully detect whole blood aggregation induced by ADP, collagen and TRAP by measuring the SFP of blood samples. The platelet aggregation threshold index (PATI), the concentration of agonist required with an inducing pressure rate of 50%, varied time-dependently after collection of blood. High values for ADP and collagen were noted immediately after blood collection, suggesting low aggregation activity of platelets, and gradually increase thereafter. 3. Cilostazol (phosphodiesterase 3 inhibitor), dipyridamole, aspirin and tirofiban all inhibited whole blood aggregation in vitro. Inhibitory effects of cilostazol and dipyridamole, but not tirofiban, were markedly enhanced 6 or 7 fold by long pre-incubation (60 min), compared with short pre-incubation (2 min). Such enhancement was only observed with ADP- and not collagen-induced whole blood aggregation. A similar phenomenon was also observed for aggregation with platelet rich plasma (PRP). Cilostazol inhibition of ADP-induced platelet aggregation was more potent with PRP than whole blood (PATI(200)=3.80+/-0.95 microM for whole blood; 2.04+/-0.61 microM for PRP). Inhibitory effects of dipyridamole were attenuated in PRP without erythrocytes. 4. These results demonstrate that the SFP aggregometer can sensitively detect anti-platelet aggregatory effects of various kinds of drugs. So that it is a useful tool for evaluation of anti-platelet drugs.

Potentiation of Ibudilast Inhibition of Platelet Aggregation in the Presence of Endothelial Cells

Although communications between platelets and endothelial cells or other blood cells are important in in vivo thrombus formation, laboratory platelet function tests are usually performed in isolation from these surrounding cells. In this study, we evaluated the effect of an antiplatelet drug, ibudilast (3-isobutyryl-2-isopropylpyrazolo[1,5- a]pyridine), on platelet aggregation in the presence and absence of human umbilical vein endothelial cells (HUVECs) and with the use of platelet-rich plasma (PRP) or whole blood as platelet samples. Stimulation-dependent platelet aggregation was weakened in the presence of HUVECs, which was especially prominent when the thrombin receptor-activating peptide SFLL (compared with ADP and epinephrine) was used as an aggregating agent. Ibudilast hardly affected SFLL-induced platelet aggregation (in PRP), while this antiplatelet agent was found to clearly inhibit this SFLL-induced response in a concentration-dependent manner, in the presence of HUVECs. Ibudilast tended to inhibit ADP- or epinephrine-induced platelet aggregation in the presence of HUVECs, but the effects were not statistically significant. Enhanced inhibition by ibudilast of SFLL-induced platelet aggregation (in the presence of HUVECs) was reproduced with the use of whole blood samples when a screen filtration pressure method was employed. It is suggested that the platelet aggregation studies in the presence of endothelial cells and/or other blood cells provide us with valuable information on platelet reactivity in vivo and improvement of antiplatelet therapy.

Characterization of Whole Blood Aggregation with a New Type of Aggregometer by a Screen Filtration Pressure Method

A new type of platelet aggregometer of whole blood, based on the screen filtration pressure method, has been developed and characterized. It measures resistance of flow of whole blood samples through a screen of microsieve with 30-μm 2 openings and provides pressure rate as an index of platelet aggregation. On optical microscopic observation, platelet aggregates, but not fibrin fibers, were found to be trapped on microsieves, and the pressure rate and protein amounts on microsieves are correlated. The aggregometer showed good reproducibility for investigations performed on different days. The time course of pressure rates indicated a bell curve change, where the pressure rate was very low immediately after blood collection and gradually increased up to 60 min thereafter. Use of the aggregometer was able to confirm that orally administered aspirin inhibits ADP- and collagen-induced whole blood aggregation as well as platelet aggregation. The results suggest that this platelet aggregometer might be useful in research and clinical diagnosis of thrombotic diseases.

全血ｓｃｒｅｅｎ ｆｉｌｔｒａｔｉｏｎ ｐｒｅｓｓｕｒｅ法によるチクロピジンおよびアスピリンの抗血小板作用の検討と比濁法との比較

Screen filtration pressure(SFP)法による全血血小板凝集計を用いて,チクロピジン(TIC)とアスピリン(ASA)の抗血小板作用を測定し,比濁法と比較した.対象は脳血栓症慢性期患者85例(TIC群51例,ASA群34例),対照群25例である.全血凝集の測定はADPとcollagenを凝集惹起物質として採血5分後と60分後に行い,血小板凝集能の指標として血小板凝集閾値係数(PATI)を算出した.TIC群とASA群の全血凝集能は,対照群に比べて抑制されていた.全血ADP凝集は,対象群とTIC群では採血5分後より60分後で高値を示したが,ASA群では変化がなかった.全血collagen凝集は,TIC群では採血5分後より60分後で高値を示したが,対照群とASA群では変化がなかった.全血凝集能と比濁法では,ADP凝集では3群で,collagen凝集ではTIC群で負の相関があった.全1血SFP法は,抗血小板薬の評価に有効であった.

塩化ランタンによる実験的家兎粥状硬化症の抑制効果について

We observed the effects of lanthanum (La3+, an inorganic Ca2+-channel blocker) on experimental atherosclerosis in rabbits fed on cholesterol.16 male Japanese white rabbits weighing 2.1-2.7kg were fed on a 1% cholesterol diet for two weeks, and then divided into two groups so as not to make statistical differences of the serum total cholesterol levels between the two groups. One group was fed on a 1% cholesterol diet plus 0.12% LaCl3 (40mg/kg/day), and the other (control) group was fed on a 1% cholesterol diet only. At the end of the 14 week period, all animals were killed and autopsied.There was no difference in serum total cholesterol between the La3+-treated rabbits and the control rabbits through the experimental period. Serum triglyceride, phospholipid, HDL-cholesterol, total protein, and albumin levels were also similar in both groups through the study period. LaCl3 was well tolerated and the increases of body weight did not differ significantly between the groups. LaCl3 had no effects on arterial pressure. Serum calcium and inorganic phosphorus were similar in both groups through the study. Serum calcium increased after six weeks and then returned to normal. Serum inorganic phosphorus increased after two weeks but decreased at six weeks and then returned to normal level. 1% Cholesterol diet itself might have influence on the metabolism of calcium and inorganic phosphorus. Platelet aggregability measured by screen filtration pressure method was inhibited significantly at the end of the study in the La3+-treated rabbits. La3+ by itself had no significant effects on platelet aggregation in vitro.Aortic lesions stainable with Sudan II covered 36.3±8.6% of the intimal surface in the control rabbits, and 25.4±5.5% in the La3+-treated rabbits. Histopathologically, intimal foam cell layer was thicker in the control rabbits than in the La3+-treated rabbits. Relative plaque deposition of intramural coronary arteries was similar in both groups. Fatty degeneration of the liver was suppressed in the La3+-treated rabbits.Although our results were not so remarkable as those of D. M. Kramsch et al., we are sure that La3+ suppressed experimental atherosclerosis in rabbits without reducing hypercholesterolemia. Inhibitory effects of other Ca2+-channel blockers on experimental atherosclerosis and the mechanisms of these drugs are currently being studied by us.

Changes in the plasma levels of thromboxane B2 and cyclic nucleotides in patients with Takayasu disease.

Plasma thromboxane B2 (TXB2), cyclic AMP and cyclic GMP levels in 31 women with Takayasu disease were measured and findings were compared with data on 34 age-matched healthy Japanese. Platelet aggregation determined by the screen filtration pressure (SEP) method and pulmonary lesions assessed by scintillation were studied in 21 patients. Plasma TXB2 levels in patients with Takayasu disease were 265.8 +/- 20.4 pg/ml, which were statistically higher than the levels of 196.3 +/- 10.7 in healthy controls. On the contrary, cyclic AMP levels in the patients were 9.6 +/- 0.7 pmols/ml, statistically lower levels than 13.5 +/- 1.0 seen in the healthy controls. A positive correlation among cyclic AMP, cyclic GMP and TXB2 levels was confirmed only in the controls. SEP values in the patients with pulmonary lesions were significantly higher than in those without lesions and also in the controls. A positive correlation was obtained between SEP and TXB2 levels in healthy controls, but not in the patients. Thus, thromboxane A2 may play an important role in the pathology of Takayasu disease.

Platelet aggregation measured by the screen filtration pressure method in hypertensive patients.

In this study platelet aggregation was measured by the screen filtration pressure method in 2 groups of hypertensives separated according to age. They were perfectly matched for levels of various "risk factors", with normotensive "controls". No significant difference in platelet aggregate filtration pressure (PAFP) was found between hypertensives and normotensives. Contrary to normotensive subjects, there was no significant increase in the PAFP values with age in the hypertensives. This might be due to the significantly higher blood urea values in the hypertensives as compared to the normotensives. An inverse relationship between blood urea concentration and PAFP values was in fact confirmed by in vivo and in vitro studies.

Enhancement of Platelet Sensitivity to ADP-Aggregation by Isometric Exercise in Arteriosclerotic Patients and its Prevention

A new method for assessment of platelet sensitivity to ADP-aggregation was devised. Its reproducibility and the correlations between the values obtained by this method, the optical density (O. D.) method, and the screen filtration pressure (SFP) method were assessed. In summary, this method may be said to have three main points: 1. It can be performed without centrifugation, avoiding mechanical stress to platelets, using only 0.8 ml. of blood and inexpensive equipment. 2. It may reflect different aspects of platelet function from the O. D. method and the SFP method, despite the positve significant correlations between the values obtained by these three methods. 3. It was proved to be highly reproducible and is thought to be useful clinically. By using this method, the effect of sustained isometric exercise by handgripping on platelet aggregability was assessed in coronary sclerotic and cerebral arteriosclerotic patients on placebo and EG-626, a newly synthesized cyclic AMP phosphodiesterase inhibitor. On placebo, an enhancement platelet sensitivity was observed after isometric exercise in coronary and cerebral arteriosclerotic patients but not in healthy control subjects. The enhancement was prevented by pretreatment of EG-626, administered orally 1.5 hours prior to exercise.

Adnormal platelet count and aggregability in bilateral cortical necrosis; A case study

A case of bilateral cortical necrosis (BCN) was reported because of her abnormal platelet count and aggregability. She was 26 years old primipara.In her past history, at the age of 11, she was operated because of papillary adenocarcinoma of the thyroid gland, when no abnormal bleeding was reported.After cesarean section, atonic hemorrhage occurred and anuria developed. Because BCN was suspected heparin and urokinase therapy were started (later, patchy BCN was verified by renal biopsy). Uremia was controlled by hemodialysis (3/week). Platelet count (Plt.) increased gradually to normal level within a week. After heparin cessation, Plt. continued to increase and exceeded 60×104/mm3. In spite of thrombocytosis, bleeding time (BT) was prolonged to more than 15 min. On 31st hospital day when Plt. was 40×104/mm3and BT more than 15 min., platelet aggregability was investigated by screen filtration pressure (SFP) method (normal range: 264.9±14.3mmHg when induced by 3μM ADP). Her aggregability was no more than 20mmHg. On 34th hospital day, she was attacked by generalized convulsion and tracheotomy was done. Despite 17 units of blood transfusion bleeding was not discontinued. Therfore, 6 units of packed platelet were transfused and bleeding was dramatically stopped within 2 hours. After this episode, BT was normalized while thrombocytosis persisted. On 59th hospital day when Plt. showed 48.1×104/mm3 and BT was 3.5min., platelet aggregability was investigated by SEP method and optical density (O. D.) method. Using SFP method 3μM ADP induced aggregability was 400mmHg. By O. D. method, 10μM ADP induced maximum aggregability (ADP max) was 32.8% (normal 70.2±2.6), 1μg/ml adrenaline induced maximum aggregability (adrenaline max) 90.8% (normal 40.6±4.0), and 1mg/ml collagen induded maximum aggregability (collagen max) 69.6% (normal 74.8±5.6), respectively.She discharged on 14th hospital day, when her creatinine clearance was 17L/day, BUN 31mg/dl, and creatinine 3.3mg/dl, and conservative management was indicated. On 178 th day after BCN, when Plt. revealed 27.6×104/mm3 and was 3min., platelet aggregability was investigated again. Using SFP method, 3μM ADP induced aggregability was 390mmHg, while by O. D. method, ADP max was 63.2%, adrenalin max 98.5%, and collagen max 82.4%, respectively.Throughout her clinical course, fibrin degradation products were 40μg/ml or less, fibrinogen 370-900mg/dl, and euglobulin lysis time 24 hours or more. CB-PC and cephalothin, which were administered when platelet aggregability decreased, were investigated in vitro by O. D. method, with no effect to platelet aggregability being found.