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PubMedDate not supplied

Dietary effect on platelet aggregation in men with and without a family history of essential hypertension.

Platelet aggregation induced by 5 microM adenosine 5'-diphosphate (ADP) was significantly higher in men with a family history of essential hypertension than in men without such a history when they were fed a low fat-cholesterol diet with low salt. Platelet aggregation activity was remarkably increased in both groups when the diet was changed from low salt into high salt. Platelet aggregation activity was higher in the group with a positive family history of hypertension on the low fat-cholesterol plus high salt diet than in the group without a family history under the same conditions. The activity was slightly increased in both groups when fed a high fat-cholesterol diet with low salt. There was no significant difference in the platelet aggregation between the two groups. The activity was significantly increased in both groups on the high fat-cholesterol diet after the diet was changed from low salt to high salt. Under both the low and high fat-cholesterol diets, the mean blood pressure was significantly elevated in response to excessive salt intake in the group with a family history of essential hypertension, but it was not elevated in the group without such a family history.

Adenosine Diphosphate↗

PubMed1992

Heparin enhances platelet aggregation irrespective of anticoagulation with citrate or with hirudin.

The effects of anticoagulation with citrate or hirudin on heparin effects on platelet aggregation was studied with whole blood aggregometry on blood from healthy volunteers. Platelet aggregation was initiated by collagen. The heparin effect was also studied with filtragometry where hirudin was used as the anticoagulant. In citrated blood, a mean collagen dose of 0.42 +/- 0.04 micrograms/ml resulted in an impedance change of 1.1 +/- 0.3 Ohm. Preincubation with heparin doses of 0.5, 2.5 and 5 IU/ml enhanced the impedance induced by the same dose of collagen by 2.9 +/- 1.4, 11.4 +/- 1.6 and 9.9 +/- 2.3 times, respectively (p less than 0.0001, ANOVA). In hirudinized blood a similar degree of change in impedance (1.5 +/- 0.2 Ohm) was achieved at significantly lower concentration of collagen (0.08 +/- 0.006 micrograms/ml, p less than 0.0001). Preincubation with heparin in doses of 0.5, 2.5 and 5 IU/ml increased impedance by 1.5 +/- 0.5, 3.9 +/- 1.6 and 1.3 +/- 0.5 times, respectively (p less than 0.0001, ANOVA). The dose-related increments were smaller in hirudinized blood as compared to citrated blood (p less than 0.04). With filtragometry, heparin dose-dependently shortened the aggregation time (p less than 0.0007). Compared to hirudin alone as anticoagulant, heparin in an equipotent dose in these experiments shortened aggregation time (p less than 0.05). In conclusion, heparin enhanced platelet aggregation both in calcium-chelated blood and in blood anticoagulated with hirudin. Heparin also dose-dependently increased platelet aggregation in filtragometry. Thus the heparin potentiating effect on platelet aggregation seems to be independent of extracellular ionized calcium and be operative at physiological calcium concentrations.

Adult↗

PubMed1983

Drug-induced inhibition of guinea pig platelet aggregation unrelated to their beta-adrenolytic actions.

Inhibitory actions on adenosine diphosphate (ADP)-induced platelet aggregation of atenolol, dl- and d-D-32, IPS-339, pindolol and propranolol were investigated in guinea pigs for the purpose of obtaining a clue about a possible mechanism for the disaggregatory phenomenon of beta-adrenoceptor blocking agents. The effects of verapamil and procaine on guinea pig platelet aggregation were also examined. All of these agents including verapamil and procaine showed a dose-dependent inhibitory effect on platelet aggregation, and their relative potencies determined on the basis of the molar concentrations producing a 50% inhibition of ADP-induced aggregation were in descending order: IPS-339 greater than propranolol greater than verapamil greater than dl-D-32 not equal to d-D-32 greater than pindolol greater than procaine greater than atenolol. This order of relative potencies of the inhibitory actions of these test compounds on platelet aggregation was well correlated to those of local anaesthetic action in guinea pigs (r = 0.932, P less than 0.01) and lipophilicity (r = -0.899, P less than 0.01), while it did not agree with the orders of potency of beta-adrenoceptor blocking action, intrinsic sympathomimetic action and vasodilator action. From these results, it may be reasonable to propose that inhibitory actions of beta-adrenoceptor blocking agents and local anaesthetics on platelet aggregation are caused through the same mechanism or through a very similar one.

Adrenergic beta-Antagonists↗

PubMed1995

Effects of haloperidol and chlorpromazine on smooth muscle contractility, platelet aggregation and neuronal calcium current.

Effects of chlorpromazine, haloperidol (neuroleptics and calmodulin antagonists), and verapamil on rat platelet aggregation induced by thrombin, on calcium current in snail neurones and on both tonic tension of high potassium contracture and phasic contraction of isolated guinea-pig ureter preparations were studied. Moreover, droperidol, sulpiride and prazosine effects were studied for models of phasic contractility and platelet aggregation. Sulpiride and prazosine were ineffective, verapamil was ineffective on platelet aggregation, while droperidol was the most potent inhibitor of platelet aggregation. These results, the similarity revealed in the blockage of neuronal calcium current by neuroleptics and verapamil, and the potent inhibitory action of haloperidol and chlorpromazine on contractility and aggregation suggest that both phenothiazine and butyrophenone neuroleptics possess some properties of calcium antagonists and may also have intracellular sites of action other than calmodulin.

Animals↗

PubMed2002

Protease-activated receptors 1 and 4 do not stimulate G(i) signaling pathways in the absence of secreted ADP and cause human platelet aggregation independently of G(i) signaling.

Thrombin is an important agonist for platelet activation and plays a major role in hemostasis and thrombosis. Thrombin activates platelets mainly through protease-activated receptor 1 (PAR1), PAR4, and glycoprotein Ib. Because adenosine diphosphate and thromboxane A(2) have been shown to cause platelet aggregation by concomitant signaling through G(q) and G(i) pathways, we investigated whether coactivation of G(q) and G(i) signaling pathways is the general mechanism by which PAR1 and PAR4 agonists also activate platelet fibrinogen receptor (alphaIIbbeta3). A PAR1-activating peptide, SFLLRN, and PAR4-activating peptides GYPGKF and AYPGKF, caused inhibition of stimulated adenylyl cyclase in human platelets but not in the presence of either Ro 31-8220, a protein kinase C selective inhibitor that abolishes secretion, or AR-C66096, a P2Y12 receptor-selective antagonist; alpha-thrombin-induced inhibition of adenylyl cyclase was also blocked by Ro 31-8220 or AR-C66096. In platelets from a P2Y12 receptor-defective patient, alpha-thrombin, SFLLRN, and GYPGKF also failed to inhibit adenylyl cyclase. In platelets from mice lacking the P2Y12 receptor, neither alpha-thrombin nor AYPGKF caused inhibition of adenylyl cyclase. Furthermore, AR-C66096 caused a rightward shift of human platelet aggregation induced by the lower concentrations of alpha-thrombin and AYPGKF but had no effect at higher concentrations. Similar results were obtained with platelets from mice deficient in the P2Y12. We conclude that (1) thrombin- and thrombin receptor-activating peptide-induced inhibition of adenylyl cyclase in platelets depends exclusively on secreted adenosine diphosphate that stimulates G(i) signaling pathways and (2) thrombin and thrombin receptor-activating peptides cause platelet aggregation independently of G(i) signaling.

Adenosine Diphosphate↗

PubMed1990

Effects of nitroglycerin at therapeutic doses on platelet aggregation in unstable angina pectoris and acute myocardial infarction.

The platelet aggregation response to adenosine diphosphate (ADP) and to thrombin was quantified in 10 patients, 5 with unstable angina pectoris and 5 with acute myocardial infarction, before, during and after a 45-minute infusion of nitroglycerin. An impedance aggregometer allowing rapid bedside studies in whole blood was used. The reproducibility of the methods was documented to be within 10%. Doses of nitroglycerin were titrated for a 10 mm Hg decrease in mean arterial blood pressure with mean doses being 1.2 +/- 0.2 (standard error of the mean) micrograms/kg/min. Nitroglycerin decreased the area under the aggregation curve induced by ADP from 43 +/- 3.6 to 30 +/- 6.3 cm2 (p = 0.007) and by thrombin from 8.9 +/- 1.7 to 4.1 +/- 0.9 cm2 (p = 0.003). Peak responses to ADP were decreased from 13.3 +/- 1 to 9.1 +/- 1.7 ohms (p = 0.005) and to thrombin from 9.3 +/- 2 to 5.0 +/- 1.2 ohms (p = 0.003). All patients had greater than or equal to 50% inhibition with 1 agent or the other and the inhibition was greater than 50% with each of the 2 aggregating agents in 6 patients. Analyses performed on blood withdrawn 15 minutes after the discontinuation of nitroglycerin showed a return to baseline before nitroglycerin results. When analyses were delayed and performed on blood preserved at room temperature for 30 minutes, no effect of nitroglycerin could be detected. Thus, bedside platelet aggregation studies document a significant and reversible effect of nitroglycerin at therapeutic doses on platelet function.

Adenosine Diphosphate↗

PubMed1991

[Changes in morning platelet aggregation in patients with peripheral obliterating arteriopathy after evening administration of picotamide].

Platelets are involved in the progressive pathogenesis of atherosclerosis. It has been shown that there is usually an increase in platelet aggregation between 6 and 9 a.m.; in the present study. in 10 patients suffering from chronic occlusive arterial disease, the impedancemetric method was used to evaluate, in whole blood, platelet aggregation induced by ADP and collagen the day prior to and the day following the evening administration of 300 mg picotamide. Analysis of the data obtained shows, in accordance with the findings of other authors, in increase of platelet aggregation from 6 a.m. to 9 a.m. This increase is suppressed by the evening administration of the anti-aggregant.

Aged↗

PubMed2002

Acute effects of ingestion of black tea on postprandial platelet aggregation in human subjects.

Results of population studies suggest that black tea can reduce cardiovascular risk. Effects of black-tea polyphenols to reduce platelet aggregability may help to explain any benefits. Given that black tea is often consumed with and after meals, and man spends much of his life in the postprandial state, the objective of the present study was to investigate the acute effects of ingestion of black tea on postprandial platelet aggregation ex vivo. Twenty healthy participants had platelet aggregation and blood lipids assessed before and 4 h after the ingestion of 50 g dairy fat on two occasions in random order, corresponding to black tea or hot water. Black tea or hot water (one cup) was consumed immediately following the dairy fat, then after 15 and 30 h. Platelet aggregation ex vivo was assessed in platelet-rich plasma in response to three concentrations of collagen (0.2, 0.6, 20 microg/ml) and ADP (2, 4, 8 microM). Urinary concentrations of 4-O-methylgallic acid were used as an indicator that tea polyphenols were absorbed. Serum total cholesterol and triacylglycerol concentrations increased significantly 4 h after ingesting the dairy fat, but there was no significant difference between black tea and hot-water treatments on the cholesterol or triacylglycerol responses. Urinary 4-O-methylgallic acid concentrations were significantly increased following ingestion of black tea (P=0.0001) but not water. Black tea in comparison to hot water did not inhibit collagen or ADP-induced postprandial platelet aggregation. The results of this study do not support the suggestion that reduced postprandial platelet aggregability contributes to any benefits of black tea on cardiovascular risk.

Adenosine Diphosphate↗

PubMed1989

Glyceryl trinitrate and platelet aggregation: effects of N-acetyl-cysteine.

The concentration range of GTN causing inhibition of platelet aggregation in vitro is much higher than the plasma concentrations achieved clinically. This action is potentiated by the sulphydryl donor N-acetylcysteine. We have investigated the effects of GTN given with and without N-acetylcysteine on ex vivo platelet aggregation in man. In a double-blind randomised crossover trial eight healthy volunteers were treated with 20 mg of transdermal GTN/24 h, together with N-acetylcysteine 200 mg three times daily or matching placebo. Platelet aggregation, measured ex vivo by whole blood impedance aggregometry in response to adenosine diphosphate, was not significantly altered by GTN acutely or after 4 days' treatment with or without N-acetylcysteine. Platelet cyclic guanosine monophosphate levels were not significantly altered by GTN either in the absence or presence of N-acetylcysteine. This result implies that previously reported beneficial effects of GTN in myocardial infarction or unstable angina are unlikely to be attributable to direct pharmacological inhibition of platelet aggregation.

Acetylcysteine↗

PubMed1983

Platelet aggregation studies in patients with angina pectoris--relationships to types of angina and coronary pathoanatomy.

Platelet aggregation was studied in patients with angina pectoris in whom coronary sclerosis was found by arteriography. The subjects consisted of 20 patients with stable angina pectoris, 12 with unstable angina pectoris and 4 with variant form of angina pectoris. Fifteen healthy subjects served as controls. ADP- and collagen-induced platelet aggregations were estimated during resting conditions before and immediately after an exercise test. In patients with unstable angina pectoris, ADP-induced as well as collagen-induced platelet aggregations during resting conditions were significantly less than those in normal subjects. After exercise, however, they significantly increased. In stable angina pectoris, they did not differ from those in the control group and their responses to exercise were also not significant. In general, platelet aggregation during resting conditions was accelerated in relation to an increase in the number of coronary arteries involved. The results demonstrate that examination of platelet aggregation during resting conditions and following exercise aids in a more accurate evaluation of the types and the stages of patients with angina pectoris.

Adult↗

PubMed1989

Effects of dietary polyunsaturated fatty acid on platelet aggregation in rats.

In the present study, we changed the fatty acid profile in blood and platelet membranes by dietary manipulation, and examined the effect on platelet aggregation in rats. Fifty-five rats were divided into five groups and fed for 56 days with 1% cholesterol and different types of fatty acid-rich diets: basal, lard, lard + fish oil, soybean oil, and soybean oil + fish oil. a decrease in serum arachidonic acid (20:4, omega-6, AA) and an increase in serum eicosapentaenoic acid (20:5, omega-3, EPA) were found in all experimental dietary groups fed with refined fish oil. Similar changes in the polyunsaturated fatty acids were also found in the platelet membrane phospholipids. Platelet aggregation, quantitated by the slope and height of the aggregation curve induced by different concentrations of ADP in a platelet aggregometer, was inhibited in all groups fed with refined fish oil. This inhibition of platelet aggregation may be related to an increase in the ratio of EPA and AA in the platelet membrane phospholipids after dietary manipulation. The differences in the platelet aggregation and thromboxane B2 (TXB2) concentration between the lard and the lard + fish oil groups were more profound than that between the soybean oil and the soybean oil + fish oil group. However, the malondialdehyde (MDA) concentration revealed no significant differences between the five groups.

Animals↗

PubMed1987

[Platelet aggregation in severe and malignant forms of hypertension: effect of treatment with prostaglandin E2].

Platelet aggregation was studied in patients with high and stable arterial hypertension that was mostly associated with the malignant syndrome, and the effect of PGE2 introduced into the blood flow as repeated intravenous infusions on platelet activity was assessed. The addition of low-dose inductor produced the greatest changes in platelet aggregation following platelet exposure to different ADP doses in the patients, as compared to normal subjects. Stimulation with 0.1 mumol ADP produced a 7-fold increase in platelet aggregation in hypertensive patients, as compared to the controls. Repeated administration of 1.2-1.5 mg PGE2 normalizes cell sensitivity to ADP. Mean arterial BP dropped by 15-45 mm Hg during the infusions and remained low for several days afterwards.

Adenosine Diphosphate↗

PubMed1996

[Effect of acute hypoxia on blood catecholamine and whole blood platelet aggregation].

Experiments were performed on 250-300 g male Sprague-Dawley rats under urethane (700 mg/kg) and alpha-chloralose (35 mg/kg) anesthesia. Plasma catecholamine concentration and the whole blood platelet aggregation were measured during normoxia, acute hypoxia, reoxygenation, acute hypoxia immediately after bilateral adrenalectomy and acute hypoxia at the end of 15 and 30 min after bilateral adrenalectomy. The plasma adrenaline concentration and the whole blood platelet aggregation increased markedly (P < 0.01), while the plasma noradrenaline concentration tended to increase (P > 0.05) during acute hypoxia. The plasma adrenaline concentration and the whole blood platelet aggregation are capable of restoring to the normal level during reoxygenation. The plasma noradrenaline concentration did not change, while the plasma adrenaline concentration and the whole blood platelet aggregation decreased significantly (P < 0.001 or 0.05) during acute hypoxia for 15 min immediately after bilateral adrenalectomy. On the other hand, plasma adrenaline and noradrenaline were not detectable during acute hypoxia 30 min after bilateral adrenalectomy while the whole blood platelet aggregation deceased markedly (P < 0.01). When adrenaline (1 ng/ml) was added to the blood (in vitro), the whole blood platelet aggregation increased significantly (P < 0.01). All the above results indicate that acute hypoxia leads to increament of whole blood platelet aggregation and plasma adrenaline concentration due to release from the adrenal gland and the increament of the whole blood platelet aggregation may be partly mediated by increased plasma adrenaline.

Acute Disease↗

PubMed2006

Bradykinin and its metabolite bradykinin 1-5 inhibit thrombin-induced platelet aggregation in humans.

Bradykinin 1-5 is a major stable metabolite of bradykinin, formed by the proteolytic action of angiotensin-converting enzyme. In vitro and animal studies suggest that bradykinin 1-5 possesses biological activity. This study tests the hypothesis that bradykinin 1-5 affects vasodilation, fibrinolysis, or platelet aggregation in humans. Graded doses of bradykinin (47-377 pmol/min) and bradykinin 1-5 (47-18,850 pmol/min) were infused in the brachial artery in random order in 36 healthy subjects. Forearm blood flow (FBF) was measured, and simultaneously obtained venous and arterial plasma samples were analyzed for tissue plasminogen activator (t-PA) antigen. In seven subjects each, alpha- and gamma-thrombin-induced platelet aggregation was measured in platelet-rich plasma obtained from antecubital venous blood at baseline and during peptide infusions. Bradykinin caused dose-dependent increases in FBF and net t-PA release (P < 0.001 for both). Bradykinin 1-5 did not affect FBF (P = 0.13) or net t-PA release (P = 0.46) at concentrations >1500 times physiologic. In contrast, both bradykinin and bradykinin 1-5 inhibited alpha-and gamma-thrombin-induced platelet aggregation (P < 0.01 versus baseline). Bradykinin 1-5 inhibited gamma-thrombin-induced platelet aggregation 50% at a calculated dose of 183 +/- 3 pmol/min. Neither bradykinin nor bradykinin 1-5 affected thrombin receptor-activating peptide-induced platelet aggregation, consistent with the hypothesis that bradykinin and bradykinin 1-5 inhibit thrombin-induced platelet aggregation by preventing cleavage of the thrombin receptor and liberation of thrombin receptor-activating peptide. This study is the first to demonstrate biological activity of bradykinin 1-5 following in vivo administration to humans. By inhibiting thrombin-induced platelet aggregation without causing vasodilation, bradykinin 1-5 may provide a model for small molecule substrate-selective thrombin inhibitors.

Adult↗

PubMed1998

A cross-sectional evaluation of spontaneous platelet aggregation in relation to complications in patients with type II diabetes mellitus.

To clarify the relationship between platelet function and diabetic complications, we investigated spontaneous platelet aggregation (SPA) and agonist-induced platelet aggregation by a particle counting method using light scattering (LS) and by a conventional light transmission method (LT) in 23 age- and sex-matched control subjects and 74 patients with type II diabetes mellitus. We also observed platelets using the FIC-2 (TOA Medical Electronics, Kobe, Japan) flow cytometer and imaging device. Observation by the FIC-2 device showed microaggregates of platelets in samples with increased SPA-LS. SPA-LS was significantly elevated in patients with type II diabetes mellitus as a whole compared with control subjects. SPA-LS also showed significant differences between control subjects and three diabetic patient subgroups with a varying severity of retinopathy, nephropathy, or neuropathy, and the mean values increased along with the increasing severity of complications. On the other hand, although SPA-LT also showed significant differences between these groups, the absolute values were all less than 10%, which we believe does not warrant quantitative analysis. Adenosine-5'-diphosphate (ADP)-induced platelet aggregation failed to show significant differences between controls and subjects with a varying severity of retinopathy by either LS or LT, which indicates that SPA is more sensitive than agonist-induced platelet aggregation in relation to diabetic complications. We observed significant correlations between SPA-LS and the patients' age, hemoglobin A1c (HbA1c) level, plasma fibrinogen level, or 6-keto-PGF1alpha (6KF) to 11-dehydro-thromboxane B2 (TXB2) ratio. Our study demonstrated a close relationship between platelet hyperaggregability and diabetic complications, and a longitudinal prospective study of SPA-LS in diabetic patients is warranted to clarify cause-and-effect relationships.

Cross-Sectional Studies↗

PubMed1994

Inhibition of platelet aggregation by transdermal glyceryl trinitrate.

OBJECTIVE: To determine the optimum conditions for the demonstration of an antiplatelet effect of nitric oxide and to use these conditions to elucidate the effects of a transdermal glyceryl trinitrate patch on platelet aggregation in normal volunteers. METHODS: An open prospective crossover study. The effects of nitric oxide on platelet aggregation in whole blood and platelet rich plasma as stimulated by adenosine diphosphate and U46619 was assessed in the presence and absence of iloprost and MB22948. Optimum conditions for the demonstration of an antiplatelet effect of nitric oxide were then applied to whole blood from normal volunteers in the presence and absence of a transdermal glyceryl trinitrate patch. SETTING: University hospital. SUBJECTS: Eight normal volunteers. MAIN OUTCOME MEASURES: Platelet aggregation in the presence and absence of transdermal glyceryl trinitrate. RESULTS: The optimum conditions for the demonstration of an antiplatelet effect of nitric oxide in whole blood were collecting blood into a tube containing MB22948 and citrate and stimulating platelet aggregation with adenosine diphosphate in the presence or absence of iloprost. Using this method a significant effect of transdermal glyceryl trinitrate on platelet aggregation was shown (P < 0.03) in the presence and absence of iloprost. CONCLUSIONS: These results are consistent with an inhibitory effect on platelet aggregation of nitric oxide liberated by transdermal glyceryl trinitrate. Optimum test conditions are needed to show this effect. The clinical significance of the antiplatelet effect of transdermal glyceryl trinitrate is unknown.

Adenosine Diphosphate↗

PubMed2002

Inhibition of rat platelet aggregation by the diazeniumdiolate nitric oxide donor MAHMA NONOate.

1. Inhibition of rat platelet aggregation by the nitric oxide (NO) donor MAHMA NONOate (Z-1-N-methyl-N-[6-(N-methylammoniohexyl)amino]diazen-1-ium-1,2-diolate) was investigated. The aims were to compare its anti-aggregatory effect with vasorelaxation, to determine the effects of the soluble guanylate cyclase inhibitor, ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one), and to investigate the possible role of activation of sarco-endoplasmic reticulum calcium-ATPase (SERCA), independent of soluble guanylate cyclase, using thapsigargin. 2 MAHMA NONOate concentration-dependently inhibited sub-maximal aggregation responses to collagen (2-10 micro g ml(-1)) and adenosine diphosphate (ADP; 2 micro M) in platelet rich plasma. It was (i). more effective at inhibiting aggregation induced by collagen than by ADP, and (ii). less potent at inhibiting platelet aggregation than relaxing rat pulmonary artery. 3. ODQ (10 micro M) caused only a small shift (approximately half a log unit) in the concentration-response curve to MAHMA NONOate irrespective of the aggregating agent. 4. The NO-independent activator of soluble guanylate cyclase, YC-1 (3-(5'-hydroxymethyl-2'-furyl)-1-benzyl indazole; 1-100 micro M), did not inhibit aggregation. The cGMP analogue, 8-pCPT-cGMP (8-(4-chlorophenylthio)guanosine 3'5' cyclic monophosphate; 0.1-1 mM), caused minimal inhibition. 5. On collagen-aggregated platelets responses to MAHMA NONOate (ODQ 10 micro M present) were abolished by thapsigargin (200 nM). On ADP-aggregated platelets thapsigargin caused partial inhibition. 6. Results with S-nitrosoglutathione (GSNO) resembled those with MAHMA NONOate. Glyceryl trinitrate and sodium nitroprusside were poor inhibitors of aggregation. 7. Thus inhibition of rat platelet aggregation by MAHMA NONOate (like GSNO) is largely ODQ-resistant and, by implication, independent of soluble guanylate cyclase. A likely mechanism of inhibition is activation of SERCA.

Adenosine Diphosphate↗

PubMed1988

The effect of red cells on platelet aggregation: a study with the electronic whole blood aggregometer.

Platelet aggregation was studied in the same platelet rich plasma (PRP) by the simultaneous use of Born's optical method and Cardinal's electronic method. The maximum rate of impedance change (electronic method) correlated well with both the rate and the extent of aggregation as measured by the optical method. The rate of impedance change was therefore the parameter chosen for the study of the effect of red cells on platelet aggregation. Erythrocytes, both at 40 and 60% haematocrit (Hct.), greatly inhibited platelet aggregation induced by ADP and adrenalin, but only minimally affected platelet aggregation induced by collagen.

Electronics↗