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PubMed1987

Effect of postprandial lipaemia on platelet function in man evaluated in whole blood.

The effect of a fatty meal (100 g of fat) on platelet function is evaluated. Two hours after the fat intake (dairy cream) there is a significant reduction in the initial stages of platelet activation by collagen (1 and 0.5 micrograms/ml) as measured by a new analytical method, the BASIC wave, and by the decrease in the beta-Thromboglobulin released by stimulated platelets. This effect is greater in platelet rich plasma (PRP) than in whole blood. Red blood cells (RBC) have a potentiating effect on platelet activation by collagen both before and after the fat intake which is indicated by an increase in the BASIC wave intensity. No significant differences were found, however, in platelet aggregation in PRP or whole blood evaluated by impedance aggregometry. These results suggest that the increase of chylomicrons after fat intake has an inhibitory effect on platelet activation but does not modify platelet aggregation. In addition, it seems that lipaemia does not modify RBC interactions with platelets in collagen stimulated samples.

Animals↗
PubMed1987

Effects of iloprost (ZK 36374), a prostacyclin derivative, on platelet function after ischaemic exercise in patients with stable angina pectoris.

The effect of a chemically stable prostacyclin analogue (Iloprost) on platelet function was investigated in a controlled study in patients with angiographically confirmed stable angina pectoris after ischaemic exercise. In placebo experiments, ADP platelet aggregation was increased after exercise only when measured in whole blood and not in PRP. While plasma thromboxane B2 levels were unchanged, those of 6-keto PGF1 alpha were significantly although transiently increased after exercise. Iloprost displayed a potent antiaggregating activity in PRP and also reversed platelet hyperaggregation occurring in whole blood determinations after exercise. Plasma thromboxane B2 levels were significantly reduced but occasionally a rebound increase occurred 30 min. after end of the infusion. In contrast plasma level of 6-keto PGF1 alpha did not change after Iloprost and its recorded post-exercise increase was counteracted, thus suggesting a negative feed-back mechanism between Iloprost and natural prostacyclin. The data also suggest that degradation of the analogue is probably accomplished through pathways different from those of PGI2.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Antiplatelet activity of dipyridamole in non anticoagulated whole blood.

Dipyridamole has been reported to inhibit platelet aggregation in citrate anticoagulated whole blood (WB). However, citrate may alter the response of platelets and/or the effect of antiplatelet drugs. The present study evaluates the "ex vivo" effect of dipyridamole, two hours after a single dose (3 mg/Kg) in 25 normal subjects in non-anticoagulated (native) WB and in WB anticoagulated with citrate or hirudin. We have used the BASIC anticoagulated with citrate or hirudin. We have used the BASIC wave as analytical method, which can evaluate the early steps of platelet activation with collagen in less than 1 min after venoclysis, thus allowing the study in native WB. The results show that dipyridamole significantly inhibits (p less than 0.001) platelet activation to collagen in citrated WB (66%) while the drug's effect is much lower (21%) and non-significant if evaluated in native or hirudine anticoagulated WB. These results suggest that citrate or low calcium concentration amplify the drug's platelet inhibitory action in WB and, therefore, the laboratory results may overestimate the drug's effect "in vivo".

Adult↗
PubMed1988

No acute effect of cigarette smoking on bleeding time of habitual smokers.

To study the influence of cigarette smoking on blood platelet function, bleeding time was measured in two groups of 14 habitual smokers before and after a 20-minute period during which the subjects either smoked two cigarettes (experimental group) or rested (control group). The second bleeding time appeared to be slightly shortened upon cigarette-smoking (-0.1 min) and was found to be prolonged in the control group (+0.4 min). These changes did not differ significantly from each other (P = 0.38). Consequently, bleeding time of habitual smokers is not affected by smoking two cigarettes.

Adolescent↗
PubMed1988

Inhibition of platelet function by low-dose plain and micro-encapsulated acetylsalicylic acid.

The effect of two acetylsalicylic acid (ASA) formulations, plain (Magnyl) and micro-encapsulated (Globentyl), on platelet aggregation, thromboxane formation, and bleeding time was studied in 12 healthy volunteers in a randomized double-blind cross-over study. All subjects were treated with Magnyl and Globentyl (75 mg daily) in periods of 2 weeks, separated by a wash-out period of 2 weeks. Both drugs significantly depressed platelet aggregation and thromboxane formation and prolonged bleeding time without difference in mode of action of the drugs. It is concluded that significant inhibition of platelet activity may be achieved by low-dose ASA treatment with micro-encapsulated as well as with plain formulations.

Adult↗
PubMed1988

Two antiplatelet agents from Magnolia officinalis.

Magnolol and honokiol are two position isomers isolated from the bark of Magnolia officinalis. Both inhibited the aggregation and ATP release of rabbit platelet-rich plasma induced by collagen and arachidonic acid without affecting that induced by ADP, PAF or thrombin. Aggregation of washed platelets was more markedly inhibited than that of platelet-rich plasma, while the aggregation of whole blood was least affected by both inhibitors. Thromboxane B2 formation caused by collagen, arachidonic acid or thrombin was in each case inhibited by magnolol and honokiol. The rise of intracellular calcium caused by arachidonic acid or collagen was also suppressed by both agents. Collagen-induced intracellular calcium increase in the presence of indomethacin was suppressed by magnolol. It is concluded that the antiplatelet effect of magnolol and honokiol is due to an inhibitory effect on thromboxane formation and also an inhibition of intracellular calcium mobilization.

Animals↗
PubMed1989

Effects of acute exercise on bleeding time, bleeding amount and blood cell counts: a comparative study.

Twenty-five men and 26 women were studied to investigate the effects of acute strenuous exercise on hemostasis after obtaining their informed consent. After familiarization, they performed exercise on a bicycle ergometer at 75% of their predetermined maximal workload until exhaustion. Bleeding time, measured by the Simplate method, and venous blood cell counts of platelets (Plt), erythrocytes (RBC), leukocytes (WBC) were determined at rest and immediately after exercise. We found that bleeding time of Chinese in our study was longer than those of the westerners in other studies and that bleeding time was significantly shortened after exercise from 8.3 +/- .7 to 6.5 +/- .5 min in men and from 11.4 +/- .9 to 8.6 +/- .8 min in women (p less than 0.001). In men, but not in women, acute exercise also augmented the initial bleeding rate and bleeding amount from standard incisions. We also observed that RBC, WBC and Plt counts were greatly increased. The increased percentages for RBC, WBC and Plt in men were 7 +/- 1%, 59 +/- 7%, 16 +/- 3%, and those in women were 5 +/- 1%, 42 +/- 6% and 17 +/- 2% respectively.

Adult↗
PubMed1989

A new index for collagen induced platelet aggregation.

In this paper, we propose a new index of platelet aggregation for optical aggregometry, the "R" value. This represents the rate of change in the half time for platelet aggregation (T1/2) induced by collagen with changes in the platelet concentration and expresses the degree of platelet sensitivity to collagen. The "R" value has been shown to reflect the aggregability of platelets due to activation of the contact factors. The "R" values were significantly different in the acute and chronic phases of occlusive arterial disease, while ordinary platelet aggregation parameters did not change. A decrease in the "R" value appears to indicate a platelet hyperfunction and hypercoagulable state, in other words a prethrombotic state.

Adenosine Diphosphate↗
PubMed1989

Measuring platelet function with platelet shape change, an early event in aggregation.

Platelet shape change precedes aggregation and is sensitive to significantly less stimulant. In this study, differences in percent light transmission (%T) through stirred suspensions of spheroid or discoid platelets are exploited for studying the response of platelets to Platelet Activating Factor (PAF). Changes in %T between stirred and non-stirred suspensions of unstimulated platelets in Platelet Rich Plasma (PRP) varied with the starting concentration. Aggregation was blocked by the presence of citrate while activation by ADP was minimized by apyrase. However, phosphatidic acid formation, ATP release and minimal serotonin release occurred. A shape change parameter (SCP) was defined which varied with the concentration of PAF. Its dependence on PAF was shifted to lower concentration with washed platelets. The dose-response curves for the SCP were found to be virtually identical for both sheep and human platelets. Human platelets were then used to correlate morphology, as determined by phase contrast microscopy, with spectrophotometric data in the form of the SCP. A linear regression analysis of SCP and percent activation revealed a virtual 1:1 correspondence with a slope of 1.066 and an intercept of 0.009 with the standard error of the estimate equal to 0.053. The correlation coefficient was 0.990, making it significant at p less than 0.001. This method provides an alternative to platelet aggregation assays as a convenient, sensitive and reliable measure of platelet activation.

Adenosine Triphosphate↗
PubMed1989

Effects of Hydergine on platelet deposition on "active" human carotid artery lesions and platelet function.

Effects of co-dergocrine mesylate (Hydergine), a drug widely used for the therapy of cerebral vascular disease on local platelet accumulation in the carotid artery region was studied by means of the platelet uptake ratio (PUR) and on the systemic platelet-vascular wall interaction as calculated from platelet half-life were investigated. A placebo controlled, double blind, randomised protocol was used, 18 patients were treated with co-dergocrine and compared to placebo (n = 18). Co-dergocrine treatment resulted in a significant decrease in platelet deposition, PUR decreased from 1.28 +/- 0.05 before treatment to 1.25 +/- 0.06 on day 5 of therapy with a statistically significant (p less than 0.001) in the paired comparison. In the control group the corresponding changes from 1.29 +/- 0.04 before to 1.28 +/- 0.04 did not show a p-value of less than 0.05 in paired comparison. Platelet half-life (72 +/- 11 before vs. 76 +/- 11 hours after 5 days of co-dergocrine treatment) showed a statistically significant (p less than 0.001) prolongation, whereas in the placebo group no relevant change of T/2 was observed (71 +/- 10 before vs. 72 +/- 10 hours on day 5, p greater than 0.10). No relevant effects on ADP-induced platelet aggregation, platelet-release reaction, platelet aggregate ratio, TXB2 plasma levels and thrombin-induced MDA-formation could be detected. These results indicate that co-dergocrine decreased in-vivo platelet residence time to atherosclerotic lesions of the carotid artery. Co-dergocrine may thereby be of benefit in prevention of mural thrombus formation and prevention of transient ischemic attacks, but also of atherosclerosis in man.

Aged↗
PubMed1990

Autologous platelet-labeling in thrombocytopenia.

Field studies performed with peripheral platelets obtained from 6 male volunteers aged 23 to 29 years revealed an extraordinary dependence of labeling efficiency on incubation time and platelet concentration after 111In-oxine platelet labeling. Since the monitoring of in vivo-platelet function in patients with thrombocytopenia may cause problems due to insufficient labeling results and homologous platelets may show a different in vivo behaviour to autologous ones, we have searched for the minimal amount of platelets necessary to allow appropriate labeling and imaging in patients with thrombocytopenia. In 15 patients with untreated thrombocytopenia aged 14 to 79 years demonstrating a mean peripheral platelet count of 2.509 +/- 1.45 x 10(4) cells/microliters autologous 111In-oxine platelet labeling was performed. The results indicate that approximately 1 x 10(8) (concentrated) platelets/ml are necessary to obtain an adequate labeling efficiency and recovery. This platelet concentration can be easily achieved by drawing one more Monovette of whole blood per each 5 x 10(4) platelets/microliter peripheral platelet count less than 2 x 10(5)/microliter. It is concluded, that calculation of the required number of platelets in advance, variation of the blood volume drawn and the volume of incubation buffer allow informative, qualitative and quantitative results using autologous platelets. The method presented effectively circumvents the requirement of homologous platelets for radiolabeling in thrombocytopenia.

Adolescent↗
PubMed1991

Inhibition of PAF-induced human platelet responses by newly synthesized ether phospholipids.

A series of 10 analogues of platelet-activating factor (PAF) was evaluated for proaggregatory and inhibitory behaviour on human blood platelets in vitro. Most of the compounds did not activate platelets but inhibited the PAF-induced aggregation. The inhibition was concentration-dependent and selective for PAF. Platelet responses to ADP and collagen were not suppressed. Schild analysis of the aggregation data was consistent with a simple competitive antagonism. The pA2 of the most effective antagonist (1-O-hexadecyl-2-O-ethylglycero-3-phosphoric acid-6'-(1-chinuclidinium)-hexylester) was 5.96. There is also evidence for its ability to inhibit the high affinity binding of [3H]PAF to the platelet receptors.

Adenosine Diphosphate↗
PubMed1991

Age, cardiovascular risk factors and coronary heart disease as determinants of platelet function in men. A multivariate approach.

Older age, the cardiovascular risk factors and arteriosclerosis have been reported to be associated with stimulated platelet function. To evaluate the relative importance of these factors in determining platelet function, a cross-sectional multivariate study in 191 men, 113 healthy subjects and 78 patients with angiographically documented coronary heart disease, was performed. In healthy subjects, stepwise multiple linear regression identified age to be a major determinant of platelet aggregability. After induction with both ADP and collagen the platelet aggregatory response markedly increased with age. In the patients, platelet function was not age dependent. In multivariate analysis of variance, neither smoking status nor hypercholesterolemia (greater than or equal to 240 mg/dl) were determinants of platelet function in either group. An increase in systolic blood pressure was associated with slightly more inhibited ADP induced aggregation in both healthy subjects and patients with coronary heart disease. In patients compared to healthy subjects, aggregation after induction with ADP and collagen was markedly enhanced and the in vitro formation of thromboxane after collagen stimulation increased. Thus, by multivariate analysis, age and the presence or absence of coronary heart disease were found to be major determinants of platelet function. In contrast, the cardiovascular risk factors smoking, hypercholesterolemia and hypertension were associated with only minor or no alterations of platelet function.

Adult↗