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PubMed1986

Platelet-aggregating activities of metastasizing tumor cells. V. In situ roles of platelets in hematogenous metastases.

Intravenous inoculations of B16 cells having high procoagulant, thrombingenerating, and platelet-aggregating (PA) activities resulted in severe platelet reduction and fibrin-rich thromboembolism in the lungs, whereas those of 3LL cells, whose activities were moderate, caused only moderate changes. MH134 cells with low procoagulant, no thrombin-generating and moderate PA activities induced moderate platelet reduction and the formation of thrombi containing less fibrin. In contrast to the respective high and moderate colonizing abilities of B16 and 3LL cells, MH134 cells failed to form lung colonies in half of the recipients. Thrombocytopenia markedly impaired lung colonization by B16 and 3LL cells. However, thrombin injection enhanced lung colonization by MH134 cells.

Animals↗
PubMed2006

Effect of sex difference on platelet aggregation using an optical method in healthy subjects.

There are many studies reporting conflicting results of sex differences on various platelet functions. The purpose of this study was to investigate whether sex differences could affect platelet aggregation results using an optical method in healthy subjects. A total of 42 subjects, 21 males and 21 females, were included in the study. Platelet aggregation was induced by adenosine diphosphate (ADP; 5 microm), collagen (2 microg/ml), and epinephrine (10 microm). Optical aggregation was performed using a turbidometric method. In all platelet aggregation tests ADP, collagen and epinephrine were studied; there was no significant difference between females and males in platelet aggregation amplitudes and slopes. As a result, sex difference does not affect platelet aggregation performed with this optical method in healthy subjects. This result supports that there is no need for sex differentiation while composing control groups in platelet aggregation studies using the optical method.

Adenosine Diphosphate↗
PubMedDate not supplied

Clinical pharmacology studies with indobufen (K 3920): inhibitor of platelet aggregation.

When given to 12 subjects at single oral doses of 100 and 300 mg, indobufen caused clear-cut, dose-dependent, reversible inhibition of epinephrine- and collagen-induced platelet aggregation. Platelet factor 3 availability and platelet factor 4 release were not affected by the lower dose but were markedly reduced by the 300-mg dose. Bleeding time was slightly influenced by 100 mg, and 300 mg had a more pronounced effect. Indobufen 300 mg was also intravenously injected to five subjects. When washed platelets obtained before indobufen were resuspended in plasma obtained after indobufen, aggregation was inhibited. This was not the case when washed platelets obtained after indobufen were resuspended in plasma obtained before indobufen. These experiments indicate tha indobufen causes reversible inhibition of platelet functions unlike the effect of acetylsalicylic acid.

Aged↗
PubMed1998

Anti-platelet activity of the peptides composing the lebetin 1 family, a new class of inhibitors of platelet aggregation.

We have purified from Vipera lebetina venom a family of inhibitors of platelet aggregation, named Lebetins. They are composed of two peptide groups of short (Lebetin 1: L1alpha: GDNKPPKKGPPNG; L1beta: DNKPPKKGPPNG) and long (Lebetin 2: L2alpha: GDNKPPKKGPPNGCFGHKIDRIGSHSGLGCNKVDDNKG; L2beta: DNKPPKKGPPNGCFGHKIDRIGSHSGLGCNKVDDNKG) size. The sequence presenting anti-platelet activity is mainly present within the Lebetin 1 sequence [Barbouche, R. Marrakchi, N., Mansuelle, P., Krifi, M., Fenouillet, E., Rochat, H. and El Ayeb, M. (1996) Novel anti-platelet aggregation polypeptides from Vipera lebetina venom: isolation and characterization. FEBS Lett. 392, 6-10]. Here, the peptides that compose the Lebetin 1 family were synthesized. Their respective activity was determined. Synthetic L1alpha and L1beta inhibited collagen-induced platelet aggregation in the nanomolar range. A peptide corresponding to L1beta deleted by D at its N terminus (L1gamma) also inhibited platelet aggregation potently; further truncation of L1gamma impaired its activity. Because L1 peptides efficiently inhibited fibrinogen-induced alpha-chymotrypsin treated-platelet aggregation, we tested whether they act mainly through the inhibition of platelet binding to fibrinogen and showed that they failed to inhibit platelet binding to fibrinogen-coated wells. The activity of L1 peptides was also tested in vivo: their intravenous administration strongly inhibited collagen-induced thrombocytopenia in rats.

Amino Acid Sequence↗
PubMed1992

[The platelet aggregation inhibiting activity in human placenta--study on the ADP degrading activity of human placental villi].

We studied the platelet aggregation inhibiting activity and ADP degrading activity of human placental villi (tissue culture supernatant) and brush border membrane vesicles (BBMV) and obtained the following results. 1. There existed a platelet aggregation inhibiting activity in tissue culture supernatant of villi (S-villi) but not in that of decidua or amnion. The S-villi inhibited the platelet aggregation induced by ADP, but not that induced by collagen, arachidonic acid or ristocetin. And, there was also ADP degrading activity (ADPase activity) in the S-villi. ADP was quickly degraded by S-villi. When ADP was preincubated with S-villi, the platelet aggregation induced by ADP was completely lost. 2. There was very strong platelet aggregation inhibiting activity in placental BBMV. The BBMV almost completely inhibited the platelet aggregation induced by ADP, collagen, arachidonic acid and ristocetin. And there was very strong ADP degrading activity in the placental BBMV. ADP was quickly degraded by BBMV. When ADP was preincubated with BBMV, the platelet aggregation induced by ADP was completely lost. 3. The enzymatic character (heat stability, enzymatic kinetics, Ca++ dependency and pH dependency) of ADP degrading activity in BBMV was very similar to that in S-villi. 4. The ADP degrading activity of both S-villi and solubilized BBMV were fractionated by anion exchange column chromatography and gel filtration column chromatography in similar patterns, and it was shown that ADP degrading substance of both S-villi and solubilized BBMV had a molecular weight of about 60K.

Apyrase↗
PubMed1999

Pharmacokinetics and pharmacodynamics of Ro 44-3888 after single ascending oral doses of sibrafiban, an oral platelet aggregation inhibitor, in healthy male volunteers.

AIMS: This study constituted the first administration of the oral platelet inhibitor, sibrafiban, to humans. The aim was to investigate the pharmacokinetics and pharmacodynamics of Ro 44-3888, the active principle of sibrafiban, after single ascending oral doses of sibrafiban. Particular emphasis was placed on intersubject variability of the pharmacokinetic and pharmacodynamic parameters of Ro 44-3888. METHODS: The study consisted of three parts. Part I was an open ascending-dose study to determine target effect ranges of sibrafiban. Part II, a double-blind, placebo-controlled, parallel-group study, addressed the intersubject variability of pharmacokinetic and pharmacodynamic parameters of the active principle at a sibrafiban dose achieving an intermediate effect. Part III was a double-blind, placebo-controlled, ascending-dose design covering the complete plasma concentration vs pharmacodynamic response curve of sibrafiban. RESULTS: At sibrafiban doses between 5 mg and 12 mg, the pharmacokinetics of free Ro 44-3888 in plasma were linear whereas those of total Ro 44-3888 were non-linear because of the saturable binding to the glycoprotein IIb-IIIa receptor. Saturation of the GP IIb-IIIa receptor was reached at plasma concentrations of 15.9 ng ml-1. At sibrafiban doses up to 2 mg, ADP-induced platelet aggregation was inhibited by 50%, whereas the inhibition of TRAP-induced platelet aggregation was about 20-30%. At the higher doses, ADP-induced platelet aggregation was almost completely inhibited while a clear dose-response could be observed with TRAP-induced inhibition of platelet aggregation at sibrafiban doses of 5 to 12 mg. Ivy bleeding time increased very steeply with dose with a significant prolongation observed at doses of 5 to 7 mg of sibrafiban (5-7 min, >30 min in one case). At a sibrafiban dose of 12 mg, the stopping criterion for dose escalation (prolongation of the Ivy bleeding time >30 min in three out of four subjects per dose group) was reached. The interindividual coefficients of variation of the integrated pharmacokinetic and pharmacodynamic parameters (AUC and AUE) were below 20%, thus lying well within the pre-set level of acceptance. CONCLUSIONS: With a low intersubject variability of its pharmacokinetic and pharmacodynamic parameters, linear pharmacokinetics and pharmacodynamic effects closely related to its plasma concentrations, Ro 44-3888 has good pharmacological prerequisites for a well controllable therapy of secondary prevention of arterial thrombosis in patients with acute coronary syndrome.

Adenosine Diphosphate↗
PubMed2006

[Effect of asymmetric dimethylarginine on platelet-aggregation and losartan intervention in spontaneous hypertensive rat models].

OBJECTIVE: To evaluate the effect of asymmetric dimethylarginine (ADMA) and the results of losartan intervention on platelet-aggregation in spontaneous hypertensive rats. METHODS: Spontaneous hypertensive rats (SHR) were randomly assigned into 3 groups: SHR control group, L-arginine treatment group (L-arg) and losartan (los) treatment group, each group consisting of 16 rats. Another 16 Wistar Kyoto rats (WKY) served as normal control group. The L-arginine and losartan treatment groups received 1.0 g/kg L-arginine or 30 mg/kg losartan in 10 mL/kg distilled water daily through gastric tube for 2 weeks respectively, while the SHR and WKY groups received distilled water alone. All the rats took tap water and standard feed freely during the experimental period. Systolic blood pressure (SBP) was monitored by the tail-cuff method. At the end of the 2-week intervention, all the rats were sacrificed and the blood samples were collected from the carotid artery. The platelet-aggregation-rate, NO levels, eNOS activity, and ADMA levels both in the plasma and the platelets were measured. We got other platelet samples from the SD rats and incubated the platelets with blood vascular endothelium from the above 4 groups of experimental rats and the platelet-aggregation-rate was monitored as well. RESULTS: (1) Systolic blood pressure of the SHR was significantly higher, compared with that of the WKY (P<0.01), which were significantly reduced both in the L-arginine and losartan groups (P<0.01). (2) Platelet-aggregation-rate of the SHR was significantly higher, compared with that of WKY (P<0.01), which was significantly reduced both in the L-arginine and losartan groups (P<0.01). (3) NO levels both in the plasma and the platelets of the SHR were lower, compared with those of the WKY (P<0.05); and were elevated significantly both in the L-arginine and losartan groups,compared with those of the SHR (P<0.05); (4) Both the plasma and the platelet eNOS activities of SHR followed the same pattern of the NO levels in these groups (P<0.01). (5) In contrast, the plasma and platelet ADMA levels showed a reverse pattern (P<0.05). (6) Platelets from the SD rats incubated with vascular endothelium of WKY exhibited lower platelet-aggregation-rate,compared with the platelets incubated with SHR vascular endothelium (P<0.05); Platelet-aggregation-rate of the SHR group increased, compared with that of the WKY group (P<0.05); Platelet-aggregation-rate both of L-arginine and losartan groups reduced, compared with that of the SHR group (P<0.05). CONCLUSION: High levels of ADMA both in the plasma and in the platelets of SHR are associated with the decline of eNOS activity and NO levels, which might be an important reason for the increased platelet-aggregation-rate. Intervention with Losartan can reduce the platelet-aggregation-rate simultaneously with its known anti-hypertensive effect. The possible mechanism might be that losartan can enhance the eNOS activity and elevate NO levels through the suppression of ADMA.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2001

Effects of oral combined hormone replacement therapy on platelet aggregation in postmenopausal women.

The effects of combined oestrogen/progestin hormone replacement therapy (HRT) on platelet aggregation were studied using women on HRT or placebo. The study involved 32 postmenopausal women (aged 50-75 years) who were enrolled in a double-blind randomized controlled trial, and who received either oral continuous combined HRT (Kliogest(R); 2 mg of oestradiol+1 mg of norethisterone) or placebo for a minimum of 6 months. Platelet aggregation was measured by whole-blood impedance aggregometry in response to the agonists collagen, arachidonic acid and ADP. To determine whether the effects of oestrogen on platelets were influenced by platelet-derived nitric oxide, exposure to collagen was repeated in the presence of the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA). Mean platelet volume was similar in the two groups. Compared with the placebo group, the women on HRT had similar rates and maximum values of platelet aggregation in response to collagen, arachidonic acid and ADP. Addition of L-NMMA did not alter the aggregation response to collagen in either the HRT or the placebo group. In conclusion, postmenopausal women on oral combined continuous HRT comprising oestradiol and norethisterone had similar whole-blood platelet aggregation rates and maximum platelet aggregation responses to higher doses of platelet agonists when compared with those on placebo. The endogenous platelet nitric oxide system did not appear to affect aggregation in either group.

Aged↗
PubMed1985

Effect of cilostazol on platelet aggregation and experimental thrombosis.

A new antithrombotic drug, cilostazol (6-[4-(1-cyclohexyl-1 H-tetrazol-5-yl)butoxy]-3,4-dihydro-2(1H)-quinolinone, OPC-13013) was studied for its inhibitory effect on platelet aggregation in vitro in various experimental animals and man and in dogs ex vivo, for its effect to disperse platelet aggregates in vitro in rabbits and man and for its antithrombotic effect in vivo using its effect to prevent death due to the formation of pulmonary thrombi in mice. Cilostazol produced a potent inhibition of platelet aggregation both in vitro and ex vivo and a dispersion of platelet aggregates in vitro. The mode of action of cilostazol was different from that of acetylsalicylic acid (ASA) in that cilostazol inhibits not only secondary platelet aggregation but also primary platelet aggregation induced by aggregating agents such as adenosine diphosphate (ADP). The drug potently prevented death due to pulmonary thrombosis by platelet aggregates in mice in vivo. Unlike ASA which prevented only death due to collagen-induced platelet aggregation, cilostazol prevented both collagen- and ADP-induced platelet aggregation. These results suggest that cilostazol is a promising antithrombotic drug.

Adenosine Diphosphate↗
PubMed1989

Visualization of vascular platelet aggregation by plastic embedding and light microscopy.

Previous studies have indicated that platelets play a role in inflammation and microvascular damage but routine histologic preparations do not permit clear visualization of the platelets in tissues. Plastic embedding was used in this study to demonstrate platelet aggregates in the pulmonary vasculature of mice exposed to complement activation. The degree of platelet aggregation in the excised lungs was graded semiquantitatively in a total of 75 mice. Control Balb/c mice had a mean aggregation score of 0.16 while mice which received 0.3 ml zymosan-activated plasma (ZAP) intravenously (iv) had a score of 2.2. Injection of 0.3 or 0.4 ml of ZAP to which epsilon-aminocaproic acid was added prior to incubation with zymosan resulted in a score of 2.6 or 4.7 respectively. Balb/c (C5 sufficient) and AKR/J (C5 deficient) mice injected iv with 1 mg zymosan had scores of 2.9 and 3.2, respectively. Cobra venom factor (CVF) injected iv to Balb/c mice induced a dose-dependent aggregation. Taken together, these results confirm that complement activation products can mediate intrapulmonary platelet aggregation and they also demonstrate the suitability of plastic embedding for visualization of intravascular platelet aggregates under light microscopy.

Animals↗
PubMed1999

Platelet aggregation in atopic dermatitis.

Many observations suggest the active role of platelets in allergic inflammation. However, this problem is poorly researched in atopic dermatitis. The aim of study was to examine the intensity and velocity of platelet aggregation and a potential relationship with some immunological parameters (total IgE and specific-IgE serum levels) in atopic dermatitis patients. Platelet aggregation was evaluated in 12 subjects with atopic dermatitis and 12 healthy, nonatopic persons, according to the Born method, in a dual-channel aggregometer, in response to three exogenous stimulators (ADP, thrombin and collagen). The intensity and velocity of platelet aggregation and total platelet counts did not differ between the two groups irrespective of the type of extrinsic stimulator used. In contrast to other atopic diseases, in atopic dermatitis platelet aggregation is not impaired.

Journal Article↗
PubMed1986

Role of heparin in tumor cell-induced platelet aggregation.

B16 mouse melanoma cell lines (B16F1, B16F10 and B16BL6) were able to induce platelet aggregation, and concomitant release of ATP in heparinized platelet-rich plasma (PRP). In citrated PRP, these tumor cells did not induce platelet aggregation. Addition of heparin to citrated PRP enabled these tumor cells to induce aggregation. In heparinized PRP, platelet aggregates induced by B16F10 cells were dissociated by the addition of either 4 mM EDTA, 10 mM CaCl2 or 0.1 micrograms/ml protamine sulfate. B16F10-induced aggregation in heparinized PRP was inhibited by preincubation with anti-fibronectin antibody, but not with antifibrinogen or anti-von Willebrand factor antibodies. B16F10 cells induced aggregation in washed platelet suspension with the addition of heparinized platelet-poor plasma (PPP). Cryoprecipitate from human plasma showed the same effect in the presence of heparin if substituted for PPP. The mixture of purified fibronectin, von Willebrand factor, fibrinogen and heparin were less effective than cryoprecipitate on B16F10-induced aggregation of washed platelets. The results suggest that an interaction between fibronectin and heparin may be important in tumor cell-induced aggregation.

Animals↗
PubMed1988

Treatment of hypertension with captopril: preservation of regional blood flow and reduced platelet aggregation.

The BP of 12 patients with essential hypertension was controlled with captopril over a period of three months. Cerebral blood flow, muscle blood flow (anterior tibialis muscle), platelet aggregation and platelet thromboxane A2 release were measured during a baseline drug-free period, and measurements repeated during the treatment phase on achieving BP control, after one and three months. Cerebral blood flow rose during the early phase of treatment and then dropped to baseline levels during chronic therapy. Muscle blood flow, both at rest and following maximal exercise, was unaffected by captopril therapy. Platelet aggregation was diminished during therapy, and this finding was paralleled by a reduction in platelet thromboxane A2 generation. Control of hypertension with maintenance of regional blood flow and beneficial changes in platelet function during treatment with captopril may improve the overall risk profile of hypertensive patients. Inhibition of platelet aggregation and thromboxane A2 release may contribute to the antihypertensive action of captopril and the maintenance of regional blood flow.

Aged↗
PubMed2004

Ingestion of quercetin inhibits platelet aggregation and essential components of the collagen-stimulated platelet activation pathway in humans.

BACKGROUND: Quercetin, a flavonoid present in the human diet, which is found in high levels in onions, apples, tea and wine, has been shown previously to inhibit platelet aggregation and signaling in vitro. Consequently, it has been proposed that quercetin may contribute to the protective effects against cardiovascular disease of a diet rich in fruit and vegetables. OBJECTIVES: A pilot human dietary intervention study was designed to investigate the relationship between the ingestion of dietary quercetin and platelet function. METHODS: Human subjects ingested either 150 mg or 300 mg quercetin-4'-O-beta-D-glucoside supplement to determine the systemic availability of quercetin. Platelets were isolated from subjects to analyse collagen-stimulated cell signaling and aggregation. RESULTS: Plasma quercetin concentrations peaked at 4.66 microm (+/- 0.77) and 9.72 microm (+/- 1.38) 30 min after ingestion of 150-mg and 300-mg doses of quercetin-4'-O-beta-D-glucoside, respectively, demonstrating that quercetin was bioavailable, with plasma concentrations attained in the range known to affect platelet function in vitro. Platelet aggregation was inhibited 30 and 120 min after ingestion of both doses of quercetin-4'-O-beta-D-glucoside. Correspondingly, collagen-stimulated tyrosine phosphorylation of total platelet proteins was inhibited. This was accompanied by reduced tyrosine phosphorylation of the tyrosine kinase Syk and phospholipase Cgamma2, components of the platelet glycoprotein VI collagen receptor signaling pathway. CONCLUSIONS: This study provides new evidence of the relatively high systemic availability of quercetin in the form of quercetin-4'-O-beta-D-glucoside by supplementation, and implicates quercetin as a dietary inhibitor of platelet cell signaling and thrombus formation.

Blood Platelets↗
PubMed2005

BMS-191095, a cardioselective mitochondrial K(ATP) opener, inhibits human platelet aggregation by opening mitochondrial K(ATP) channels.

We evaluated the antiplatelet effects of two classes of ATP-sensitive potassium channel openers (K(ATP) openers) on washed human platelets, and the study's emphasis was on the role of mitochondrial K(ATP) in platelet aggregation. Collagen-induced platelet aggregation was inhibited in a dose dependent manner by lemakalim and SKP-450, which are potent cardio-nonselective K(ATP) openers, and also by cardioselective BMS-180448 and BMS-191095 (IC50: 1,130, >1,500, 305.3 and 63.9 microM, respectively), but a significantly greater potency was noted for the cardioselective K(ATP) openers. The latter two K(ATP) openers also inhibited platelet aggregation induced by thrombin, another important blood-borne platelet activator, with similar rank order of potency (IC50: 498.0 and 104.8 microM for BMS-180448 and BMS-191095, respectively). The inhibitory effects of BMS-191095 on collagen-induced platelet aggregation were significantly blocked by a 30-min pretreatment of platelets with glyburide (1 microM) or sodium 5-hydroxydecanoate (5-HD, 100 microM), a nonselective and selective mitochondrial K(ATP) antagonist, respectively, at similar magnitudes; this indicates the role of mitochondrial K(ATP) in the antiplatelet activity of BMS-191095. However, glyburide and 5-HD had no effect when they were added to the platelet cuvette immediately prior to the addition of BMS-191095. These findings indicate that cardioselective mitochondrial K(ATP) openers like BMS-191095 are able to exert cardioprotective effects in cardiac ischemia/reperfusion injury via dual mechanisms directed at the inhibition of platelet aggregation and the protection of cardiomyocytes, and both these mechanisms are mediated by mitochondrial K(ATP).

Adenosine Triphosphate↗
PubMed1985

Fibrinogen mediated activation of platelet aggregation and thromboxane A2 release: pathological implications in vascular disease.

The effect of a human fibrinogen preparation on in vitro platelet aggregation was assessed. Platelets were obtained from healthy volunteers. Human fibrinogen induced platelet aggregation in 65% of platelet rich plasma samples and enhanced submaximal platelet aggregation induced by heparin or by several conventional agonists in all samples. Aggregation induced by fibrinogen alone was reversed by the in vitro addition of human albumin. Fibrinogen induced aggregation was associated with the release of the vasoconstrictor, thromboxane A2. Preincubation with indomethacin inhibited both the aggregation and the release of thromboxane A2. Fibrinogen had no effect on in vitro vascular prostaglandin I2 synthesis (rat aortic rings) during a 60 minute incubation. The observed effects of fibrinogen on platelet function may be relevant to clinical conditions in which hyperaggregability of platelets is associated with hyperfibrinogenemia and thrombosis.

Animals↗
PubMed1991

The alpha 2-adrenergic receptor antagonist yohimbine inhibits epinephrine-induced platelet aggregation in healthy subjects.

Onset of sudden death, myocardial infarction, and stroke occurs more likely in the morning hours. Similarly, a morning increase in epinephrine-induced platelet aggregation was observed accompanied by an increase in plasma catecholamines. Inhibition of the morning increase in platelet aggregation would be of therapeutic benefit. In this study the effect of the selective alpha 2-adrenergic receptor antagonist yohimbine on platelet aggregation was evaluated in healthy subjects. Yohimbine administered orally selectively antagonized epinephrine but not collagen, arachidonic acid, or adenosine diphosphate-induced ex vivo platelet aggregation. The lowest dose of yohimbine that significantly inhibited epinephrine-induced platelet aggregation was 8 mg. The inhibitory effect of yohimbine on platelet aggregation lasted 10 hours with the 12 mg dose. At the doses studied (4, 8, and 12 mg), yohimbine did not modify blood pressure, standing heart rate, or plasma catecholamine or glucose concentrations. Twelve milligrams of yohimbine moderately but significantly accelerated supine heart rate (mean maximal increase, 7 +/- 3 beats/min). Further clinical studies are needed to evaluate whether bedtime administration of 12 mg yohimbine may block the morning increase in epinephrine-induced platelet aggregation.

Administration, Oral↗
PubMed1979

Platelet function studies in heart disease. VI. Enhanced platelet aggregate formation activity in congestive heart failure: inhibition by sodium nitroprusside.

We studied 11 patients with congestive heart failure and 10 normal volunteers for in vivo platelet aggregate formation activity. The patients with heart failure had significantly (p less than 0.01) more circulating platelet aggregates than the normal volunteers. During sodium nitroprusside infusion, the number of circulating platelet aggregates declined to normal levels and in vitro platelet aggregation responses to epinephrine and adenosine diphosphate were also suppressed significantly (p less than 0.01). This was associated with a 30% decline in systemic vascular resistance and a 28% increase in cardiac output. In other in vitro experiments, sodium nitroprusside was found to have direct, dose-related platelet aggregation inhibitory actions. This study suggests that an increase in vascular resistance in certain heart failure patients may in part be related to an increase in circulating platelet aggregates. Direct inhibition of platelet aggregation by sodium nitroprusside may be a mechanism of its beneficial effects in heart failure.

Adult↗