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PubMed1982

Antithrombotic activity and the mechanism of action of trapidil (Rocornal).

Antithrombotic activity and the mechanism of action of trapidil were investigated, as compared with those of aspirin and dipyridamole. Trapidil at oral doses of 30 and 100 mg/kg inhibited arterial thrombosis in rats, while aspirin and dipyridamole at doses up to 300 mg/kg showed only a mild activity. This action may be explained by the fact that trapidil at concentrations ranging from 139 microM to 251 microM exerted 50% inhibition of platelet aggregation induced by ADP, arachidonic acid, thrombin or thromboxane A2 mixture, inhibition of platelet release reaction induced by ADP, arachidonic acid or thrombin, disaggregatory effect on aggregated rabbit platelets by arachidonic acid and potentiating action on antiaggregatory action of prostacyclin in vitro. In vitro actions of trapidil were apparently different from those of aspirin and dipyridamole. Trapidil also showed inhibition of platelet phosphodiesterase activity and thromboxane synthetase activity. Trapidil was expected to be an effective antithrombotic agent. The antithrombotic action of trapidil may be mediated by the inhibition of platelet function which is characterized by the inhibition of both thromboxane synthetase and phosphodiesterase activities, and by the potentiation of the antiaggregatory action of prostacyclin.

Adenosine Triphosphate↗
PubMed1999

Effects of aspirin and trapidil on cardiovascular events after acute myocardial infarction. Japanese Antiplatelets Myocardial Infarction Study (JAMIS) Investigators.

Aspirin therapy confers conclusive net benefits in the acute phase of evolving myocardial infarction, but no clear evidence of benefit from the long-term use of aspirin after acute myocardial infarction (AMI) has been shown in any single study. This multicenter study, the Japanese Antiplatelets Myocardial Infarction Study, was performed to find out whether aspirin or trapidil would improve clinical outcome compared with no antiplatelets in postinfarction patients. The study was a multicenter, open-label, randomized controlled trial of aspirin 81 mg/day, trapidil 300 mg/day, and no antiplatelets in patients with AMI admitted within 1 month from the onset of symptoms. Seven hundred twenty-three patients were enrolled at 70 hospitals in 18 prefectures of Japan; 250 were randomly assigned to treatment with 81 mg aspirin (aspirin group), 243 to that with trapidil (trapidil group), and 230 were not given antiplatelet agents. The mean follow-up period was 475 days. This study demonstrated that long-term use of aspirin at the dose of 81 mg/day reduced the incidence of recurrent AMI compared with the group receiving no antiplatelets after AMI (p = 0.0045) and that trapidil also reduced the occurrence of reinfarction compared with the group receiving no antiplatelets, but the difference was not significant (p = 0.0810). The incidence of cardiovascular events including cardiovascular death, reinfarction, uncontrolled unstable angina requiring admission to hospital, and nonfatal ischemic stroke was reduced in the group receiving 300 mg trapidil daily compared with the group receiving no antiplatelets (p = 0.0039). The use of aspirin 81 mg/day provided almost no benefit over no antiplatelets therapy in the incidence of cardiovascular events. In conclusion, low-dose aspirin (81 mg) effectively prevented recurrent AMI in postinfarction patients after thrombolysis or coronary angioplasty when used over a long term. Furthermore, the long-term use of trapidil resulted in a significant reduction in the incidence of cardiovascular events.

Aged↗
PubMed2001

The TRAPIST Study. A multicentre randomized placebo controlled clinical trial of trapidil for prevention of restenosis after coronary stenting, measured by 3-D intravascular ultrasound.

BACKGROUND: Studies have reported benefit of oral therapy with the phosphodiesterase inhibitor, trapidil, in reducing restenosis after coronary angioplasty. Coronary stenting is associated with improved late outcome compared with balloon angioplasty, but significant neointimal hyperplasia still occurs in a considerable proportion of patients. The aim of this study was to investigate the safety and efficacy of trapidil 200 mg in preventing in-stent restenosis. METHODS: Patients with a single native coronary lesion requiring revascularization were randomized to placebo or trapidil at least 1 h before, and continuing for 6 months after, successful implantation of a coronary Wallstent. The primary end-point was in-stent neointimal volume measured by three-dimensional reconstruction of intravascular ultrasound images recorded at the 6 month follow-up catheterization. RESULTS: Of 312 patients randomized at 21 centres in nine countries, 303 (148 trapidil, 155 placebo) underwent successful Wallstent implantation, and 139 patients (90%) in the placebo group and 130 (88%) in the trapidil group had repeat catheterization at 26+/-2 weeks. There was no significant difference between trapidil and placebo-treated patients regarding in-stent neointimal volume (108.6+/- 95.6 mm(3)vs 93.3+/-79.1 mm(3);P=0.16) or % obstruction volume (38+/-18% vs 36+/-21%;P=0.32), in angiographic minimal luminal diameter at follow-up (1.63+/-0.61 mm vs 1.74+/-0.69 mm;P=0.17), restenosis rate (31% vs 24%;P=0.24), cumulative incidence of major adverse cardiac events at 7 months (22% vs 20%;P=0.71) or anginal complaints (30% vs 24%;P=0.29). CONCLUSION: Oral trapidil 600 mg daily for 6 months did not reduce in-stent hyperplasia or improve clinical outcome after successful Wallstent implantation and is not indicated for this purpose.

Aged↗
PubMedDate not supplied

Effects of trapidil on forearm veins and arteries in man.

To understand the mechanisms of antianginal effects of trapidil, we examined the effects of trapidil, 100 mg i.v., on forearm veins and arteries in nine young healthy volunteers and compared the results with those of nitroglycerin, 0.3 mg s.1. At the doses used in the study, which are those in clinical use, trapidil and nitroglycerin increased forearm venous distensibility (p less than 0.05 for both) and decreased central venous pressure (CVP; p less than 0.01 for both). These results suggest that both drugs dilate veins. Forearm vascular resistance was decreased by trapidil but not by nitroglycerin. To examine the possibility that reflex vasoconstriction triggered by the decrease in CVP counteracted the direct vasodilator effect of the drugs, we studied the relationship between CVP and forearm vascular resistance while altering CVP by lower body negative pressure. Forearm vascular resistance at a comparable level of CVP was less after than before trapidil or nitroglycerin. These results suggest that both trapidil and nitroglycerin dilate forearm arteries in humans. Thus, we conclude that at a clinical dose, trapidil, as well as nitroglycerin, dilates forearm veins and arteries in humans.

Adult↗
PubMed1992

Vasorelaxant effect of trapidil on human basilar artery.

We have investigated the vasorelaxant effect of trapidil on human isolated basilar artery. Trapidil (10(-5)-10(-4) M) dose-dependently caused relaxation in vascular strips with or without endothelium, with no significant difference between the two types of strips. The relaxation responses were not inhibited by atropine, propranolol or methylene blue. Trapidil increased the concentration of 6-keto-PGF1 alpha, a prostacyclin degradation product, released from an artery ring in the incubation medium, but trapidil-induced relaxation was not inhibited by indomethacin. Pretreatment of vascular strips with 10(-5) M trapidil increased the relaxation responses to forskolin and dibutyryladenosine cyclic monophosphate but not to sodium nitroprusside or 8-bromoguanosine cyclic monophosphate. Trapidil induced a significant increase in the cAMP concentration but not in the cGMP concentration in artery strips. These results suggest that the relaxation response to trapidil is not caused by prostacyclin release or an increase in cGMP in the smooth muscle, but possibly by an increase in the cAMP levels, probably via an inhibitory effect on cAMP phosphodiesterase.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Bronchodilatory effect of trapidil in man.

Trapidil (Rocornal) is clinically used as a coronary vasodilator and inhibitor of coagulation of the platelet. Recently trapidil has been reported to have a bronchodilatory action in excised dog's tracheal smooth muscle. In the present study the bronchodilatory effects of trapidil were investigated in man. For 21 patients with asthma, 6 patients with emphysema and 2 patients with chronic bronchitis, 100 mg of trapidil was infused intravenously. Subjects were divided into two groups. Group I was infused for about 30 min and Group II for about 10 min. After administration of trapidil, forced vital capacity increased in both groups (p less than 0.01), forced expiratory volume at 1.0 s (p less than 0.01) and peak expiratory flow rate (p less than 0.05) increased in Group II. Respiratory resistance decreased (p less than 0.01) in Group II. From these results, it was confirmed that trapidil has bronchodilatory effect. We think trapidil is useful for the treatment of the patients not only with ischemic heart disease but with chronic obstructive lung disease.

Adult↗
PubMed1981

Effects of trapidil on musculature and vasculature of the dog trachea in situ.

In anesthetized dogs the trachea in situ was perfused with blood through the cannulated cranial thyroid arteries. The effects of trapidil on tracheal musculature and vasculature were assessed in comparison with those of isoproterenol and theophylline. All drugs were injected intra-arterially. Isoproterenol (0.03--0.3 microgram), trapidil (10--300 micrograms) and theophylline (30--300 micrograms) all produced an increase in tracheal blood flow (tracheal vasodilatation) and a decrease in the tracheal intraluminal pressure elevated by neostigmine (tracheal dilatation). In high doses the three drugs all produced maximal tracheal dilatation. Dose-response curves for tracheal vasodilatation to the three drugs were all parallel together, and trapidil was about 2700 time less potent than isoproterenol and about 3 times more potent than theophylline on a weight basis in producing tracheal vasodilatation. Dose-response curves for tracheal dilatation to the three drugs were also parallel together, and trapidil was about 880 times less potent than isoproterenol and about 3 times more potent than theophylline on a weight basis. When compared with isoproterenol, trapidil was about 3 times more effective on tracheal musculature than on tracheal vasculature, and theophylline resembled trapidil. The results suggest that trapidil can also be used as a bronchodilator.

Animals↗
PubMed1996

Pharmacokinetics of trapidil in patients with chronic liver disease.

The pharmacokinetics of trapidil were studied in 15 patients with chronic liver disease (12 with hepatic cirrhosis, 2 with alcoholic fatty liver, 1 with liver fibrosis). Trapidil was administered intravenously as a 100-mg bolus. Serum samples were analyzed for trapidil by means of high-performance liquid chromatography. Mean pharmacokinetic parameters were compared with those found in a previous study of 12 healthy volunteers. Total plasma clearance was decreased significantly in patients with hepatic cirrhosis (96 mL/ min versus 258 mL/min in healthy individuals and 252 mL/min in patients with noncirrhotic liver disease). No difference in clearance was observed between patients with compensated or decompensated cirrhosis, and portal hypertension did not affect this clearance of trapidil. It can be concluded that trapidil clearance is a parameter that is very sensitive to alterations in hepatic clearance caused by liver cirrhosis, and that the dosage of trapidil should be adjusted accordingly in such patients.

Adult↗
PubMed1981

Trapidil stimulation of slow Ca2+ current in cardiac muscle.

The effect of trapidil, a coronary vasodilator and positive inotropic agent (associated with elevated tissue cyclic AMP levels due to phosphodiesterase inhibition), was examined on the electrophysiological properties of cardiac muscle. Specifically, the trapidil was tested for its ability to induce slow action potentials (APs), and to affect the maximum upstroke velocity (+Vmax) of the slow APs in the ventricular myocardial cells of isolated perfused chick hearts. The effect of trapidil on the contractions accompanying the slow APs and on the tissue cyclic AMP levels was also examined. To study the slow channels exclusively, the fast Na+ channels were voltage-inactivated by elevated (25 mM) K+. In this condition of functional removal of the fast channels, the hearts could not be excited even by intense electrical stimulation. It was found that trapidil (10(-4)--10(-3) M) induced slow APs accompanied by contractions. Elevation of the trapidil concentration produced dose-dependent increases in +Vmax, dT/dt (first derivative of developed tension) and cyclic AMP. These effects of trapidil were not affected by propranolol, suggesting that they were not mediated by beta-adrenergic receptors. These results support the hypothesis that intracellular cyclic AMP levels regulate the number of available slow channels, thereby controlling contractile force in the heart muscle via the Ca2+ influx mediated by slow channels.

Action Potentials↗
PubMed1983

Antianginal drug trapidil (Rocornal) inhibits spreading of platelets and formation of surface-bound thrombi-like aggregates.

Effects of an antianginal drug trapidil (Rocornal) on platelet interaction with a surface coated with fibrillar calf skin collagen (CSC) have been studied by scanning electron microscopy. Gel filtered human platelets were incubated with the CSC substrate in the absence or in the presence of soluble inducers of platelet activity: arachidonic acid (AA), stable analogue of prostaglandin (PG) endoperoxides, U46619, and thrombin. In the absence of soluble inducers, trapidil does not alter the total number of adherent platelets. At the same time, trapidil inhibits the shape change of adherent platelets, induced by the CSC substrate, increasing the percentage of discoid and decreasing the percentage of spread platelets. It was demonstrated earlier (1) and in the present study that soluble inducers of platelet activity stimulate massive spreading of platelets and formation of surface-bound thrombi-like aggregates on the CSC substrate. Trapidil completely prevents the effects of the exogenous AA and U46619 on platelet-substrate interactions, but inhibits the AA-stimulated synthesis of thromboxane A2 (TXA2) in platelets by 40-50% only. Trapidil also blocks platelet aggregation in suspension, spreading and formation of surface-bound aggregates induced by low, but not high, concentrations of thrombin. Possible sites of trapidil action are discussed.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2004

Trapidil inhibits monocyte CD40 expression by preventing IFN-gamma-induced STAT1 S727 phosphorylation.

Trapidil is a triazolopyrimidine that has been found to prevent restenosis after vascular injury. Although its precise mode of action is still unclear, several biological effects have been described including inhibition of IFN-gamma-induced CD40 expression on monocytes. Herein, we investigated the molecular mechanisms by which Trapidil exerts this inhibitory action. First, we observed that the inhibition of CD40 expression is associated with the suppression of CD40 gene transcription, as demonstrated by a clear decrease of CD40 nuclear RNA (nRNA) levels and unchanged CD40 mRNA half-life. IFN-gamma-induced CD40 transcription has been shown to be mediated by STAT1alpha dimers (p91/p84) which, after nuclear translocation, bind to GAS elements present in the promoter of IFN-gamma responsive genes. Electrophoresis mobility shift assay (EMSA) with both STAT1 consensus and CD40 mGAS probes showed that Trapidil did not affect the DNA binding ability of STAT1 dimers. STAT1 dimerization and activation are conferred by upstream phosphorylation of two amino acid residues of the STAT1 protein. The subsequent studies on these two potential STAT1 phosphorylation sites (Tyr701, Ser727) revealed that Trapidil attenuated IFN-gamma-induced Ser727 but not Tyr701 phosphorylation. The inhibition of CD40 transcription by Trapidil could at least partially owing to the impaired Ser727 phosphorylation of STAT1, since IFN-gamma failed to trigger CD40 expression in U3A S727A cells, a cell line displaying a point mutation at the Ser727 site. Collectively, our results indicate that phosphorylation of STAT1 at the Ser727 site enhances CD40 transcription and that Trapidil might be used as a selective inhibitor that could differentially modulate STAT1 target genes.

CD40 Antigens↗
PubMed2006

Effects of trapidil on renal ischemia-reperfusion injury.

There is increasing evidence to suggest that reactive oxygen and nitrogen species play a role in the pathogenesis of renal ischemia-reperfusion (I/R) injury. This study was designed to determine the possible protective effects of trapidil treatment against oxidative and nitrosative tissue injury of kidney induced by I/R. A renal I/R injury was induced by a left renal pedicle occlusion by ischemia for 45 minutes, followed by 1 hour of reperfusion with contralateral nephrectomy in I/R and I/R + trapidil groups. Trapidil (8 mg/kg intravenously) was administrated immediately before reperfusion phase. At the end of the reperfusion period, rats were killed. Then, renal tissue samples were taken for biochemical analysis and histopathological evaluation, and blood samples were obtained to determinate serum urea, aspartate aminotransferase (AST), and tumor necrosis factor-alpha (TNF-alpha) levels. Ischemia-reperfusion injury caused significant increases in myeloperoxidase activity and malondialdehyde and 3-nitrotyrosine levels in renal tissue and elevated serum urea, AST, and TNF-alpha levels. In addition, severe deterioration of renal morphology was seen in the I/R group. Trapidil treatment significantly reduced in biochemical parameters, as well as serum urea, AST, and TNF-alpha levels. Furthermore, renal tissue injury was markedly attenuated with trapidil treatment. These data suggest that reactive oxygen species and reactive nitrogen species play a causal role in I/R-induced renal tissue, and trapidil has a renoprotective effect against oxidative and nitrosative kidney damage.

Animals↗
PubMed2004

Matrix metalloproteinase 2 is suppressed by trapidil, a CD40-CD40 ligand pathway inhibitor, in human abdominal aortic aneurysm wall.

BACKGROUND: The activation of inflammatory cells and the production of matrix metalloproteinases (MMPs) are important in the pathogenesis of abdominal aortic aneurysm (AAA). Previous studies have demonstrated that the antiplatelet agent trapidil has multiple actions, including suppression of MMP expression through the inhibition of the CD40-CD40 ligand (CD40-CD40L) pathway in cultured cells. A recent clinical study suggested that trapidil might have functions beyond its antiplatelet action. Methods and results In the present study, we performed immunohistochemical analysis and semiquantitative reverse transcription-polymerase chain reaction to evaluate the effect of trapidil on the production of MMPs in cultured aortic tissues from patients with infrarenal AAA (n = 9) and control patients with aortoiliac occlusive disease (n = 7). The tissue concentrations of both MMP-2 and MMP-9 were significantly higher in AAA walls than in control aortic walls. Both trapidil and an anti-CD154 (CD40L) antibody significantly suppressed the protein production and mRNA expression of MMP-2 but did not inhibit those of MMP-9 in organ cultures of AAA wall specimens. MMP-9 was produced by macrophages and a lot of neutrophils in AAA tissues, whereas MMP-2 was derived from macrophages. CD40 was expressed on macrophages but not on neutrophils, and this expression could explain the differential effect of trapidil on the production of MMP-2 and MMP-9. CONCLUSIONS: Trapidil, a CD40-CD40L pathway inhibitor, suppressed mRNA expression and protein production of MMP-2 in AAA tissues, suggesting a potential therapeutic approach for the prevention or treatment of AAA.

Aortic Aneurysm, Abdominal↗
PubMed2003

Effect of trapidil on cardiovascular events in patients with coronary artery disease (results from the Japan Multicenter Investigation for Cardiovascular Diseases-Mochida [JMIC-M]).

A large-scale study was conducted to assess the effect of long-term administration of trapidil on the prognosis of patients with angiographic evidence of coronary artery disease (CAD). A large-scale, multicenter study, the Japan Multicenter Investigation for Cardiovascular Diseases-Mochida was an open-label, randomized trial of 1,743 patients with CAD who were < or =70 years old and had angiographic evidence of >25% stenosis in any coronary artery. We randomly assigned the patients to receive medical treatment either with trapidil 100 mg 3 times daily (trapidil group, n = 873) or without trapidil (control group, n = 870). The mean follow-up period was 924 days. The incidence of cardiovascular events, including cardiac death, nonfatal myocardial infarction, angina pectoris/heart failure requiring hospitalization, and cerebrovascular events was 11.1% in the trapidil group and 14.9% in the control group (relative risk 0.75, 95% confidence interval 0.58 to 0.98, p = 0.036). Thus, long-term intervention with trapidil in CAD reduces the incidence of cardiovascular events and improves the prognosis of patients with CAD.

Angina Pectoris↗
PubMed2001

Effect of trapidil on effector functions of monocytes related to atherosclerotic plaque.

The infiltration and activation of inflammatory cells play an important role in the formation and stability of coronary atherosclerotic plaque in patients with acute coronary syndrome. In this study, we evaluated the effect of trapidil, an anti-platelet agent, on atheroma-related functions of human T cells and monocytes. Trapidil and anti-CD154 (CD40 ligand) antibody inhibited the increase of procoagulant activity in the mixed lymphocyte reaction; trapidil also suppressed the induction of tissue factor, monocyte chemoattractant protein-1 (MCP-1) and matrix metalloproteinase-9 in the mixed lymphocyte reaction. Trapidil did not alter CD154 expression on isolated T cells, but it diminished CD40 expression on isolated monocytes and human monocytic leukemia THP-1 cells stimulated with interferon-gamma. Moreover, trapidil reduced MCP-1 production of isolated monocytes and THP-1 cells stimulated with interferon-gamma plus CD154-transfected cells. This effect was not seen with other tested anti-platelet agents and coronary vasodilators. In conclusion, trapidil directly acts on monocytes/macrophages to lower their susceptibility to CD154 on T cells.

Animals↗
PubMed1999

Inhibitory effects of trapidil on PDGF signaling in balloon-injured rat carotid artery.

Trapidil, which was originally developed as an anti-platelet agent, is among the few agents thus far proven to be clinically effective in preventing restenosis after percutaneous coronary interventions. Trapidil was previously shown to inhibit platelet-derived growth factor (PDGF)-induced cellular responses in vitro in cultured cells. However, its mechanism of action is poorly understood. In this study, we investigated by using a rat carotid balloon-injury model whether and how trapidil inhibited the in vivo action of PDGF, which is regarded as a most important growth factor implicated in proliferation and migration of vascular smooth muscle cells. The combination of both oral and topical administration of trapidil reduced the intimal lesion size by more than 70% and nearly completely suppressed injury-induced increases in phosphotyrosine content of PDGF alpha- and beta- receptors of carotid artery. Moreover, trapidil was found to decrease mRNA levels of PDGF alpha- and beta- receptors strongly and of PDGF A- and B- chains moderately in injured arteries. These results indicate that trapidil potently suppresses the action of PDGF with inhibition of neointima formation in injured artery, which is mediated at least in part through decreasing the expression of both PDGF ligands and their receptors.

Angioplasty, Balloon↗
PubMed2003

Effects of trapidil on the healing of colonic anastomoses in an experimental rat model.

BACKGROUND: Trapidil has various properties including vasodilatation, inhibition of lipid peroxidation and platelet aggregation as well as, and reduction of, the inflammatory response to injury. The aim of the present study was to investigate the effects of trapidil on dexamethasone-impaired colonic anastomotic healing in an experimental rat model. METHODS: Twenty-four Wistar rats underwent colonic transsection and primary anastomosis. Rats were divided into four groups of six: group 1 (G1), control; group 2 (G2) trapidil, 8 mg/kg per day intravenously; group 3 (G3) dexamethasone, 0.1 mg/kg per day intramuscularly; and group 4 (G4) dexamethasone 0.1 mg/kg intramuscularly and trapidil 8 mg/kg intravenously per day, for 1 week. Anastomotic bursting pressure, hydroxyproline level, histopathological grading, malondialdehyde and nitrite/nitrate levels were determined. RESULTS: Dexamethasone-impaired anastomotic healing was found to be improved by trapidil administration in terms of anastomotic bursting pressure and hydroxyproline content (P = 0.026, and P = 0.017). In addition, histopathological examination revealed an increase in fibroblast proliferation and collagen deposition (P = 0.004, and P = 0.015) and a decrease in leucocyte infiltration (P = 0.004). Moreover, serum nitrite/nitrate and malondialdehyde levels decreased when G3 was compared to G4 (P < 0.001, P = 0.38). CONCLUSIONS: Trapidil may improve the dexamethasone-impaired anastomotic healing due to its preventive effects on inflammatory response and lipid peroxidation in rats.

Anastomosis, Surgical↗
PubMed1995

Trapidil inhibits endothelial cell proliferation and angiogenesis in the chick chorioallantoic membrane and in the rat cornea.

The effects of trapidil, a coronaro-active drug which has been shown to inhibit the mitogenic activity of platelet derived growth factor (PDGF), have been investigated on the proliferation of the human endothelial cells (HUV-EC-C), on the neovascularization in the chorioallantoic membrane of the chick embryo (CAM) as well as on the angiogenesis of rat cornea following chemical injury. The proliferation of HUV-EC-C in the presence of trapidil (25 and 250 micrograms/mL) was significantly inhibited by 19 and 25% respectively, compared to controls. On 2-days old CAMs, agarose disks containing 100-150 micrograms of trapidil produced an avascular zone indicating significant antiangiogenic activity, while control agarose disks were without effect. Corneal neovascularization was induced by applying a silver nitrate/potassium nitrate applicator to the rat eyes. A 6-day-treatment with eye drops of a solution of 10 mg/mL trapidil significantly decreased the rate of vessel growth compared with vehicle controls. The antiangiogenic activity of trapidil was markedly increased by the association with hydrocortisone (1.34 mg/mL). These results suggest that trapidil, alone or in combination with a steroid, could be a promising candidate for the therapy of corneal diseases in which alterations induced by neovascular growth play a substantial role.

Allantois↗