Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Trapidil”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMed1993

Effect of trapidil on serum lipid and apolipoprotein levels in patients with ischemic heart disease.

1. Serum total cholesterol (TCH), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein (LDL-C), atherosclerotic index (AI) and apolipoprotein (apo A-I, A-II, B, C-II, C-III and E) levels were investigated in patients with ischemic heart disease before and after medication of trapidil. 2. Twenty-one patients were orally given 100 mg of trapidil, three times daily (300 mg/day). After 8 weeks' administration, serum HDL-C level increased (P < 0.01) and AI decreased (P < 0.02) significantly, whereas TCH, TG and LDL-C levels tended to decrease but not significantly. 3. Among the parameters of apolipoproteins, apo A-I, a main protein of HDL-C, was significantly increased (P < 0.05) by trapidil. 4. These results indicate that trapidil has a beneficial effect on the coronary risk profile as reflected by lipid measurements.

Aged↗
PubMed2006

Trapidil decreases the aggregation of platelets from heart transplant recipients ex vivo.

Heart transplant recipients show platelet hyperaggregability, which may be related to the incidence of graft vasculopathy. We investigated whether trapidil can inhibit the aggregation of platelets from these patients. Platelet count, mean platelet volume (MPV), and adenosine diphosphate (ADP)-induced platelet aggregation were determined in 18 heart transplant recipients and 12 healthy subjects. Additionally, platelet-rich plasma from the patients was incubated with trapidil or with saline, prior to measuring ADP-induced aggregation. The MPV was significantly greater in patients compared to controls (9.4+/-1.1 vs 8.5+/-0.7 fL; P=.01), and ADP-induced platelet aggregation was significantly increased in patients compared to controls (81.2%+/-13.1% vs 69.6%+/-16.2%; P=.04, respectively). The trapidil-treated samples showed significantly decreased platelet aggregation compared to the control samples (24.2%+/-12.6% vs 66.7%+/-11.7%; P<.001). Platelets from heart transplant recipients showed an increased MPV and increased ADP-induced aggregation. Trapidil effectively reduced the ADP-induced aggregation ex vivo.

Adenosine Diphosphate↗
PubMed1998

Trapidil effects on intimal thickening and mRNA levels for platelet-derived growth factor A in human saphenous vein smooth muscle cells.

BACKGROUND: Platelet-derived growth factor (PDGF) A chain, basic fibroblast growth factor (bFGF), and tissue-type plasminogen activator (tPA) from smooth muscle cells (SMCs) have been postulated to initiate SMC proliferation and migration in the process of intimal thickening. OBJECTIVE: In this study we tested whether trapidil, which is reported to reduce intimal thickening, would suppress mRNA increases for all or only some of these genes in human SMC. METHODS: Cultured human saphenous vein SMCs made quiescent by 72-hour incubation in 0.5% serum were stimulated with 3U/mL alpha-thrombin +/- trapidil. Changes in mRNA transcript levels were analyzed by Northern blot. RESULTS: Trapidil decreased thrombin-induced mRNA levels for bFGF and appeared to decrease mRNA for PDGF-A chain, but not for tPA. CONCLUSION: These results suggest that trapidil may reduce intimal thickening at least partly via the suppression of increased bFGF and PDGF-A chain mRNA levels in vascular SMCs.

Autoradiography↗
PubMed1996

Trapidil modifies mesangial cell proliferation and collagen accumulation in anti-thymocyte serum (ATS)-induced glomerulonephritis.

This study was designed to assess whether the glomerular mesangial-cell proliferation and the increased extracellular matrix (ECM) accumulation that occur in anti-thymocyte serum (ATS)-induced glomerulonephritis (GN) are affected by Trapidil, a potent antagonist for platelet-derived growth factor (PDGF). Fifteen male Wistar rats were divided into three groups. In group I, GN was induced by injecting a single dose of ATS. In group II, rats were given a single dose of ATS followed by daily treatment with Trapidil. In group III, the rats (controls) were treated with a single dose of phosphate buffered saline. All the rats were killed on the 10th day of the experiment. ATS induced marked mesangial cell proliferation (P < 0.01) in group I rats and Trapidil treatment (group II) significantly suppressed such proliferation (P < 0.01). Increased type III and IV collagen immunolabelling was observed in the expanded mesangial matrix in group I rats. In group II, immunolabelling for type III and IV collagen was much less than in group I. The study suggests that Trapidil therapy is effective in suppressing both mesangial cell proliferation and mesangial matrix expansion by reducing collagen accumulation.

Animals↗
PubMed2002

Resolution of cerebral vasospasm with trapidil; an animal model.

Cerebral vasospasm and rebleeding are important clinical phenomena associated with a high mortality rate. Therefore, any promising finding in the laboratory deserves assessment in clinical practice. The present study was designed to examine the possible effects of trapidil on the basilar artery of the rabbit through a cerebral vasospasm model. This experimental study was carried out on 26 adult New Zealand albino rabbits of both sexes weighing 2.5-3.0 kg. A transclival exposure was performed. Vasospasm was produced by an intracisternal injection of autologous blood. After observation of the vasospasm, trapidil was locally applied in increasing concentrations (10(-5)-10(-4) M). The effect of each concentration was measured independently after 10 minutes for each application and was extended to three hours. Trapidil was shown to have a clear spasmolytic effect on the rabbit's basilar artery. These data suggest that trapidil can have a potential use in the treatment of patients suffering from cerebral vasospasm.

Animals↗
PubMedDate not supplied

Angiographic evaluation of the coronary vasodilating effect of trapidil in anesthetized closed-chest dogs.

We studied the effect of trapidil on coronary diameters of anesthetized closed-chest dogs using coronary angiography. Trapidil 2 mg/kg i.v. significantly (p less than 0.01) increased the diameter of the proximal (1.96 +/- 0.08 mm), middle (1.29 +/- 0.05 mm), and distal (0.86 +/- 0.03 mm) coronary arteries by 4.2 +/- 1.0, 7.6 +/- 1.2, and 10.8 +/- 2.2%, respectively. Nitroglycerin 20 micrograms/kg i.v. significantly (p less than 0.01) increased the diameter of classes I, II, and III arteries by 4.0 +/- 0.7, 7.7 +/- 1.3, and 7.5 +/- 1.8%, respectively. Ergonovine (0.4 mg i.v.; n = 13) reduced (p less than 0.01) the diameter of all three classes of coronary arteries by 8.2 +/- 1.2, 9.0 +/- 1.0, and 13.3 +/- 1.9%. After pretreatment with ergonovine, trapidil (n = 8) relaxed the coronary arteries from -10.4 +/- 1.7 to -2.4 +/- 1.7% constriction (p less than 0.05). These results indicate that in dogs trapidil dilates coronary arteries in a fashion similar to nitroglycerin and reverses ergonovine-induced coronary vasoconstriction.

Animals↗
PubMedDate not supplied

Reduction of myocardial infarct size by trapidil in anesthetized dogs.

We studied the effect of trapidil on acute experimental myocardial infarction in anesthetized, openchest dogs. The size of myocardial infarction 8 h after ligation of the left anterior descending coronary artery was determined by planimetry of myocardial slices stained by the nitroblue tetrazolium method. Systemic hemodynamic variables, epicardial ST-segment elevation, activity of serum creatine phosphokinase (CPK), and changes of myocardial blood flow in the ischemic area were measured. Infusion of 3 mg/kg trapidil reduced the size of infarction and ameliorated the infarction-induced deterioration of systemic hemodynamic variables, such as the decrease in left ventricular dP/dt, aortic blood flow, and regional endomyocardial blood flow in the ischemic area. This dose of trapidil also suppressed ST elevation and significantly inhibited the increase in activity of serum CPK. Hyaluronidase also reduced the size of infarction significantly. These results suggest that trapidil alters the course of acute myocardial infarction favorably, presumably by increasing regional endomyocardial blood flow.

Animals↗
PubMedDate not supplied

Suppression of mesangial-cell proliferation by trapidil in glomerulonephritis induced by anti-thymocyte serum in rats.

Trapadil (Mochida Pharmaceuticals, Japan), an antiplatelet drug, suppresses the growth of several cell types and is thought to antagonize platelet-derived growth factor. The effects of trapidil on mesangial-cell proliferation in glomerulonephritis induced by anti-thymocyte serum in Wistar rats were investigated. Control rats were treated with phosphate-buffered saline (group I); group II rats were injected with a single dose of anti-thymocyte serum (8 ml/kg body weight), and group III rats were treated with both a single dose of anti-thymocyte serum (8 ml/kg body weight) and with trapidil (5 mg/kg body weight/day). Three rats in each group were killed on day 3, and the other three on day 10. Control rats showed no significant histological changes on day 3 or day 10. In group II, on day 3, there was a marked decrease in glomerular cell numbers, with mesangiolysis. Histologically severe mesangial-cell proliferation with expansion of mesangial areas was noted on day 10. None of the rats in group III showed mesangial alterations, histologically, indicating that mesangial-cell proliferation was suppressed by trapidil. This suppression may result from antagonism of the binding of platelet-derived growth factor to the specific surface receptors in the mesangial cells. Trapidil may have clinical value in the treatment of mesangial-cell proliferative glomerular diseases.

Animals↗
PubMed2003

Triazolopyrimidine (trapidil), a platelet-derived growth factor antagonist, inhibits parathyroid bone disease in an animal model for chronic hyperparathyroidism.

Parathyroid bone disease in humans is caused by chronic hyperparathyroidism (HPT). Continuous infusion of PTH into rats results in histological changes similar to parathyroid bone disease, including increased bone formation, focal bone resorption, and severe peritrabecular fibrosis, whereas pulsatile PTH increases bone formation without skeletal abnormalities. Using a cDNA microarray with over 5000 genes, we identified an association between increased platelet-derived growth factor-A (PDGF-A) signaling and PTH-induced bone disease in rats. Verification of PDGF-A overexpression was accomplished with a ribonuclease protection assay. Using immunohistochemistry, PDGF-A peptide was localized to mast cells in PTH-treated rats. We also report a novel strategy for prevention of parathyroid bone disease using triazolopyrimidine (trapidil). Trapidil, an inhibitor of PDGF signaling, did not have any effect on indexes of bone turnover in normal rats. However, dramatic reductions in marrow fibrosis and bone resorption, but not bone formation, were observed in PTH-treated rats given trapidil. Also, trapidil antagonized the PTH-induced increases in mRNA levels for PDGF-A. These results suggest that PDGF signaling is important for the detrimental skeletal effects of HPT, and drugs that target the cytokine or its receptor might be useful in reducing or preventing parathyroid bone disease.

Animals↗
PubMed1987

Trapidil does not affect serum levels and cardiotonic action of digoxin in healthy humans.

The influence of trapidil on serum levels and cardiac effects of digoxin was investigated in 10 healthy men, intraindividually compared with placebo. Each subject took digoxin orally for 9 days (0.375 mg daily on days 1 to 8, 0.25 mg on day 9) either combined with trapidil (400 mg daily on days 1 to 8, 200 mg on day 9) or combined with placebo in a cross-over design. Trapidil failed to change significantly the steady-state serum digoxin concentrations on day 9 of treatment. It did also not alter significantly the following digoxin effects: shortening in QS2c time indicating the cardiotonic digoxin effect, shortening in QTc time, increase in PTQ index. But trapidil prevented the negative chronotropic digoxin effect.

Adult↗
PubMed1986

[Effect of trapidil on neuropathy in diabetic mice].

Long term oral administration of trapidil at the doses of 20 and 60 mg/kg/day restored the decrease in motor nerve conduction velocity in genetically diabetic mice (C57BL/KsJ db+/db+). Trapidil also suppressed the increase in sorbitol content and the decrease in myoinositol content in the sciatic nerve. The elevation of serum total cholesterol level and the decrease in the ratio of serum HDL-cholesterol level to total cholesterol level were suppressed by trapidil. The blood glucose level and the serum triglyceride level were not affected by the drug administration. These results suggest that trapidil may restore the decrease in nerve conduction velocity in diabetic mice through amelioration of the metabolite abnormalities in nerve and microcirculatory disorders.

Animals↗
PubMed1983

Improvement by trapidil of cardiac function of the dog heart-lung preparation depressed by pentobarbital.

The effect of trapidil on depressed cardiac function was investigated in 5 dog heart-lung preparations. Trapidil at a dose of 60 mg improved cardiac function which had been severely depressed by 70 +/- 32 (S.D.) mg of sodium pentobarbital. This dose of trapidil, however, produced no significant increase in heart rate. The results suggest that trapidil would be useful in the treatment of heart failure.

Animals↗
PubMed2005

Trapidil, an inhibitor for phosphodiesterase and platelet-derived-growth factor, ameliorates corrosive esophageal burn in rats.

Corrosive esophageal burn is a common health problem in the pediatric age group and causes serious esophageal injuries. The medical treatment in acute phase of corrosive esophageal injury is of particular importance for prevention of esophageal stricture. We therefore aimed to investigate the possible beneficial effect of trapidil (triazolopyrimidine), an inhibitor for phosphodiesterase and platelet-derived-growth-factor, during acute phase of esophageal corrosive injury. Wistar albino rats were randomly allocated to untreated, treated, and sham-operated groups (n = 10 for each group). Corrosive esophageal burn was generated with 10% NaOH solution. The rats were left untreated (untreated group) or treated with trapidil as a single dose of 40 mg/kg intraperitoneally after one hour of the injury (treated group). Abdominal esophageal segment was isolated and tied in sham-control group. The studied esophageal segment was removed from each animal after 24 hours. Malondialdehyde (MDA) and nitric oxide (NO) levels were measured in the esophageal tissues. The ulcer depth was graded by histopathologic examination. MDA and NO levels were significantly higher in the untreated group than in the treated group. Namely, trapidil treatment significantly decreased MDA and NO levels in the injured tissues, the levels of which are similar to those in the tissues of control animals. The grades of ulcer depth were significantly improved in the treated group. These results indicate that the reactive oxygen radicals increase in the early phase of corrosive esophagitis and cause tissue damage. We suggest that trapidil treatment may be useful in acute phase of corrosive esophageal injury.

Animals↗
PubMed1990

[Oral trapidil treatment of Fontaine stage II arteriosclerotic circulatory disorders of the legs--a double-blind study].

In a double blind study altogether 41 patients with obliterating arteriosclerosis at stage II after Fontaine have been treated for 26 weeks either with 3 X 100 mg Trapidil (Rocornal) daily or placebo. In the second half of the study under Trapidil in contrast to placebo a clinically relevant additional increase of the distance of the intermitent claudication was the result. On the other hand, the plethysmographically measured reserve of the arterial blood supply did not show any changes in the two groups. A specific influence of Trapidil on the lipoprotein metabolism is apparently not present, since there appeared favourable influence on the hyperlipoproteinaemia diagnosed in 37 out of 41 patients both under placebo and under Trapidil.

Aged↗
PubMed1986

[Is there a renaissance for trapidil?].

In a survey experimental and clinical investigations on Trapidil (Rocornal) are briefly demonstrated. The great number of recent investigations, particularly by Japanese authors, render it necessary anew to think over the application of Trapidil in the GDR. Apart from possibilities of the treatment of the ischaemic heart disease, the survey shows further possible indications, such as inhibitions or the aggregation of thrombocytes, improvement of the microcirculation and treatment of hyperlipidaemias. It was made evident that Trapidil induces no steal phenomenon and thus a restriction as an antianginal pharmacon it not justified. A renaissance for Trapidil indicates itself.

Angina Pectoris↗
PubMed1985

Acute haemodynamic effects of intravenous administration of trapidil in man.

In 6 patients affected by coronary artery disease, undergoing right and left heart catheterization, under resting conditions and after intravenous injection of 100 mg trapidil, the following haemodynamic parameters were recorded: heart rate, cardiac output, right atrial pressure, pulmonary artery pressure, capillary wedge pressure, aortic and left ventricular pressure. Furthermore, left ventricular angiography was performed before and after trapidil administration and the end-diastolic and systolic images were digitized on a computer. After administration of trapidil, an increase of the heart rate, a significant decrease of the systemic systolic pressure and of the pulmonary artery pressure together with a reduction of the systemic and pulmonary vascular resistances were noticed. Even end-diastolic volume and end-diastolic pressure significantly decreased. The results point out a remarkable effect of trapidil on the peripheral and pulmonary circulation.

Aged↗
PubMed1981

Difference in site and time course of coronary dilating effects of trapidil, nitroglycerin and dipyridamole in anesthetized dogs.

Effects of trapidil, a non-nitrate type coronary vasodilator, nitroglycerin and dipyridamole on epicardial coronary diameter and total coronary resistance were studied in anesthetized open-chest dogs. The epicardial coronary diameter of the left circumflex coronary artery was measured by sonomicrometry and total coronary resistance was calculated by aortic pressure and coronary blood flow. Intravenous administration of Trapidil, as well as nitroglycerin, produced transient decreases in total coronary resistance followed by sustained dilation of the large coronary artery. Dipyridamole increased coronary blood flow by 2.7-fold, whereas diameter of the large coronary artery decreased along with the reduction of aortic pressure. The first peak of the biphasic increases in coronary blood flow and subsequent dilation of the large coronary artery appeared after an i.v. bolus administration of trapidil or nitroglycerin and remained even after beta adrenergic blockade. Intracoronary administration of either drug produced monophasic increases in coronary blood flow along with subsequent dilation of the large coronary artery. Thus, trapidil, like nitroglycerin, directly dilates the large and small coronary arteries.

Animals↗
PubMed1982

Effect of trapidil on regional myocardial function during acute coronary occlusion in the dog.

The effects of an antianginal agent, N,N-diethyl-5-methyl[1,2,4]triazolo[1,5-a]pyrimidine-7-amine (trapidil, Rocornal) (5-10 mg/kg), on regional myocardial function were studied in 17 open-chest dogs. The animals were instrumented with a micromanometer for measurement of left ventricular pressure, an electromagnetic flow probe around the left circumflex coronary artery, and 3 pairs of ultrasonic crystals in control, marginal and ischemia-induced segments. In cases of an intact coronary artery, trapidil increased peak dP/dt by 48%, heart rate by 19%, and coronary blood flow by 40%. End-diastolic segment length decreased by 7% with an increase of 17% in shortening. Coronary occlusion increased end-diastolic length of all three segments. In the ischemic segment, active shortening was rapidly replaced by systolic expansion. In the marginal segment, percent shortening decreased by 58%, while in the control segment, shortening was augmented by 11%. Trapidil administered during coronary occlusion significantly improved the shortening of control and marginal segments, as associated with a reduction in end-diastolic length. There was no significant change in function of the ischemic segment. These effects of tripidil during coronary occlusion were not blocked by propranolol (0.5-1.0 mg/kg). These data suggest that trapidil may be an effective treatment for left ventricular failure due to myocardial ischemia by virtue of its potent positive inotropic effects associated with substantial increases in myocardial blood supply sufficient to counteract the increase in oxygen consumption.

Acute Disease↗