Antiplatelet Drugs, Controlled by Platelet Survival

1979 ◽  
Author(s):  
G. Bremer ◽  
O. Richter ◽  
E. Jacobi

The mean Platelet survival is an in-vivo parameter in the analysis of platelet function. Thromboembolic diseases are associated with shortened platelet survival, because platelets are consumed in the thrombus generanation. Platelet survival therefore is an parameter for controlling the effectiveness of antiplatelet drugs. In order to investigate the effect of several antiplatelet drugs, platelet survival is measured in Patients suffered from long-standing diabetes mellitus with secondary complications with and without the following antiplatelet drugs: 3 times of 500 mg per day SH 1117 (Sulfinylaceticacidemethylester), 3 times of R 149 per day (75 mg Dipyridamole + 330 mg Acetyl-Salicylic-Acid) and a third group treated with 3 times per day 150 mg Anturano + 150 mg Dipyridamole. The shortened platelet survival in Diabetes mellitus can be normalized by R 149, whilest SH 1117 increases the platelet survival only moderately. Under the treatment with Anturano combined with Dipyridamole platelet survival is prolonged, but not normalized.

1981 ◽  
Author(s):  
G Bremer ◽  
O Richter ◽  
E Jacobi ◽  
T Koschinsky

It is well kown that microangiopathy is associated with shortened platelet survival. Therefore a pilot study was performed to test several antiplatelet drugs with respect to their ability to increase platelet survival. The study was confined to 18 patients with long standing Diabetes mellitus and microangiopathv of I.- II. degree, exhibiting platelet survival times less than 7 days. The patients were treated with antiplatelet drugs. Dipyridamole with several combination of Acetylsali- cylicacid (ASA) and Sulfinpyrazon.1. 225 mg Dipyridamole and 990 mg ASA per day, 2. 225 mg Dipyridamole and 300 mg ASA per day, 3. 150 mg Dipyridamole and 150 mg Sulfinpyrazon per day.Platelet survival was determined by the method described by Harker. The resultant survival curves were analysed by a computer program written by Murphy and Francis which is based on the multine hit model for platelet survival.The results of the study are: After 10 days treatment the platelet survival was markedly increased under each of the combination.If one assumes that there exists a causal relationship between microangiopathy and platelet survival,a long-term treatment by antiplatelet drugs may be a prophylaxis against microangiopathy in diabetics.


2017 ◽  
Vol 17 (1) ◽  
pp. 47
Author(s):  
Wahyu Dewi Tamayanti ◽  
Ratna Megawati Widharna ◽  
Catherine Caroline ◽  
Bambang Soekarjo

The new compounds of salicylic acid derivatives, 2- (3- (chloromethyl) benzoiloksi)benzoic acid and 2-(4-(chloromethyl)benzoiloksi) benzoate was synthesized to produce a greater analgesic activity and lower stomach irritation from salicylic acid. 2-(4-(chloromethyl) benzoiloksi)benzoic acid and 2-(3-(chloromethyl)benzoiloksi) benzoate was synthesized by Schotten-Baumann acylation reaction. In this study, the analgesic test activity with plantar test method. The compound was given to test animals in doses of 12.5; 25; 50; 100; and 200 mg.kg-1. Analgesic activity was determined by the response time of mice to pain infra-red heat. The percentage is calculated by the mean pain barrier time response to pain. The results showed percentation of pain barrier: 74.28%; 105.58%; 110.58%; 115.29%; and 175.87% after administration of the compound 2-(4-(chloromethyl) benzoiloksi) benzoate at doses of 12.5; 25; 50; 100; and 200 mg.kg-1, respectively. The results of calculations percent pain barrier 2-(3-(chloromethyl)benzoiloksi) benzoate, obtained 85.30%; 92.48%; 124.96%; 180.36%; and 208.01% consecutive for the doses compound of 12.5; 25; 50; 100; and 200 mg.kg-1. Five doses of acetyl salicylic acid ranging from 12.5 mg. kg-1 to 200 mg.kg-1 resulted in percent pain barrier as follows: 26%; 34.34%; 45.68%; 60.38% and 114.12%. This study indicates that 2-(3-(chloromethyl)benzoiloksi)benzoic acid and 2-(4-(chloromethyl)benzoiloksi) benzoate are capable of producing higher analgesic activity than acetyl salicylic acid. Keywords: analgesic, benzoate, plantar test method 


1985 ◽  
Vol 53 (02) ◽  
pp. 260-263 ◽  
Author(s):  
A Boneu ◽  
P Sié ◽  
R Bugat ◽  
C Caranobe ◽  
M Eber ◽  
...  

SummaryA simultaneous investigation of platelet regeneration time (PRT) based upon malondialdehyde (MDA) recovery after a single oral intake of 500 mg of aspirin and of platelet survival time (PST) after labelling with 51chromium or 111Inindium oxine was performed in 25 cancerous patients. A pilot study conducted with 9 healthy volunteers demonstrated that the MDA assay was highly reproducible and specific for the platelet cycloxygenase activity. The pattern of MDA recovery after aspirin ingestion was linear in the healthy volunteers and in the patients presenting both a normal and an accelerated platelet turnover. PST were calculated using the four mathematical models recommended by the International Committee for Standardization in Hematology; the best fit was given by the multiple hit model in 22 cases and by the linear regression model in 3 cases. The mean results obtained in the patients investigated with the 51chromium were consistently shorter than those obtained in the patients investigated with the mindium oxine while the mean PRT were almost identical in the two groups. An excellent correlation between PRT and PST was observed after 111Indium oxine labelling and using the weighted mean method for PST determination. These results suggest that the 111Indium oxine technique is a better method for platelet labelling and that the results provided by the weighted mean method reflect more closely the in vivo platelet turnover than those provided by the multiple hit model.


1976 ◽  
Vol 9 (5) ◽  
pp. 467-471 ◽  
Author(s):  
Alan I. Fleischman ◽  
Marvin L. Bierenbaum ◽  
Arleane Stier ◽  
Helen Somol ◽  
Portia B. Watson

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Rajeshwary Ghosh ◽  
Sarbashri Bank ◽  
Rabindra Bhattacharya ◽  
Nighat N. Khan ◽  
A. Kumar Sinha

The effect of dermcidin isoform 2 (dermcidin), an environmentally induced stress protein, was investigated on the genesis of diabetes mellitus and hypertension, the two major atherosclerotic risk factors. The role of dermcidin as an atherosclerotic risk factor related to the impaired systemic insulin level was investigated. Dermcidin was prepared by electrophoresis using plasma from the subjects with acute ischemic heart disease. Injection of 0.2 μM dermcidin in mice increased the blood glucose level from98±2.45 mg/dL to350 ±10.2 mg/dL which was normalized by the oral administration of acetyl salicylic acid (aspirin) after 24 h. Hypertensive subjects with systolic and diastolic blood pressure of 165 mm and 95 mm of Hg, respectively, had plasma dermcidin level of 95 nM. Ingestion of acetyl salicylic acid (aspirin) (150 mg/70 kg body weight) decreased the systolic and diastolic pressures to 125 mm and 80 mm of Hg, respectively, with decrease of dermcidin level to 15 nM. Incubation of kidney cortex cells with 0.2 μM dermcidin-inhibited synthesis of (r)-cortexin, an antihypertensive protein, and the basal (r)-cortexin level was reduced from 33 nM to 15 nM. Addition of 25 μunits of insulin/mL was found to reverse the inhibition of cortexin synthesis. The effect of dermcidin as a diabetogenic and a hypertensive agent could be controlled either by aspirin or by insulin.


1967 ◽  
Vol 126 (1) ◽  
pp. 171-188 ◽  
Author(s):  
M. A. Packham ◽  
E. S. Warrior ◽  
M. F. Glynn ◽  
A. S. Senyi ◽  
J. F. Mustard

Sulfinpyrazone and phenylbutazone block the aggregating action of collagen, antigen-antibody complexes, and gamma globulin-coated surfaces on blood platelets. These drugs do not block the action of ADP or thrombin. Inhibition of surface-induced aggregation appears to be the result of a decreased response of the platelets to surface stimuli, giving rise to diminished release of platelet constituents, such as ADP and serotonin. The intravenous infusion of these drugs produced results similar to those found in the in vitro experiments. Administration of phenylbutazone in doses sufficient to produce marked suppression of the platelet-collagen reaction impaired hemostatic plug formation at the ends of transected mesenteric vessels in rabbits. Since platelet function is considered a factor influencing platelet survival, the effect of phenylbutazone on platelet survival was examined. It was found that phenylbutazone prolonged platelet survival to more than twice the normal time and reduced platelet turnover by nearly 50%. These studies show that drugs which suppress platelet response to surface stimuli alter platelet function in vivo.


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