Suppression Of Platelet Aggregation By A New Beta-Adrenergic Blocker

1981 ◽  
Author(s):  
M Small ◽  
J T Douglas ◽  
Morna Orr ◽  
G D O Lowe ◽  
C D Forces ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Blood Viscosity ◽  
Beta Blockers ◽  
Protective Action ◽  
Plasma Viscosity ◽  
Significant Inhibition ◽  
Variable Effect ◽  
Adrenergic Blocker ◽  
Artery Disease ◽  
Long Acting

Beta-blockers have been reported to have a variable effect on a number of haemostatic parameters. In view of their possible protective action in coronary artery disease, we studied the effect of the new long-acting beta-blocker, carteolol, on platelet function, coagulation and blood viscosity in 10 healthy male volunteers. Following carteolol (5 mg. orally) blood was taken at 2, 5 and 24 hours and we were able to demonstrate a significant inhibition of platelet aggregation to ADP, adrenaline and collagen (p< 0.05) at 5 hours post ingestion, but not at 2 or 24 hours. Platelet release as measured by plasma levels of beta-thromboglobulin, platelet count, fibrinopeptide A, whole blood viscosity and plasma viscosity was also unaltered.

Takotsubo cardiomyopathy: a novel beta-adrenergic blocker withdrawal syndrome

2013 ◽  
Vol 154 (7) ◽  
pp. 267-271 ◽  
Author(s):  
János Tomcsányi ◽  
Kinga Jávor ◽  
Hrisula Arabadzisz ◽  
András Zsoldos ◽  
Vince Wagner ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Takotsubo Cardiomyopathy ◽  
Cardiac Dysfunction ◽  
Drug Withdrawal ◽  
Beta Blockers ◽  
Stress Cardiomyopathy ◽  
Abrupt Withdrawal ◽  
Adrenergic Blocker ◽  
Artery Disease ◽  
Long Acting

The authors describe two cases of takotsubo cardiomyopathy developing after an abrupt withdrawal of carvedilol and bisoprolol. Takotsubo or stress cardiomyopathy is characterized by acute and reversible cardiac dysfunction without coronary artery disease. It is triggered by acute emotional or physical stress, drugs or drug withdrawal. The immediate discontinuation of the long acting vasodilator beta-blocker, carvedilol has not yet been described to cause takotsubo cardiomyopathy. The authors recommend cautious withdrawal of beta-blockers. Orv. Hetil., 2013, 154, 267–271.

scholarly journals UPLC-Q-TOF/MS-Based Plasma Metabolomics to Evaluate the Effects of Aspirin Eugenol Ester on Blood Stasis in Rats

Molecules ◽  
2019 ◽  
Vol 24 (13) ◽  
pp. 2380 ◽  
Author(s):  
Dongshuai Shen ◽  
Ning Ma ◽  
Yajun Yang ◽  
Xiwang Liu ◽  
Zhe Qin ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Blood Viscosity ◽  
Metabolic Profile ◽  
Blood Stasis ◽  
Thromboxane A2 ◽  
Plasma Viscosity ◽  
Inhibit Platelet Aggregation ◽  
Underlying Mechanisms ◽  
Aspirin Eugenol Ester ◽  
Metabolomic Study

Aspirin eugenol ester (AEE) is a novel compound that is formed from the esterification of aspirin (acetylsalicylic acid (ASA)) and eugenol. This study aimed to investigate the effects of AEE on blood stasis in rats and to characterize the underlying mechanisms using a plasma metabolomic study. The results indicate that AEE and ASA could modulate whole blood viscosity (WBV), plasma viscosity (PV), blood coagulation parameters, platelet count, platelet aggregation, lactate dehydrogenase (LDH), creatinine (CR) and the levels of thromboxane A2 (TXA2) and 6-keto prostaglandin F1α (6-keto-PGF1α). The metabolic profiles of the plasma samples from all groups were clearly separated in the score plots. Nineteen potential metabolites were selected and identified, and disordered levels of these metabolites could be regulated by AEE and ASA. Pathway analysis showed that the mechanism of action of AEE on blood stasis might be principally related to the metabolism of amino acid, fatty acid, energy and glycerophospholipid. The above results indicate that AEE protected the rats against blood stasis, and that this effect might have been caused by the anticoagulation activity of AEE and its abilities to maintain a balance between TXA2 and PGI2, reduce blood viscosity, inhibit platelet aggregation and normalize the plasma metabolic profile.

P6374Effectively treated hypertension: secrets of blood rheology

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
O Svirida ◽  
F T Ageev ◽  
N V Fgeeva ◽  
M D Smirnova ◽  
Z N Blankova ◽  
...  
Keyword(s):  
Blood Viscosity ◽  
Independent Predictor ◽  
Beta Blockers ◽  
Blood Rheology ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Plasma Viscosity ◽  
Angiotensin Ii Receptor ◽  
Rotational Viscometer ◽  
Converting Enzyme Inhibitors ◽  
Hypertensive Patients

Abstract Background The contributions of the effectively treated hypertension on blood viscosity remain unclear, as well as impact of clinical and demographic parameters, biochemical variables, level of anxiety. Aim Aim of the study is to research viscosity state in patients with effectively treated hypertension and to reveal factors affecting blood viscosity. Materials 58 treated hypertensive patients (36 females and 24 males aged 62,9±9,7 years) with achievement of target blood pressure (BP) level (systolic BP was 130,9 (126,6; 135,4), diastolic BP - 81,4 (79,7; 83,1) mmHg. 71.7% of patients were treated with beta-blockers, 46.7% - angiotensin converting enzyme inhibitors (ACE inhibitors), 31.7% - angiotensin II receptor blockers, 38.3% - calcium channel antagonists, 18.3% - diuretics, 71.3% - statins, 60% - acetylsalicylic acid. Coronary heart disease (CHD) were presented in 24 (40%). The average cholesterol level was 5.11 (4.76; 5.46) mmol/l, creatinine 71.83±12.6 mmol/l, sodium 143.4 (143.0; 143.9) mmol/l. The level of anxiety disorders determined on Sheehan's Patient-Rated Anxiety Scale (SPRAS) was 33.7 (23.1; 39.2) points. Methods Whole blood viscosity at high (η1) and low (η2) shear rates, plasma viscosity (ηpl) were measured by a rotational viscometer. Aggregation of erythrocytes (η2/ η1) was studied also. The statistical analysis was carried out by nonparametric method of Spearman and multivariate regression analysis with STATISTICA 6. Results Hemorheological profile was as follows: η1 4,7 (4,7; 5,0) sec–1, η 2 24,6 (23,5; 26,5) sec–1, η2/η 1 5,4 (4,9; 5,3), η pl 1,52 (1,51; 1,55) sec–1. Blood viscosity in men was higher than in women in all indices studied: η1 5,4 (5,1; 5,7) sec–1 in men vs 4,6 (4,6; 5,0) sec–1 in women (p<0,001), η 2 28,6 (26,0; 31,9) sec–1 vs 23,0 (21,6; 25,8) sec–1 (p=0,004), η2/η1 - 5,3 (5,1; 5,6) vs 4,9 (4,7; 5,2) (p=0,03) respectively. It was revealed η1 correlation with patient growth (r=0,468, p=0,001), η2 –with creatinine (r=0,551, p=0,001) and sodium (r=0,488, p<0,001) level. η2 /η1 positively correlated with the level of creatinine (r=0,383, p 0,04), sodium (r=0,543, p=0,0001), and with the level of anxiety as well (r=0,374, p=0,01). The level of anxiety is defined as an independent predictor of η2/η1 in the model including gender, age, creatinine, sodium, anxiety level. In patients treated with an ACE inhibitor η2/η1 was higher compared to patients who were not prescribed: 5,3 (4,6; 5,2) vs 5,0 (5,0; 5,5), (p=0,04). However, a multivariate analysis showed a loss of the prognostic value of antyhypertesive treatment (in model included gender, age, height, creatinine, sodium). Blood viscosity does not depend on the level of total cholesterol, the presence of CHD. Conclusion In effectively treated hypertensive patients the level of anxiety, indirectly reflected the activity of the sympatho-adrenal system, proved to be an independent predictor of a higher value of η2/η1.

The Effects of KBT-3022, a New Anti-platelet Agent, on Hemorheological Properties in Guinea Pigs

1995 ◽  
Vol 73 (01) ◽  
pp. 118-121 ◽  
Author(s):  
Noriko Yamamoto ◽  
Koichi Yokota ◽  
Akira Yamashita ◽  
Minoru Oda
Keyword(s):  
Shear Stress ◽  
Blood Viscosity ◽  
Guinea Pigs ◽  
Direct Action ◽  
Plasma Viscosity ◽  
Fibrinogen Concentration ◽  
Anti Platelet Agent ◽  
Blood Filterability ◽  
2,3 Dpg ◽  
Rbc Deformability

SummaryUsing guinea pigs, a study was conducted on the effects of KBT-3022, a new anti-platelet agent, on hemorheological properties in various tests including blood filterability, blood viscosity, shear stress-induced red blood cell (RBC) deformability and contents of ATP and 2,3-diphosphoglycerate (2,3-DPG). Oral administration of KBT-3022 at 1 and 10 mg/kg significantly increased blood filterability, and significantly reduced blood viscosity at 10 mg/kg without changing the hematocrit, plasma fibrinogen concentration or plasma viscosity. KBT-3022 (10 mg/kg, p.o.) improved RBC deformability in response to shear stress, which was evoked by passing the blood through a thin tube. This dose of KBT-3022 also increased the contents of ATP and 2,3-DPG in RBC. These findings indicate that KBT-3022 may reduce blood viscosity as a sequel to improvement of RBC deformability through direct action on RBC. The increase in the intracellular levels of ATP and 2,3-DPG was considered to be involved in this improvement of hemorheological properties. These hemorheological effects of KBT-3022 appear to be promising for the treatment of patients with ischemic vascular disease.

The Effects of Acute Smoking on Platelet Behaviour, Fibrinolysis and Haemorheology in Habitual Smokers

1984 ◽  
Vol 51 (01) ◽  
pp. 006-008 ◽  
Author(s):  
J J F Belch ◽  
B M McArdle ◽  
P Burns ◽  
G D O Lowe ◽  
C D Forbes
Keyword(s):  
Platelet Aggregation ◽  
Factor Viii ◽  
Plasminogen Activator ◽  
Arterial Thrombosis ◽  
Plasma Viscosity ◽  
Red Cell ◽  
Cell Deformability ◽  
Red Cell Deformability ◽  
Cigarette Smokers ◽  
Smoking Group

SummaryThere is an increased frequency of arterial thrombosis in cigarette smokers. The changes in blood coagulation seen in these subjects have been studied by many workers but results have not always been in agreement. We wished to study the effects of acute .smoking on platelet behaviour, fibrinolysis and haemorheology in ten habitual smokers, and to compare these results with nonsmoking controls. Results show that the smoking group had higher plasma fibrinogen (p <0.04), lower plasminogen (p <0.02) and plasminogen activator (p <0.05), and higher plasma viscosity (p <0.003). The changes seen in cigarette smokers after smoking three cigarettes were an increase in the rate of platelet aggregation to ADP (p <0.02), an increase in α2M, (p <0.02), and factor VIII RAG (p <0.05). Plasma viscosity was decreased (p <0.02) as was red cell deformability (p >0.02).We confirm an increased tendency to hypercoagulability in smokers compared to controls which becomes more pronounced immediately after smoking three cigarettes.

Inhibition of Platelet Function by Antiarrhythmic Drugs, Verapamil and Disopyramide

1982 ◽  
Vol 47 (02) ◽  
pp. 150-153 ◽  
Author(s):  
P Han ◽  
C Boatwright ◽  
N G Ardlie
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Antiarrhythmic Drugs ◽  
Adenosine Diphosphate ◽  
Inhibitory Effect ◽  
Second Phase ◽  
Ionophore A23187 ◽  
High Concentrations ◽  
Artery Disease

SummaryVarious cardiovascular drugs such as nitrates and propranolol, used in the treatment of coronary artery disease have been shown to have an antiplatelet effect. We have studied the in vitro effects of two antiarrhythmic drugs, verapamil and disopyramide, and have shown their inhibitory effect on platelet function. Verapamil, a calcium channel blocker, inhibited the second phase of platelet aggregation induced by adenosine diphosphate (ADP) and inhibited aggregation induced by collagen. Disopyramide similarly inhibited the second phase of platelet aggregation caused by ADP and aggregation induced by collagen. Either drug in synergism with propranolol inhibited ADP or collagen-induced platelet aggregation. Disopyramide at high concentrations inhibited arachidonic add whereas verapamil was without effect. Verapamil, but not disopyramide, inhibited aggregation induced by the ionophore A23187.

Blood Viscosity and Platelet Aggregation in Male and Female Patients with Transient Ischaemic Attacks (TIA)

1979 ◽  
Author(s):  
G. Palareti ◽  
M. Poggi ◽  
G. Fortunato ◽  
S. Coccheri
Keyword(s):  
Platelet Aggregation ◽  
Blood Viscosity ◽  
Indirect Evidence ◽  
Vascular Lesions ◽  
Transient Ischaemic Attacks ◽  
Group A ◽  
Circulating Platelet Aggregates ◽  
Male Patients ◽  
Group B ◽  
Almost All

A series of 40 patients with TIA (25 males and 15 females) was thoroughly investigated by means of angiography and computerized tomography, and divided into a group (A) of 15 “sine materia”, and a group (B) of 25 with direct or indirect evidence of vascular occlusive or stenotic changes. Blood viscosity at 230 sec-1 37° was cp 4.2 ± 0.3 in the controls, cp 4.7 ± 0.7 in all patients (p < 0.05) cp 4.98 ± 0.7 in all male patients (p < 0.01 versus male controls), and cp 4.75 ± 0.8 in group B (p < 0.02). Haematocrit and Fibrinogen were also significantly increased in all male patients and in group B. Circulating platelet aggregates (CPA) were increased in 40% of the patients. Almost all patients with elevated CPA were males, with a slight prevalence in group B. Changes in blood viscosity parameters and in platelet aggregation in TIA patients were therefore related both to evidence of vascular lesions, and to sex, since they were found to prevail in male patients of both groups.

Dipyridamole Inhibits Platelet Aggregation in Whole Blood

1983 ◽  
Vol 50 (04) ◽  
pp. 852-856 ◽  
Author(s):  
P Gresele ◽  
C Zoja ◽  
H Deckmyn ◽  
J Arnout ◽  
J Vermylen ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Whole Blood ◽  
Ex Vivo ◽  
Platelet Rich Plasma ◽  
Significant Negative Correlation ◽  
Significant Inhibition ◽  
Oral Drug ◽  
Human Blood Samples ◽  
Induced Aggregation

SummaryDipyridamole possesses antithrombotic properties in the animal and in man but it does not inhibit platelet aggregation in plasma. We evaluated the effect of dipyridamole ex vivo and in vitro on platelet aggregation induced by collagen and adenosine- 5’-diphosphate (ADP) in human whole blood with an impedance aggregometer. Two hundred mg dipyridamole induced a significant inhibition of both ADP- and collagen-induced aggregation in human blood samples taken 2 hr after oral drug intake. Administration of the drug for four days, 400 mg/day, further increased the antiplatelet effect. A significant negative correlation was found between collagen-induced platelet aggregation in whole blood and dipyridamole levels in plasma (p <0.001). A statistically significant inhibition of both collagen (p <0.0025) and ADP-induced (p <0.005) platelet aggregation was also obtained by incubating whole blood in vitro for 2 min at 37° C with dipyridamole (3.9 μM). No such effects were seen in platelet-rich plasma, even after enrichment with leukocytes. Low-dose adenosine enhanced in vitro inhibition in whole blood.Our results demonstrate that dipyridamole impedes platelet aggregation in whole blood by an interaction with red blood cells, probably involving adenosine.

Viscosity and Red Cell Deformity in Arterial Disease

1979 ◽  
Author(s):  
G Cella ◽  
H de Haas ◽  
M Rampling ◽  
V Kakkar
Keyword(s):  
Vascular Disease ◽  
Blood Viscosity ◽  
Whole Blood ◽  
Arterial Disease ◽  
Plasma Viscosity ◽  
Control Group ◽  
Fibrinogen Concentration ◽  
Red Cell ◽  
Whole Blood Viscosity ◽  
Significant Difference

Haemorrheological factors have been shown to be affected in many kings of vascular disease. The present study was undertaken to correlate these factors in normal subjects and patients suffering from peripheral arterial disease. Twenty-two patients were investigated; they had moderate or severe intermittent claudication, extent of disease being confirmed by aorto-arteriography and ankle-systolic pressure studies. Twenty-five controls with no symptoms or signs of arterial disease were selected with comparable age and sex distribution. Whole blood viscosity was measured at shear rates of 230 secs-1 and 23 secs-lat 37°c using a Wells Brookfield cone plate microvisco meter. Plasma viscosity was also measured in an identical manner. Erythrocyte flexibility was measured by centrifuge technique and fibrinogen concentration as well as haematocrit by standard techniques. The fibrinogen concentration appeared to be the only significant parameter; the mean concentration in patients with peripheral vascular disease of 463 ± 73mg/l00ml in the control group ( < 0.05). Although whole blood viscosity was high in patients, when corrected to a common haematocrit, there was no significant difference between patients and controls. The same megative correlation was found for plasma viscosity. The red cell flexibility was found to be increased in patients as compared to the control group, but this effect appeared to be simply proportional to the fibrinogen concentration.

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