Thrombospondin 1 expression and angiogenesis in breast carcinoma and their relation with platelet activity.

This study investigates angiogenesis and the expression of thrombospondin 1 in invasive ductal carcinoma of the breast and their possible relation to platelet counts and platelet activity. The study included 20 cases of invasive ductal carcinoma. Platelet activity was evaluated by determining thromboxane B2 and cyclic guanosine monophosphate (cGMP) levels by enzyme immunoassay (EIA).Thrombospondin (TSP) 1 and CD34 expression was studied immunohistochemically. Mean platelet count of the patient group was significantly greater than the mean platelet count of the control group (P < 0.05). The platelet counts were positively correlated with tumour size (r=0.609; P < 0.01). Platelet counts were higher in the patients who had grade 3 microvessel density (P < 0.05). The mean basal platelet cGMP level in the patient group was significantly lower than it was in the control group (P < 0.05). Focal TSP immunoreactivity was detectable in 5 (20%) cases in the tumour cells, and in 9 (45%) cases in the stroma. We did not find any correlation between TSP-1 staining and angiogenesis, platelet counts, platelet activity, and the histological prognostic parameters. Our study confirms the essential role of platelets in tumour growth and angiogenesis. Decreased levels of cGMP in the patient group may cause platelet hyperreactivity. Although thrombospondin 1 may be upregulated in malignant breast tissue, this is not sufficient for tumour growth and dissemination according to our results.

Doppler ultrasound evaluation of the structural and hemodynamic changes in the brachial artery following two different exercise protocols.

PURPOSE: Examine the effects of incremental and submaximal exercise on structural and hemodynamic changes in the brachial artery flow parameters using Doppler ultrasonography. MATERIALS AND METHODS: Twenty four healthy sedentary males (aged 19.54+/-0.59) performed submaximal (15 minutes heart rate to 75% maximal) and incremental (workload was increased 20W every 3 minutes until exhaustion) exercises by upper extremity ergometer. Before and after exercises the brachial artery diameter, peak systolic maximum velocity (Vmax), end-diastolic minimum velocity (Vmin) and time-averaged mean flow velocity (Vmean), volume blood flow and flow waveform patterns were recorded in a controlled environment. RESULTS: The diameter of the brachial artery, flow velocities, and blood flow increased significantly after each exercise protocol (p < 0.001). The Vmax (p < 0.05), Vmean (p < 0.01), and volume blood flow (p < 0.01) after the incremental exercise were significantly higher than those measured after the submaximal exercise. However, no significant differences were noted between the two exercise protocols when arterial diameters and Vmin were concerned. The flow pattern was monophasic in all subjects after incremental exercise. Nevertheless, the flow pattern remained triphasic in two of the subjects after submaximal exercise. CONCLUSION: Blood flow velocities played important role in hemodynamic mechanism than conduit arterial diameter during arm exercises. Changes in conduit artery diameter did not significantly contribute to blood flow increase during high and moderate intensity exercises. There is minimal variation in waveform shapes of normal individuals after exercise. Doppler ultrasonography proved a practical tool in the studies of the dynamic responses of blood flow and vascular resistance during rest and exercises.

Effect of sodium selenite treatment on platelet aggregation of streptozotocin-induced diabetic rats.

INTRODUCTION: There is a well-known association between diabetes and atherosclerosis. Platelets are involved in the development of atherosclerotic vascular diseases and play a key role in atherosclerotic complications. Diabetes mellitus is related to alteration in the homeostasis of selenium and the protective role of selenium against lipid peroxidation in diabetes is reported. In the present study, thrombin-induced platelet aggregation and thromboxane A2 (TxA2) formation in diabetes and the effect of sodium selenite were evaluated. MATERIALS AND METHODS: Diabetes was induced by intraperitoneal injection of streptozotocin (STZ) in Wistar rats (n = 21). Thirty of them were used as control rats. A week after streptozotocin injection, 11 of the control rats and 12 of the diabetics were injected with 5 micromol/kg/day of sodium selenite for 4 weeks. Thrombin-induced aggregation of the platelets was evaluated by optical technique. Thromboxane B2 (TxB2), TxA2 metabolite, was measured by enzyme-linked immunoassay (EIA) in thrombin-induced platelets. RESULTS AND CONCLUSION: The platelet aggregation and TxB2 level increased in diabetic rats. Sodium selenite reversed the increase in platelet aggregation and TxB2 and caused a small but significant (p < 0.05) decrease in the glucose level. The hyperaggregability of platelets in STZ-induced diabetic rats was thought to be related to the enhanced TxA2 formation of platelets. Increase in TxA2 formation implies lipid peroxidation. Sodium selenite decreased the TxA2 formation. Besides its antioxidative effect, further studies are needed to establish the insulin-like effect of selenite because of a small decrease in blood glucose.

Differential effect of aspirin on platelet aggregation in patients with coronary artery disease in relation with associated risk factors.

Platelets play a key role in the pathogenesis of atherosclerosis and acute coronary syndromes and antiplatelet therapy offers a clinical benefit. Although aspirin is the most widely used agent, there are several conditions in which aspirin may fail to provide a full antithrombotic benefit. Furthermore, data concerning the relationship between platelet function, aspirin, and the associated risk factors are limited. In the present study. ADP and collagen-induced platelet aggregation of 200 consecutive patients with suspected coronary artery disease (CAD) who underwent coronary angiography were evaluated. The patients were classified into three groups according to the number of stenotic vessels. One hundred and eight patients were using 300 mg/day of aspirin. The associated cardiovascular risk factors were also considered. The collagen-induced platelet aggregation of smokers was significantly higher than non-smokers (P < 0.05). Although platelet aggregation was higher in diabetic and hypertensive patients, the difference was not statistically significant. No significant correlation was found between platelet aggregation and other risk factors. The collagen-induced platelet aggregation of the subjects with non-stenotic vessels was reduced by aspirin (P < 0.05). Aspirin did not sufficiently inhibit ADP and collagen-induced aggregation in patients with CAD. This finding supports the idea that the nonplatelet-mediated effects of aspirin could be more important than its antiplatelet effect in clinical use and the use of new potent antiplatelet drugs may complete its antiplatelet effect.