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A study on the in vivo production of thrombosis in rat mesenteric arterioles and action of prostaglandin (PG) I2 on the thrombosis.

We have investigated reproducible and quantitative thrombus formation in rat mesenteric arterioles using electrical stimulation under an inverted microscope. In vivo thrombi were formed in arterioles of 30-40 micrometers diameter by electrical stimulation using a tungsten electrode with a tip of 5 micrometers diameter. A "threshold" response was defined as one in which platelets adhered to the injured site of vascular wall and formed a white body which flowed away intermittently. The thrombus formations were classified into three stages: stage I, thrombi covering up less than 20% of the vessel lumen; stage II, when 20% to 40% of the lumen was covered; or state III, when more than 40% was covered. This preparation was demonstrated to be valuable for testing the potency of anti-thrombotic drugs if we performed the experiment within 2 hr after removing the mesentery from the peritoneal cavity which exposed it to air. PGl2, t a dose of 0.5 micrograms/100 g intravenously administered, inhibited the growth of the thrombus at stage II and III. PGE1, PGD2 and PGE2 had no effect at the same dose on these stages. The threshold response was significantly suppressed by both PGI2 and PGE1 at doses of 5 micrograms/100 g.

Alprostadil↗

Risk of thrombosis associated with oral contraceptives of women from 97 families with inherited thrombophilia: high risk of thrombosis in carriers of the G20210A mutation of the prothrombin gene.

BACKGROUND AND OBJECTIVES: Oral contraceptives (OC) and inherited thrombophilia are well-known risk factors associated with venous thromboembolism (VTE). However, there are only few studies on the risk of VTE in women with inherited thrombophilia who use oral contraceptives. DESIGN AND METHODS: We performed a retrospective family cohort study of 325 women belonging to 97 families with inherited thrombophilia, including antithrombin, protein S and C deficiencies, the factor V Leiden mutation (FVL) and the G20210A mutation of the prothrombin gene (PT20210A) to determine the risk of VTE associated with OC intake. RESULTS: For carriers of the PT20210A mutation, the risk of VTE in OC users was 3-fold higher (95% CI 1.3-6.8) than that in non-carriers. Carriers of FVL mutation taking OC showed an OR of 1.4 (95% CI 0.6-3.3), indicating a tendency to increase the risk of VTE. INTERPRETATION AND CONCLUSIONS: Because of the high prevalence of the PT20210A (6.5%) and FVL (2%) mutations in the general Spanish population and the increased risk of VTE associated with OC intake, genetic screening for these mutations should be considered in potential OC users belonging to families with thrombophilia.

Adolescent↗