bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluation Of Thigh Length Sequential Leg Compression In The Prevention Of Deep Venous Thrombosis
Authors: Hartman J T , Yost R P , Robertson W W , Janssen H F 
Published: July 2018

The present study is designed to evaluate the effectiveness of a thigh length sequential compression device (SCD) in the prevention of deep venous thrombosis (DVT) in patients undergoing hip operations (either fracture or elective). The night before the operation phleborheography, doppler ultrasound and, when possible, 125I fibrinogen scanning were used to evaluate venous flow in the patients’ legs. The patients identified as being free of DVT complications were then fitted with the compression sleeves. Following surgery the venous evaluation tests were repeated on alternate days to determine if DVT complications had developed. Evidence of DVT formation was identified in 10 of the 52 control patients (who received leg elevation only) and in 1 of the 52 treated patients (who received the SCD plus leg elevation). The chi square statistic demonstrates a significant difference between the two groups (P<.05).Data evaluation indicates that surgical approach and patient obesity did not contribute to the risk of DVT formation. However, patients who are either over the age of 66, females, or have suffered a hip fracture appear to be at greater risk than other groups. The amount of data in this study makes it difficult to evaluate with statistical significance the additional risk produced by other factors such as heart condition, previous history of clotting problems, estrogen therapy, etc.
Thrombectomy For Ilio-Femoral Thrombosis In Fertile Women
Authors: Swedenborg J , Delin A , Hellgren M , Jacobsson H , Nilsson E 
Published: July 2018

Thirteen women, age 29-48 years, with iliofemoral venous thrombosis were subjected to thrombectomy via the femoral vein, and construction of an arteriovenous fistula. Anticoagulant therapy was given from the operation and 6 months on. The AV fistula was closed after 3 months. After cessation of anticoagulant therapy the patency of the iliac vein was evaluated by plethysmography and, if this was inconclusive, by phlebography. A work-up for coagulation abnormalities was also made.All thromboses were left-sided. Several risk factors were present: pregnancy in 9 of 13 (2 early) contraceptive pills in 2 of 13, and iliac vein stenosis in 9 of 10. In 8 of 12 decreased levels of plasminogen activators were noted. Of the 9 pregnancies, three were complicated and required interruption, one was terminated by normal delivery one week before thrombectomy, two were interrupted at the time of thrombectomy, and three continued to normal deliveries several weeks after thrombectomy.No pulmonary embolism was observed. At follow up, the iliac vein was patent in eleven patients. It is concluded that the pathogenesis of iliofemoral venous thrombosis in fertile women is multifactorial, involving hormonal and mechanical components. This study draws attention to decreased fibrinolytic activity in many of the patients. Thrombectomy resulted in iliac vein patency in eleven of thirteen patients. The procedure is well tolerated by mother and child during pregnancy.
Monitoring Low-Dose Heparin Administration In Hip Surgery
Authors: Poller L , Tabemer D A 
Published: July 2018

Fifty-five patients requiring selective hip replacement or emergency surgery for hip fractures were randomly given fixed low-dose subcutaneous calcium heparin 5,000 units 8-hourly (30 patients) or monitored subcutaneous calcium heparin (25 patients). The aim was to prolong the activated partial thromboplastin time (APTT), using the NRLARC method, to 5 seconds above the upper limit of normal.Adjusting the dose of heparin was moderately successful in achieving the target value for the APTT (46% of observations) compared to the fixed dose group (27%) p<0.005. In nine patients prophylaxis failed to prevent DVT detected by 125I-fibrinogen scan; three were in the adjusted dose, six in the fixed dose heparin group. In all nine patients the APTT showed less than the desired prolongation the day before the scan became positive although in six patients with positive scans, measurable heparin levels were detected by anti-factor Xa assay. The APTT appears, therefore, to give a better guide during hip surgery to the antithrombotic effect of heparin than the anti-factor Xa assay in low-dose heparin prophylaxis. Maintaining the APTT at or above 50 seconds with the NRLARC method protected these high risk patients from post-operative DVT.
Histochemical Studies On The In Vitro 5-HT Uptake In Endothelial Cells
Authors: Kjellström T , Ahlman H , Dahlström F , Hansson G , Stenberg B , Risberg B 
Published: July 2018

Previous studies have shown that 5-HT is rapidly taken up by the endothelial cells and some investigations also suggested that serotonin is metabolized within these cells. In earlier studies on rat-lungs using a fluorescence histo- chemical method according to Hillarp - Falk we demonstrated that 5-HT was accumulated within the mast cells. Using this technique we could not demonstrate any specific uptake in the pulmonary endothelial cells. It was the purpose of the present investigation to further study the 5-HT uptake by isolated pulmonary endothelial cells.Methods Cells from the vascular intima of the pulmonary artery in adult rats were grown in a growth medium containing FCS. The endothelial nature of these cells was demonstrated using transmission electron microscopy and factor VIII analysis. Confluent endothelial cells were incubated with 5-HT and the cellular uptake was studied with fluorescence microscopy according to the Hillarp - Falk procedure.Results The endothelial cells were identified by the presence of Weibel-Palade bodies using transmission electron microscopy and the immunofluorescent demonstration of cellular factor VIII antigen. Cells not exposed to serotonin had no specific 5-HT fluorescense. After incubation with 5-HT at different concentrations there was a progressive uptake of the amine within the cells.Conclusions This study confirms previous reports on the specific serotonin uptake in endothelial cells. The Hillarp-Falk procedure seems suitable for further studies of serotonin uptake in cultured endothelial cells.
The Effect Of Ticlopidine On Cultured Human Endothelial Cells: Possible Influence On Extracellular Matrix Formation
Authors: Piovella F , Piovella L , Almasio P , Ricetti M M , Ascari E 
Published: July 2018

Endothelial cells derived from human umbilical cord vein were seeded and grown to confluence in culture medium TC 199 with 20% foetal calf serum without other growth factors supplement. Cells were then detached utilizing a trypsin-EDTA solution, harvested in fresh culture media containing different concentrations of Ticlopidine, poured on glass coverslips placed on 35 mm Petri dishes and cultured for six days without further medium replacement. Control dishes were prepared using fresh medium without Ticlopidine.Treated cells revealed a decreased tendency to adhere to the substratum as well as morphological changes in comparison with controls when examined by phase contrast microscopy. This effect was more evident with higher concentration (0.33 mg/ml) of Ticlopidine, while lower concentrations (0.05 mg/ml) caused morphological changes only. Indirect immunofluorescence for fibronectin utilizing monospecific antibodies, revealed a different fluorescent pattern if compared with controls. In particular a less pronounced intracellular granular fluorescence and a delay in the appearance of the fibrillar extracellular matrix.
Arterial Thrombosis In Heparin-Induced Thrombo Cytopenia Is Not Accompanied By A Decreased PGI2 Stimulating Activity In Plasma
Authors: Kulzer R , Schäfer G , Budde U , Popov S 
Published: July 2018

A patient developed severe thrombocytopenia and acute arterial occlusion 6 days after onset of heparin therapy. Heparin was ad ministered because of venous thrombosis in the lower limbs. Aggregometry showed the typical signes of heparin-induced thrombocytopenia with all evaluated heparins of different origin. PGI2 stimulating activity of plasma was in the range of normal plasma samples. No aggregating activity of the plasma could be shown without heparin(Method of Lian et al.). Heparin activity was determined before and after aggregation with a chromogenic substrate.After cessation of heparin therapy the platelets raised into the lower normal range within a few days.
Platelet Factor 4, Heparin Neutralizing Activity And Fibrinogen
Authors: Etherington M D , O’Brien J R 
Published: July 2018

To investigate the relationship between the heparin neutralizing activity in platelets (intra-plat HNA = IP HNA) and in plasma (PPP HNA) as measured by the heparin thrombin clotting time (HTCT) and the plasma PF4 (PPP PF4) and the intra-platelet PF4 (IP PF4), we selected 15 people with contrasting amounts of HNA in their plasma; these included young and old controls, patients after operations and myocardial infarcts and pregnant women. Platelet rich plasma (PRP) and PPP were prepared from citrated blood processed entirely at 4°C. 2ml sub-samples of PRP and PPP were then frozen and thawed × 3, centrifuged and the supernatants collected. IP PF4 and PPP PF4 were measured by radioimmunoassay (ABBOTT KIT). To measure IP HNA and PPP HNA a modified Harada and Zucker clotting assay was performed. On each study day PPP was prepared from a control and used as substrate. All test plasmas were added to this PPP and the amount of heparin required to give a clotting time of 30 seconds was measured. IP HNA was calculated by subtraction of PPP units heparin from PRP units. The plasma fibrinogen was estimated by Clauss’ method.The IP PF4 was significantly correlated with IP HNA (r=0.95, n=15, p<0.001). The plasma PF4 in all volunteers was less than 10ng/ml-1 and bore no relation to the PPP HNA. However the plasma fibrinogen was significantly correlated to PPP HNA (r=0.91, n=15, p<0.001).Thus the IP HNA accurately reflects IP PF4 (with presumably a parallel small contribution from β-thromboglobulin). The PPP HNA, previously thought perhaps to reflect liberated PF4 or another intra-platelet anti-heparin substance, is now shown to be independent of PF4 but at least in part reflects the plasma fibrinogen (which neutralizes heparin). This quick and simple clotting assay is well suited to a routine laboratory and might be used to measure total IP HNA, and monitor the a granule content of platelets in disease.
Glutathione Peroxidase And Malondialdehyde Production In The Arachidonic Acid Metabolism Of Human Platelets
Authors: Guidi G C , Schiavon R , Avventi G L , Perona G 
Published: July 2018

A series of functional parameters, including the aggregability triggered by various agents, the in vitro malondialdehyde production and the glutathio ne peroxidase activity, has been investigated in platelets from normal blood donors.Glutathione peroxidase activity assays showed a significant inverse correlation with malondialdehyde induced by arachidonic acid but not with aggregation data and malondialdehyde induced by thrombin. Moreover, arachidonic acid generates in human platelets lysates large amounts of hydrogen acceptor substrate(s) for the glutathione peroxidase with peculiar kinetic features. These are related to ma londialdehyde production and to partial inhibition by acetyl-salicilic acid and are likely connected with prostaglandin metabolism.Our data suggest that physiological variations in glutathione peroxidase activity are important in human platelet arachidonic acid metabolism, because they modulate the biosynthesis of key end-products, as thromboxane A2, whose malondialdehyde is an inde.
Clinical Evaluation Of Ticlopidine In The Inhibition Of Platelet Function - A Multiclinic Double Blind Study In Comparison With Aspirin
Authors: Abe T , Kuramoto A , Yasunaga K , Sakuragawa N , Maekawa T , Yamazaki H , Toyama K , Ogawa N 
Published: July 2018

Clinical effect of ticlopidine, a new inhibitor of platelet aggregation, at a daily dose of 300 mg was compared with that of aspirin at its daily dose of 500 mg by means of double blind assay. The suppression of platelet aggregations induced by ADP, collagen and epinephrine was compared among platelet samples obtained from 38 cases with thrombotic tendency or at enhanced platelet functions.The inhibitory efficacy of ticlopidine on platelet aggregations induced by collagen or epinephrine was found as potent as that of aspirin in their overall judgement, but the ticlopidine inhibition on the ADP aggregation was apparently more potent than aspirin. The maximum aggregation rate was significantly decreased and the frequency of the second aggregation pattern was more remarkably minimized in the ticlopidine-treated group than the aspirin-group. The maximum aggregation rates induced by collagen or epinephrine were significantly decreased in both of ticlopidine- and aspirin-groups to the same extent.Blood filtration velocity through Nuclepore filter of 5μm pore size was significantly enhanced in the ticlopidine- group but no change found in the aspirin-group. Other coagulation parameters and laboratory data were not changed in both groups, except bleeding and prothrombin times which were slightly prolonged in the aspirin-group.From the results mentioned above, it was expected that ticlopidine might exert superior clinical effect to aspirin on thrombotic diseases and microcirculatory disorders
Differing Effects Of Ticlopidine And Two Prostaglandin Synthetase Inhibitors On Maximum Rate Of Adp-Induced Aggregation
Authors: Bruno J J , Yang D , Taylor L A 
Published: July 2018

Many platelet inhibitors are known which block the secondary (2°) phase of ADP-induced aggregation. These agents normally inhibit platelet cyclooxygenase (CO). Agents which are able to inhibit primary (1°) ADP-induced aggregation usually cause elevation of platelet cAMP. Ticlopidine hydrochloride (T), a drug which does net stimulate platelet adenylate cyclase or inhibit platelet cAMP phosphodiesterase, or platelet CO, inhibits 1° ADP-induced aggregation. Healthy human volunteers were dosed orally from 3-8 days with doses of T from 125 to 500 mg/day. When the maximum rate of ADP-induced aggregation on the day following cessation of dosing was compared with that obtained predosing, statistically significant inhibition of maximum rate was obtained at each dose. Similar studies were done with naproxen (N) a CO inhibitor. Healthy human volunteers were given 125 to 1000 mg/day of N. When the rates of ADP-induced aggregation at 3 and 8 hours postdosing were compared to predose rates, there were no statistically significant differences at any dose. At these times collagen and arachidonic acid-induced aggregation were essentially totally inhibited. An experimental agent, 5-benzoyl-l, 2-dihydro-3H-pyrrolo [l,2-a]-pyrrole- 1.carboxylic acid, with potent platelet CO inhibiting activity, given orally to human volunteers at 2.5 to 200 mg/day showed the same results at 3 and 24 hours post dosing as did N.We conclude that T is an inhibitor of 1°phase of ADP- induced aggregation, and that agents with CO-inhibiting action alone are incapable of inhibiting 1° phase of ADP- induced aggregation despite occasional reports to the contrary.
Selective Inhibition Of Thromboxane Synthesis By 1-(3-Hydroxy-1-Octenyl)-Imidazole And Its Nicotinic Ester In Human And Rat Platelets
Authors: Bonne C , Martin B , Sincholle D , Regnault F 
Published: July 2018

Since Thromboxane A2 (T×A2) is considered to play an important role in platelet aggregation, attempts to develop selective inhibitors of T×A2- synthetase are being made. In this report the activity of 1-(3-hydroxy-1-octenyl)-imidazole, chlorhydrate (CBS612) and of its nicotinic ester, die hiorhydrat e (CBS63b) will be presented.The inhibitory activity was determined in isolated platelets from human and rat by radiochemical assay and in whole blood by radioimmunoassay of T×B2 and of PGE2 as a criteria of specificity. Human enzyme was more sensitive than the rat one’s (CBS634 : IC50 human = 0.7μM, IC50 rat = 10μM) and the two compounds were more active than imidazole in human platelets (IC50 : imidazole = 50μM, CBS612 = 2μM ; CBS631+ = 0.7μM). Collagen- induced aggregation was inhibited by the drugs at concentrations which suppressed T×B2 formation.The results of these experiments showed that CBS612 and CBS634 selectively inhibited thromboxane-synthetase since they increased the formation of PGE2. Besides, these compounds did not inhibit PGI2 release from rat aorta ring. The selectivity of the inhibition by the drugs was further shown by the absence of any effect on the first phase of ADP-induced platelet aggregation.These compounds seemed potentially interesting for the management of thrombotic diseases and for elucidating the role of Thromboxane in physiological and pathological processes.
Adenosine 3‘,5‘-Cyclic Monophosphate (C-AMP) And Inhibitors Of Platelet Aggregation: A Possibility Of A Double C-AMP Pool In Human Platelets
Authors: Zahavi M , Kakkar V V 
Published: July 2018

A new method was developed for determining platelet c-AMP in platelet rich plasma (PRP) and washed platelets.In PRP, using an adenyl cyclase activator Prostaglandin El (PGEl) and phosphodiesterase inhibitors (papaverine, theophylline) and an inhibitor of platelet function, pyridoxal-5-phosphate (PALP) it was found that the phosphodiesterase inhibitors and PALP are more effective than PGEl in inhibiting platelet function at identical c-AMP accumulation. In washed platelets aggregation induced by thrombin was greatly inhibited by papaverine and by PALP with concomitant comparatively small c-AMP accumulation but was in most preparations inhibited by PGEl only to a small extent, although c-AMP accumulation was substantial. This indicated that in platelets there may be two pools of c-AMP, one of them more closely correlated to platelet aggregation.PALP acts like a phosphodiesterase inhibitor rather than an adenyl-cyclase activator with respect to c-AMP accumulation. However, in contrast to papaverine the small c-AMP accumulations cannot be increased in washed platelets, therefore, it seems that another site in addition to phosphodiesterase inhibition is involved in inhibition of platelet function by PALP. c-AMP accumulation seems to be the main cause for inhibition of platelet function by papaverine, however, at higher concentrations an additional site is also possible. This additional inhibition is more important in inhibition of platelet function by papaverine and PALP in a diabetic patient whose platelets seem to be impaired in ability to accumulate c-AMP.
Storage Pool Disease Associated With Von Willebrand?
Authors: Meschengieser S , Schattner M , Elgue G , Lazzari M A 
Published: July 2018

We evaluated a group of 11 patients (10 female, 1 male) complaining of minor bleeding symptoms that showed the pattern of storage pool disease (SPD) and besides, presented a lack of aggregation induced by ristocetin, which corrected with the addition of normal plasma (pool of 15 donors). Only two patients had familiar history of bleeding tendency. Bleeding time (Ivy) was prolonged in 63% of the patients and platelet retention (Pellem II) was decreased in 72% of them.Three of the patients showed, apart from the SPD, a clear pattern of VW disease (low factor VIII: C and VIII: Ag). In four patients the levels of factor VIII: C and f, VIII:Ag were normal, but one of them presented a Ristocetin Cofactor (McFarlane) below normal, associated with a prolonged bleeding time and low adhesiveness. Three patients had low levels of VIII: C with normal levels of VIII:Ag. The last patient with border line levels of VIII: C and VIII:Ag, presented a low Ristocetin Cofactor. Thus, 5 of the 11 patients have undoubtful elements of VW. In the others this diagnosis could not be accomplished clearly.As a conclusion, the presence of a characteristic aggregation pattern of SPD with absence of ristocetin induced aggregation, could suggest a variant of SPD or perhaps an association of both diseases
Megakaryocytic Progenitors (CFU-M) Increase Nonspecifically In Chronic Immune Thrombocytopenia
Authors: Burstein S A , Erb S K , Adamson J W , Harker L A 
Published: July 2018

Previous studies from our laboratory have suggested that the numbers of CFU-M do not increase primarily in response to acute thrombocytopenia. To determine the effect and specificity of prolonged thrombocytopenia on CFU-M number, mice were given 4 intravenous injections on alternate days of multiply absorbed rabbit anti-mouse platelet serum (APS), while control animals received a similar regimen of rabbit anti-mouse red cell serum (ARS), normal rabbit serum (NRS), or phosphate-buffered saline (PBS). Two days aftefcthe final injection, the mean platelet count was.0.314 ± 0.129 × 106/ul in animals given APS vs. 1.105 ± 0.048 × 106/ul in animals given other regimens. The numbers of CFU-M, day 7 and day 14 erythroid burst forming cells (BFU-E), and granulocyte-macrophage colony forming cells (CFU-C) were determined in humerus and spleen.The generalized increase in progenitor cells in marrow in response to APS together with increases in CFU-M in spleen following ARS and NRS indicate that these cells may respond nonspecifically to foreign protein. The data suggest that the elevation in CFU-M numbers with chronic immune thrombocytopenia is at least partially independent of the platelet count.
The Effect Of A Proteinase Inhibitor On Platelet Function In Stored Blood
Authors: Haas S , Wendt P , Blümel G 
Published: July 2018

Blood platelets are markedly traumatized by the withdrawal of blood from the donor. Hereby the function of thrombocytes is activated and this platelet stimulation is closely related with the early formation of microaggregates in stored blood. Therefore it is clinically desired to stabilize the platelets but without inhibiting their function irreversibly and causing hemorrhage. Concerning this question an experimental study was carried out.Blood was drawn from 10 volunteers under blood bank conditions and was stored in presence of 200 KIU aprotinin per ml ACD-blood resp.the same volume of saline at a temperature of +4°C. Immediately after the withdrawal of blood and 1,2,3 and 7 days later blood samples were taken and the following parameters were studied: platelet aggregation induced by ADP, aggregate ratio, PF 4, beta-thromboglobulin and tx B2 in plasma and serum.In the aprotinin blood the aggregability was slightly diminished and was longer present than in the control group. In addition, the aggregate formation was significantly decreased. The release reaction of platelets was not effected by aprotinin;the increase of PF 4 and beta-thromboglobulin was similar to that of the control group. Also the thromboxane formation was not effected. Thus the protective effect of aprotinin is independent from the prostaglandin metabolismThis study shows that a high dose of aprotinin has a stabilizing effect on platelets in stored blood and that the thrombocyte function is not irreversibly inhibited by this substance. Therefore, aprotinin can be regarded to be effective in the prophylaxis of disseminated platelet aggregation without causing a bleeding risk.