bluuebunny/crossref_metadata_2025_split huggingface dataset:
Retention Of Platelets In A Protein A-Sepharose Column As A Measure Of Platelet Associated IgG
Authors: Chesterman C N , McVeigh D J 
Published: July 2018

Employing the biological property of staphylococcal protein A to bind human IgG a test system has been devised to detect platelet associated IgG (PAIg) by quantitating platelet retention in an agarose column with immobilised protein A.Platelets were washed free of plasma and resuspended in Tyrode’s buffer with EDTA and 0.1% BSA. Platelet counts were performed on the suspension prior to and following passage through a miniature protein A column and the percentage of platelets retained calculated. An indirect test for serum platelet antibody utilised washed normal platelets following their incubation in patient serum.Less than 30% normal platelets or normal platelets incubated in normal serum were retained in the affinity column. Similarly in four samples from patients with thrombocytopenia of nonimmune origin there was less than 15% retention in the column. Platelets from two of five patients with probable ITP (all treated with corticosteroids) showed 85% retention in the column. The remaining patients fell within the normal range. The sera from three patients with proven platelet antibody using other techniques produced 65-80% retention in an indirect test. Four other sera from possible ITP patients (with comparatively high platelet counts) showed less than 30% retention. Specificity for PAIg was suggested by inhibition of retention from 80% to less than 30% following pretreatment of the colurrai with purified IgG or normal serum.The optimum conditions for the technique are being studied and its specificity and sensitivity ascertained in patients with thrombocytopenia of various kinds. If these preliminary results are extended, such a simple technique may prove of diagnostic value.
Differences In The Appearance Of Immunoprecipitate 16 (GP IIb/Gp IIIa) By Crossed Immunoelectrophoresis Of Triton Solubilized Platelet Proteins Depending On The Solubilization Conditions
Authors: Hagen I , Korsmo R , Bjerrum O J , Gogstad G , Solum N O 
Published: July 2018

Crossed immunoelectrophoresis (CIE) of Triton solubilized platelet proteins has demonstrated that the major immunoprecipitate (16) represents GP IIb and GP IIIa. CIE of proteins solubilized from isolated membranes has often showed patterns with reduced area or absence of immunoprecipitate 16 concomitant with the appearance of new arcs.The aim of this study was to establish conditions to control this phenomenon. By CIE of proteins solubilized from platelet membranes isolated in the presence of EDTA, the area of immunoprecipitate 16 was reduced, and two new arcs, one at the cathodic side (16a) and one at a similar position (16b) as immunoprecipitate 16 appeared. In contrast, CIE of extracts from corresponding membranes which had been washed once in an EDTA-free medium revealed one major 16 peak. Despite the major differences between these patterns, SDS PAGE of these extracts showed no differences in the glycoprotein patterns. The anodic leg of immunoprecipi- tate 16a fused with 16, and a specific antibody obtained by immunozation with immunoprecipitate 16 also reacted with 16a. Partial or total disappearance of immunoprecipitate 16 was also seen after CIE of proteins solubilized from whole platelets in the presence of EDTA, whereas leupeptin had no such effect. The different patterns may reflect biochemical alterations related to platelet activation.
Activation Of Platelets In Chronic Glomerulonephritis (CGN) And Nephrotic Syndrome (NS)
Authors: Yamazaki H , Motomiya T , Sakakibara C , Ariga S , Ida T , Kuriyama R , Kuriyama R , Chida Y , Takeuchi J , Tomura S 
Published: July 2018

Platelet count, volume, aggregation, adenine nucleotide contents, plasma β-thromboglobulin (β-TG) , plasma platelet factor 4 (PF-4) and urineβ-TG were measured in 31 patients with CGN, 20 patients with NS and 51 healthy controls. Platelet counts were higher and volumes were smaller in NS than in controls significantly. Platelet aggregation induced by ADP, adrenaline and collagen was significantly higher in the patients than in controls and it markedly increased in the cases of progressive glomerular lesions. Plasma levels of β-TGwere significantly elevated in the patients (65.8± 7.5(SE) ng/ml) compared with controls (22.2±1.6 ng/ml) and NS showed markedly elevated plasma β-TG levels (124.3±28.6 ng/ml). Plasma levels of PF-4 were also significantly higher in the patients (28.6±3.6 ng/ml) than in controls (13.2±1.1 ng/ml). There was a significant inverse correlation between plasmaβ-TG and creatinine clearance (r=-0.47, P<0.01).
Urine β-TG excretion was higher in patients with decreased renal function than in those with normal renal function. Plasma β-TG remarkably decreased in 3 of 4 patients with markedly increased β-TG levels when they were given antiplatelet drugs. Platelet ATP contents were 6.98±0.24 in the patients and 8.06±0.42 μmoles/1011platelets in controls. There was a significant difference (P<0.05). Platelet ADP contents were 3.08±0.15 in the patients and 3.27±0.19 in controls.The results suggest that platelet aggregation and release reaction increased in patients with CGN and NS. However the decrease in adenine nucleotides in platelets was more marked in ATP than in ADP content. There may be an abnormal metabolism of adenine nucleotides in platelets related to the energy metabolism in addition to a decrease in storage pool in such diseases. Also it is suggested that activated platelets may be an important factor in the genesis of thrombotic tendency in NS.
The Effects Of Prostacyclin (PGI2) On Intravascular Platelet Aggregation
Authors: Duncan G G , Mallarkey G , Smith G M 
Published: July 2018

Intravascular aggregation can be measured by counting the number of circulating platelets before and after the injection of aggregation agents. The Technicon Autocounter was modified to count platelets continuously and connected via a double cannula in a carotid artery to an anaesthetised animal.Adenosine diphosphate (ADP) and collagen gave dose- dependent falls in the circulating platelet count when injected into rats, guinea pigs and rabbits. This enabled aggregation to be accurately quantitated in vivo.The infusion of PGI2 (0.25-1 ug/kg/min) in anaesthetised rats and rabbits produced a dose-dependent inhibition of the fall in platelet count produced by ADP and collagen. The formation of PGI2 can be inhibited in vitro by 15- hydroperoxyarachidonic acid (15HPAA). When 20 ug/kg/min of 15HPAA was infused into rats, aggregation produced by collagen was significantly increased suggesting that PGI2 is continuously formed by the rat vascular endothelium. This observation was confirmed by infusing 6-keto PGF1α antiserum. This antibody also prevented the inhibitory activity of PGI2 on collagen-induced aggregation. The study of continuous platelet counting in guinea pigs has been hampered by the occurrence of thrombocytopenia in certain animals. When 2 ug/kg/min of PGI2 was infused for 10 mins, a rise in the circulating platelet count to a steady plateau 4-5 × 105 platelets occurredThese experiments have shown that PGI2 will prevent aggregation by ADP and collagen and will reverse spontaneous thrombocytopenia and that PGI2 is continuously released from the vessels of anaesthetised rats.
A Study Of The Mechanisms Involved In Collagen-Induced Intravascular Platelet Aggregation
Authors: Smith G M , Mallarkey G 
Published: July 2018

Intravascular platelet aggregation can be monitored by measuring the fall in the number of circulating platelets after the injection of an aggregating agent. The Technicon Auto-counter was modified to count platelets continuously. Rats were anaesthetised and the trachea and jugular vein were cannulated. A double cannula was inserted into a carotid artery.Collagen gave consistent and dose-dependent falls in platelet count. Infusion of trisodium citrate gave a dose- dependent inhibition of collagen-induced aggregation with 2 mg/kg/min producing 100% inhibition. Indomethacin 1-8 mg/kg and aspirin 10-l60 mg/kg produced up to 60% inhibition of collagen-induced aggregation giving a biphasic dose-response curve. Sulphinpyrazone 20-160 mg/kg and piroxicam 1-8 mg/kg gave dose-dependent inhibitions of aggregation. None of the cyclo-oxygenase inhibitors studied or sulphinpyrazone completely inhibited collagen- induced aggregation. Attempts to produce 100% inhibition by infusing adenosine or low doses of citrate with indomethacin were unsuccessful. High doses of collagen were more resistant to cyclo-oxygenase inhibitors than low doses of collagen.This study has shown that trisodium citrate will completely inhibit collagen-induced aggregation and that both high and low doses of collagen produce aggregation in the rat that is partially mediated by products of arachidonic acid metabolism. The biphase nature of the dose-response curves obtained with indomethacin and aspirin suggests that the higher doses are inhibiting the cyclooxygenase in the walls of blood vessels as well as in platelets thus reducing the endogenous release of prostacyclin. The nature of the arachidonic acid- independent pathway has yet to be demonstrated.
Platelet Uptake On Bioprosthetic Heart Valves
Authors: Oyama C , Klein S , Magilligan D J 
Published: July 2018

Single and aggregated platelets have been a consistent finding on the surface of 28 degenerated porcine bioprosthetic heart valves. Both the degenerated valves as well as unimplanted commercially available valves exhibit loss of endocardium with bare collagen fibers on scanning electron microscopy. The role of platelet adherence to the collagen fibers of these glutaraldehyde treated bioprostheses in causing degeneration is an unanswered question. Platelet adherence to porcine (P) valve (Type III collagen) and bovine (B) pericardium (Type I collagen) was measured in the glutaraldehyde treated bioprosthesis and in the fresh state with saline (F, S) and with plasma (F, P). Single cusps or similar samples of pericardium were rotated at 200 RPM for 10 min in a concentration of human platelets tagged with 51Cr. The tissue was trimmed to standard size, counted in a gamma counter and adherence calculated as platelets (pits)/mm2.Our experimental observations did not show a difference in platelet adherence between porcine or bovine tissue either G-treated or F. The G-treated valves showed significantly less (p=<.01) adherence than the F tissue. Although G- treated bioprostheses have collagen fibers exposed to circulating blood, platelet collagen reaction probably does not play a primary role in degeneration of the bioprosthetic heart valve.
Vascular Changes During Resolution Of Pulmonary Arterial Hypertension
Authors: Rawlings Clarence A , Keith James C , Schaub Robert G 
Published: July 2018

Pulmonary hypertension associated with myointimal proliferation is produced by low grade, sustained damage to the arterial surfaces by Dirofilaria immitis (DI) infection in dogs. This study correlated changes during and after infection in pulmonary vascular hemodynamics, arteriograms, and morphology {scanning electron microscopy (SEM) and light microscopy (LM)}. Seven beagles were infected with 50 infective DI larvae. Twelve months after infection, mild pulmonary hypertension {mean pulmonary arterial pressure (MPAP) during normoxia was 26.4 mmHg versus 16.0 pre-infection, during isoproterenol infusion was 37.6 vs. 14.3 pre-infection and reduction of pulmonary vascular resistance was 31.1% versus 47.2% pre-infection} was present. Angiograms at this time revealed dilation and tortuosities of the main and intralobar pulmonary arteries. SEM revealed large villus proliferations, disoriented cell axis, and pore formation. The villi projected (LM) into the vessel lumen and consisted of intimai thickening with multiplying smooth muscle cells and collagen.Seven months after treatment to eliminate the DI as a cause of the arterial trauma, pulmonary hypertension was resolved (MPAP of 19.8 during normoxia, 17.7 during isoproterenol infusion, and reduction of pulmonary vascular resistance of 45.2%). The arteriographie changes of dilation, aneurysms, and tortuosities were decreased, especially in the main and lobar arteries. LM revealed that larger arteries, which had greater arteriographie resolution, had relatively more elastic tissue and that the intralobar arteries had more collagen. SEM revealed that the villus proliferations were markedly reduced in numbers and sizes. This study characterized a reduction of hypertension as related to resolution of the muscular hypertrophy of arteries and related arteriographie changes to the type of connective tissue being produced by smooth muscle cells in the arterial wal.
Treatment Of Impaired Rheologic Conditions With Pentoxifylline (PO) In Patients With Cerebrovascular Disease (CVD)
Authors: Lechner H , Ott E 
Published: July 2018

Investigations have been performed in 55 patients (25 femals, 30 males) with a mean age of 61 years presenting focal neurological deficit due to acute or subacute CVD. Impairment of hemorheologic conditions has been diagnosed in more than one third of the patients using blood viscosity, hematocrits, fibrinogen and spontaneous as well as induced platelet aggregation (PA) as indicators. Blood viscosity has been determined by a cone - plate viscometer at four different shear rates and PA has been investigated using a modification of BORN’S method.Impaired hemorheologic conditions have been treated with Pentoxifylline (PO) during a period of 3 weeks administering 4,2 - 17,1 mg/kg body weight intravenously and/or by mouth. Thus, blood viscosity decreased significantly with a maximum decrease at low shear rates (11 sec -1) while hematocrits did not change. Likewise, mean fibrinogen levels decreased significantly during PO medication. Epinephrine as well as ADP induced PA have been succesfully inhibited by PO. However, drug induced changes of rheologic parameters were more pronounced when 17 mg/kg body weight were administered.It was concluded that PO is an effective drug for treatment of impaired rheologic conditions in patients with CVD.
The Anatomical Distribution Of Adpase Activity In The Rabbit Aorta
Authors: Emms Helen , Lewis G P 
Published: July 2018

Human and rabbit aorta have been shown to be capable of degrading ADP and a role for this ADPase enzyme has been suggested in the regulation of arterial thrombosis.The anatomical distribution of ADPase activity in the rabbit aorta has been investigated. The whole aorta, removed from exsanguinated rabbits, was divided into 6 sections and intact cells prepared by digestion with a mixture of enzymes. The cells were suspended in 0.25M sucrose and incubated for up to 40 minutes at 37°C with 14C- ADP (480µM-30µM) . ADP remaining in the incubation mixture was assayed by platelet aggregation and radiochromatography (which also enabled identification of the ADP metabolites).All 6 sections of aorta were capable of degrading ADP and its removal was time-dependent. The aortic arch and upper thoracic aorta, however, metabolised ADP only slowly and the rate of metabolism increased from the upper to the lower aorta. The lower abdominal sections removed ADP at the fastest rat.The major metabolite produced from ADP by the aortic arch and upper thoracic aorta was AMP. Middle and lower thoracic sections produced only AMP at 480µM ADP, whilst AMP,inosine and adenosine were produced at lower substrate concentrations. However, upper and lower abdominal sections produced AMP, inosine and adenosine at all concentrations of ADP.Atherosclerosis in rabbits has been reported to be more severe in the aortic arch and upper thoracic aorta than in the abdominal aorta. These results therefore suggest a connection between ADPase activity and the incidence of atherosclerosis. In the aortic arch and upper thoracic aorta, where ADPase activity is low, and adenosine, an inhibitor of aggregation, is not formed, there is a high incidence of the disease and conversely in the abdominal regions where ADPase activity is high and adenosine is formed the incidence of the disease is low.
Does Uremia Promote Atherogenesis?
Authors: Horsch A , Heuck C C , Hofmann W , Kühne W , Bisson M , Ritz E 
Published: July 2018

The development of experimental atherosclerosis was studied in subtotally nephrectomized rats which were subjected to preimmunisation with horseradish peroxidase and subsequent feeding with atherogenic diet. Both in sham operated pairfed control animals and in uremic animals, the atherogenic diet caused hyperlipemia which was more pronounced in uremic than in control animals (control animals: triglycerides 1.11 ± 0.04 mmol/1; cholesterol 5.82 ± 0.21 mmol/1; uremia: triglycerides 1.33 ± 0.06; cholesterol l0.9 ± 0.31). An increase of cholesterol was seen both in the VLDL and in the LDL fractions. Despite more pronounced hyperlipemia, lipid concentration in the aortic wall was not increased nor were more marked histological abnormalities encountered in the aorta of uremic animals.The results suggest that despite hyperlipemia short term experimental renal insufficiency does not promote atherogenesis.
Is It Possible To Increase The Effectiveness Of Heparin In Acute Thromboembolism?
Authors: Fontáyi S 
Published: July 2018

The purpose of this study is to call attention to the possibility to increase the effectiveness of Heparin basing on our 25 years experience in the treatment of acute thromboembolism.Our method developed gradually. First the only aim was to achieve limb salvage by preventing apposition of the thrombi and keeping the patency of segment below the occlusion. After unexpected and surprising recanalizations (tested by pedal pulses) in some cases, the aim to achieve recanalization has been endeavoured consciously. Technique: prolonged local massive intermittent Heparin dosage supported by simultaneous local Acetylcholine. Dosage: directed individually by daily clotting time control (Lee-White).Material: 1955-79. 232 arterial embolism, 114 thrombosis (112 underwent embolectomy or thrombectomy) and 44 deep phlebothrombosis.Results: according to some comparative studies on Heparin versus fibrinolytic treatment 2,5-23% of clearance (recanalization) of thrombosed veins has been achieved by Heparin with conventional intravenous doses. In our arterial material 33% recanalization and 46%b limb salvage represents the success. In deep phlebothrombosis only 4 cases showed mild postphlebitic symptoms at follow up.Conclusions: To explain the increased effectiveness of Heparin the following factors have been taken into consideration: 1. synergistic pharmacological and 2. hemodynamic effects of Heparin and Acetylcholine, 3. pathological factor (solubility of fresh thrombi), clinical factors: advantages of 4. local and 5. intermittent (stoss) dosage, 6. keeping the principles of urgency, 7. economical factors (cheap, simple labor-control).
Effects Of Aspirin (ASA) And Sulfinpyrazone (SPZ) On The Coagulopathy Of Diabetic Nephropathy (DN)
Authors: Mariscal I , Fernandez de Castro J 
Published: July 2018

In diabetics, changes in the vessel wall and platelet hyperaggre- gability are well documented. Fg/Fn deposits in the glomeruli among other changes as well as cDIC have been described in DN. Based on these data this study was planned to explore the role of platelets in the coagolopathy of DN.Eighteen patients with DN characterized by mild to severe urea retention, significant proteinuria and creatinine clearance of 67 ml/min or less participated in a study which was prospective,dou ble blind, random in distribution and subject to the patient's own control. ASA 1.0 gm or SPZ 600 mgs or placebo 3 pills/day was used. Coagulation and fibrinolysis tests were done regularly. ASA shortened thrombin time (Biggs) from 22.0 to 19.3 sec *, - raised plasminogen (Mancinni-M Partigen Plasminogen) from 12 to 13 mgs P=NS and decreased FDP (Merskey) in serum from 56 to 32 Ug ** and in urine from 2.8 to 1.0 Ug **. SPZ raised plasminogen from 12 to 13 mgs **.Both ASA and SPZ decreased fibrinogen (Ingram) P=NS and produce no change on PT (Quick), PTT (Proctor) and platelet count (Bratcher & Cronkite). SPZ changes were interesting but barely significant up to now. The changes induced by ASA are suggestive that cDIC was inhibited. Since ASA has no direct effect on the modified parameters, it can be considered that the action was due to ASA antiplatelet activity.We can propose that platelets play an important role in maintaining the coagulopathy of DN and possibly in initiating it.
The Effects Of Chemical Alterations Of The Benzoic Acid Nucleus On Platelet Function And Prostacyclin Activity In The Arterial Wall
Authors: Killackey B A , Killackey J J , Philp R B 
Published: July 2018

The effects of a series of benzoic acid derivatives (ASA analogs) on prostacyclin (PGI2) synthesis by rabbit aorta rings and on human platelet function were examined to determine if antiplatelet activity could be separated from anti-PGI2 activity.Rings of rabbit aorta were incubated with or without drugs in Tris 0.05 M, pH 7.5 for 6 m at room temperature (R.T.). Supernatant was then transferred to platelet-rich plasma incubated at 37°C for 3 m. ADP was added 60 s later and aggregation was measured and compared to controls. Rings were also incubated with 14C-arachidonic acid (14C-AA) for 60 m at R.T. in Tris with or without drugs. Products were extracted and measured by radio-T.L.C. along with known standards. Platelet aggregation and release of ATP were measured using a ChronoLog Lumi aggregometer. The effects of these agents on PGI2 activity were similar to their effects on platelet aggregation. ASA however did not exhibit the marked inhibitory potency that it had on the second phase of platelet aggregation and ATP release. Changing the 2-acetoxy group of A.S.A. to a 2-acetyl or 3-propionyloxy resulted in a loss of inhibitory activity in both systems. 2-Propionyloxy substitution resulted in a similar spectrum of activity to ASA. The effects of these agents on the metabolism of 14C-AA by rabbit aorta rings generally confirmed the bioassay results although some of the agents had novel effects on blood vessel arachidonic acid metabolism.Despite potential species differences, this study demonstrates an inability to separate antiplatelet and anti-PGI2 effects with this series of benzoic acid derivatives. Further study of the effects of these agents on the metabolism of 14C-AA by rings of rabbit aorta may lead to a better understanding of PGI2 formation.