scholarly journals Mechanisms for elevated fibrin/fibrinogen degradation products in acute experimental pulmonary embolism

Blood ◽  
1975 ◽  
Vol 45 (4) ◽  
pp. 563-568 ◽  
Author(s):  
J Cade ◽  
J Hirsh ◽  
E Regoeczi
Keyword(s):  
Pulmonary Embolism ◽  
Degradation Products ◽  
Blood Clot ◽  
Autologous Blood ◽  
Peak Level ◽  
Fibrin Deposition ◽  
Experimental Conditions ◽  
Fibrin Degradation Products ◽  
Serial Measurements ◽  
Autologous Blood Clot

Abstract The mechanism and significance of elevated levels of serum fibrin degradation products (FDP) in pulmonary embolism were investigated experimentally. Dogs were embolized with autologous blood clot-incorporating canine 125I-fibrin and were infused with either saline, heparin, or streptokinase. Serial measurements were made of total FDP by hemagglutination inhibition assay and of radioactive FDP. After saline, the peak level of total FDP was 323 mug/ml, but radioactive FDP was only 8 mug/ml. After heparin, these values were 44 and 11 mug/ml, respectively, and after streptokinase, 415 and 20 mug/ml. The results suggest that under these experimental conditions the elevated levels of FDP in pulmonary embolism are derived mainly from lysis of fibrin deposited after embolization rather than from lysis of the original embolus. Heparin inhibits both fibrin deposition and elevation of FDP levels after embolism.

scholarly journals Mechanisms for elevated fibrin/fibrinogen degradation products in acute experimental pulmonary embolism

Blood ◽  
1975 ◽  
Vol 45 (4) ◽  
pp. 563-568
Author(s):  
J Cade ◽  
J Hirsh ◽  
E Regoeczi
Keyword(s):  
Pulmonary Embolism ◽  
Degradation Products ◽  
Blood Clot ◽  
Autologous Blood ◽  
Peak Level ◽  
Fibrin Deposition ◽  
Experimental Conditions ◽  
Fibrin Degradation Products ◽  
Serial Measurements ◽  
Autologous Blood Clot

The mechanism and significance of elevated levels of serum fibrin degradation products (FDP) in pulmonary embolism were investigated experimentally. Dogs were embolized with autologous blood clot-incorporating canine 125I-fibrin and were infused with either saline, heparin, or streptokinase. Serial measurements were made of total FDP by hemagglutination inhibition assay and of radioactive FDP. After saline, the peak level of total FDP was 323 mug/ml, but radioactive FDP was only 8 mug/ml. After heparin, these values were 44 and 11 mug/ml, respectively, and after streptokinase, 415 and 20 mug/ml. The results suggest that under these experimental conditions the elevated levels of FDP in pulmonary embolism are derived mainly from lysis of fibrin deposited after embolization rather than from lysis of the original embolus. Heparin inhibits both fibrin deposition and elevation of FDP levels after embolism.

Changes in Regional Ventilation after Autologous Blood Clot Pulmonary Embolism

2002 ◽  
Vol 97 (3) ◽  
pp. 671-681 ◽  
Author(s):  
Marcos F. Vidal Melo ◽  
R. Scott Harris ◽  
Dominick Layfield ◽  
Guido Musch ◽  
Jose G. Venegas
Keyword(s):  
Positron Emission Tomography ◽  
Pulmonary Embolism ◽  
Pulmonary Artery ◽  
Dead Space ◽  
Blood Clot ◽  
Autologous Blood ◽  
Emission Tomography ◽  
Central Vein ◽  
Positron Emission ◽  
Autologous Blood Clot

Background Previous studies have suggested that pulmonary embolism (PE) and pulmonary artery occlusion result in a shift in alveolar ventilation away from unperfused regions. This study aimed to directly assess changes in regional specific ventilation (sV(A)) due to autologous blood clot PE using positron emission tomography. Methods Pulmonary embolism was created in six anesthetized, paralyzed, and mechanically ventilated sheep by injecting cylindrical clots of autologous blood (7 mm in diameter and height). Clots were progressively infused into a central vein until a stable mean pulmonary artery pressure between 30 and 40 mmHg was achieved. A multislice positron emission tomography camera was used to image 15 contiguous, 6.5-mm-thick transverse cross-sections of the chest beginning just above the diaphragm. sV(A) from perfused regions (sV(A),(p)) was assessed as the ventilatory turnover rate of the tracer NN after central venous injection of NN-labeled saline. Results Pulmonary embolism obstructed flow to 64% of imaged areas. Before PE, (sV(A),(p))was equivalent in areas that would remain perfused and those that would become embolized after PE (0.021 +/- 0.007 0.021 +/- 0.006 s(-1); P = nonsignificant). After PE, sV(A),(p) of areas remaining perfused increased to 0.033 +/- 0.011 s (-1) (P < 0.005). This effect on regional sV(A),(p) could have been caused by active redistribution of sV(A),(p) or by a reduction in tracer concentration of perfused areas due to the dead space common to perfused and embolized regions. Model simulations indicated that the common dead-space effect could only explain a small part of the sV(A),(p) increase. Conclusions An increase in sV(A),(p) of perfused regions occurs following PE with 7-mm autologous blood clots. This increase is most likely caused by a shift in ventilation away from embolized areas mediated by hypocapnic pneumoconstriction.

Embolus size affects gas exchange in canine autologous blood clot pulmonary embolism

1993 ◽  
Vol 74 (3) ◽  
pp. 1140-1148 ◽  
Author(s):  
M. Delcroix ◽  
C. Melot ◽  
P. Vanderhoeft ◽  
R. Naeije
Keyword(s):  
Pulmonary Hypertension ◽  
Gas Exchange ◽  
Blood Clot ◽  
Autologous Blood ◽  
Inert Gas ◽  
Experimental Conditions ◽  
Arterial Ph ◽  
Pulmonary Arterial ◽  
Vascular Obstruction ◽  
Autologous Blood Clot

Embolic pulmonary hypertension is associated with alterations in gas exchange of variable severity, which we hypothesized to be related to embolus size. We therefore examined the effects of different-size autologous blood clot embolization on pulmonary arterial pressure-cardiac output relationships (Ppa/Q) and on the distribution of ventilation-perfusion ratios (VA/Q) in 18 intact anesthetized and ventilated (inspired fraction of O2 0.4) dogs. Multipoint Ppa/Q plots were generated by a manipulation of venous return before and 60 min after sufficient amounts of small (1 mm, n = 6 dogs), medium (5 mm, n = 6 dogs), or large (10 mm, n = 6 dogs) clots to increase Ppa to 50 mmHg. The distribution of VA/Q was determined by the multiple inert gas elimination technique at the same intermediate Q in each of these experimental conditions. All three sizes of emboli resulted in an 82–92% mean angiographic pulmonary vascular obstruction and increased both the extrapolated pressure intercepts and the slopes of the linear Ppa/Q plots. Gas exchange was altered the most after large clots, which were associated with lower arterial pH, higher physiological and inert gas dead spaces, higher dispersion of ventilation, and also lower mean VA/Q of perfusion distributions. In contrast, inert gas dead space was decreased after small clots. We conclude that, in autologous blood clot embolic pulmonary hypertension, Ppa/Q characteristics are unaffected by embolus size but that gas exchange is affected differently, mainly in high-VA/Q regions and most often after the largest clots.

A Monoclonal Antibody-Based Enzyme Immunoassay for Fibrin Degradation Products in Plasma

1988 ◽  
Vol 59 (02) ◽  
pp. 310-315 ◽  
Author(s):  
P W Koppert ◽  
E Hoegee-de Nobel ◽  
W Nieuwenhuizen
Keyword(s):  
Enzyme Immunoassay ◽  
Degradation Products ◽  
Blood Clot ◽  
Tissue Type ◽  
Fibrin Degradation Products ◽  
Type Plasminogen Activator ◽  
Strong Positive Reaction ◽  
Sandwich Type ◽  
Capture Antibody

SummaryWe have developed a sandwich-type enzyme immunoassay (EIA) for the quantitation of fibrin degradation products (FbDP) in plasma with a time-to-result of only 45 minutes.* The assay is based on the combination of the specificities of two monoclonal antibodies (FDP-14 and DD-13), developed in our institute. FDP-14, the capture antibody, binds both fibrinogen degradation products (FbgDP) and FbDP, but does not react with the parent fibrin(ogen) molecules. It has its epitope in the E-domain of the fibrinogen molecule on the Bβ-chain between amino acids 54-118. Antibody DD-13 was raised using D-dimer as antigen and is used as a tagging antibody, conjugated with horse-radish peroxidase. A strong positive reaction is obtained with a whole blood clot lysate (lysis induced by tissue-type plasminogen activator) which is used as a standard. The EIA does virtually not detect FbgDP i. e. purified fragments X, Y, or FbgDP generated in vitro in plasma by streptokinase treatment. This indicates that the assay is specific for fibrin degradation products.We have successfully applied this assay to the plasma of patients with a variety of diseased states. In combination with the assay previously developed by us for FbgDP and for the total amount of FbgDP + FbDP (TDP) in plasma, we are now able to study the composition of TDP in patients plasma in terms of FbgDP and FbDP.

Appearance of Nuclear-sorted Caspase-12 Fragments in Cerebral Cortical and Hippocampal Neurons in Rats Damaged by Autologous Blood Clot Embolic Brain Infarctions

2011 ◽  
Vol 31 (5) ◽  
pp. 795-802 ◽  
Author(s):  
Koji Shimoke ◽  
Yoshinori Matsuki ◽  
Kenji Fukunaga ◽  
Yoshinobu Matsumura ◽  
Eriko Fujita ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Blood Clot ◽  
Autologous Blood ◽  
Caspase 12 ◽  
Autologous Blood Clot

scholarly journals Intranasal salvinorin A improves neurological outcome in rhesus monkey ischemic stroke model using autologous blood clot

2020 ◽  
pp. 0271678X2093813
Author(s):  
Longfei Wu ◽  
Di Wu ◽  
Jian Chen ◽  
Chunhua Chen ◽  
Tianqi Yao ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Rhesus Monkeys ◽  
Infarct Volume ◽  
Blood Clot ◽  
Autologous Blood ◽  
Control Group ◽  
Stroke Model ◽  
Neurological Outcomes ◽  
Observation Period ◽  
Autologous Blood Clot

Salvinorin A (SA) exerts neuroprotection and improves neurological outcomes in ischemic stroke models in rodents. In this study, we investigated whether intranasal SA administration could improve neurological outcomes in a monkey ischemic stroke model. The stroke model was induced in adult male rhesus monkeys by occluding the middle cerebral artery M2 segment with an autologous blood clot. Eight adult rhesus monkeys were randomly administered SA or 10% dimethyl sulfoxide as control 20 min after ischemia. Magnetic resonance imaging was used to confirm the ischemia and extent of injury. Neurological function was evaluated using the Non-Human Primate Stroke Scale (NHPSS) over a 28-day observation period. SA significantly reduced infarct volume (3.9 ± 0.7 cm3 vs. 7.2 ± 1.0 cm3; P =  0.002), occupying effect (0.3 ± 0.2% vs. 1.4 ± 0.3%; P =  0.002), and diffusion limitation in the lesion (−28.2 ± 11.0% vs. −51.5 ± 7.1%; P =  0.012) when compared to the control group. SA significantly reduced the NHPSS scores to almost normal in a 28-day observation period as compared to the control group ( P =  0.005). Intranasal SA reduces infarct volume and improves neurological outcomes in a rhesus monkey ischemic stroke model using autologous blood clot.

scholarly journals Production and characterization of a monoclonal antibody reactive with a specific neoantigenic determinant (comprising B beta 54-118) in degradation products of fibrin and of fibrinogen

Blood ◽  
1986 ◽  
Vol 68 (2) ◽  
pp. 437-441 ◽  
Author(s):  
PW Koppert ◽  
J Koopman ◽  
F Haverkate ◽  
W Nieuwenhuizen
Keyword(s):  
Degradation Products ◽  
Blood Clot ◽  
Immunoaffinity Chromatography ◽  
Tissue Type ◽  
Spleen Cells ◽  
Fibrin Degradation Products ◽  
Type Plasminogen Activator ◽  
Complete Lysis ◽  
Fibrin Monomers

Abstract Balb/c mice were immunized with a mixture of fibrin degradation products (XDPs) prepared by complete lysis of a human blood clot by tissue-type plasminogen activator and purified by immunoaffinity chromatography. Spleen cells of the mice were fused with P3 X 63 Ag 8653 myeloma cells. A clone (FDP 14) was selected that produces monoclonal antibodies (MoAbs) of the IgG1 kappa type that react with a neoantigenic determinant exposed in these XDPs, but not in intact fibrinogen or in fibrin monomers. Furthermore, the MoAb is reactive with some pure, individual degradation products of fibrinogen (fragments X, Y, E, and the N-terminal disulphide knot) and with the fibrinogen B beta-chain but not with A alpha- and gamma-chains or with fragments D, FCB-2 and FCB-3. Comparison of the known primary structures of these fibrinogen fragments indicates that the stretch B beta 54–118 comprises at least an important part of the epitope recognized by FDP-14. Apparently, this stretch contributes importantly to a neoantigenic determinant that is not functional in intact fibrinogen and fibrin monomer and that can be made functional by reduction of fibrinogen, or by digestion with plasmin or CNBr.

scholarly journals Hematologic and Coagulation Measurements in Autotransfused Blood

1977 ◽  
Author(s):  
F.N. McKenzie ◽  
W. Wall ◽  
R.O. Heimbecker ◽  
R. Barr ◽  
A. Robert
Keyword(s):  
Degradation Products ◽  
Autologous Blood ◽  
Significant Risk ◽  
Major Surgery ◽  
Clot Lysis ◽  
Plasma Hemoglobin ◽  
Fibrin Degradation Products ◽  
Excellent Preservation ◽  
The Mean

Reinfusion of blood shed during elective or emergency vascular surgery (autotransfusion) is an under utilized technique. This is due in part to doubts as to the quality of autotransfused blood and concern about the risk of inducing a coagulopathy in the recipient. We have measured coagulation and hematologic parameters in autotransfused blood in the recipient before and at intervals after operation in 62 patients, none of whom received bank blood or blood products at the time of the study. The patients were heparinized (3 mg/Kg) during operation and this was reversed by protamine at the end of the procedure. The salvaged blood was reinfused immediately after appropriate samples had been taken. The mean volume of blood autotransfused was 1.8L in 58 patients and 9.4L in 4 patients. There was excellent preservation of platelets and fibrinogen, normal levels being maintained both in the autotransfused blood and in the recipients. Values for fibrin degradation products and euglobulin clot lysis remained normal. The mean plasma hemoglobin in the autotransfused blood was 416 mg% and this was not correlated to the volume autotransfused. Partial thromboplastin time which was prolonged by heparin during surgery was consistently normal post-operatively. No patient developed complications which could be attributed to autotransfusion and, in particular, re-operation for post-operative bleeding was never required and wound hematoma was not seen. We conclude that autologous blood may be returned to patients in large amounts without significant risk using the technique described. The technique deserves wider application in major surgery.

A NEW QUANTITATIVE ENZYME-IMMUNOASSAY FOR FIBRIN DEGRADATION PRODUCTS (FbDP) IN PLASMA, BASED ON MONOCLONAL ANTIBODIES

1987 ◽  
Author(s):  
P W Koppert ◽  
E Hoegee-de Nobel ◽  
W Nieuwenhuizen
Keyword(s):  
Monoclonal Antibodies ◽  
Enzyme Immunoassay ◽  
Degradation Products ◽  
Blood Clot ◽  
Tissue Type ◽  
Fibrin Degradation Products ◽  
Type Plasminogen Activator ◽  
Strong Positive Reaction ◽  
Sandwich Type

We have developed a sandwich-type enzyme immunoassay (EIA) for the quantitation of fibrin degradation products (FbDP) in plasma with a time-to-result of only 45 minutes. The assay is based on the combination of the specificities of two monoclonal antibodies (FDP-14 and DD-13), developed in our institute. FDP-14, the catching antibody, binds both fibrinogen degradation products (FbgDP) and FbDP. It has its epitope in the E-domain of the fibrinogen molecule on the BB-chain between amino acids 54-118 (Blood 68, 437, 1986). Antibody DD-13 was raised using D-dimer as antigen and was used as a tagging antibody, conjugated with horse-radish peroxidase.A strong positive reaction is obtained with a whole blood clot lysate (lysis induced by tissue-type plasminogen activator) which is used as a standard.The EIA does not detect FbgDP i.e. purified fragments X, Y, D:E complexes or FbgDP in plasma treated in vitro with streptokinase. This indicates that the assay is specific for fibrin degradation products.We have successfully applied this assay to the plasma of patients with a variety of diseases. In combination with the assays previously developed by us for FbgDP (Thromb. Haemostas. 1987, in press) and for the total amount (TDP) of FbgDP + FbDP in plasma (J. Lab. Clin. Med. 1987, in press), we are now able to study the composition of TDP in terms of FbgDP and FbDP in patients.

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