Placental Sars-Cov-2 distribution correlates with level of tissue oxygenation in Covid-19-associated necrotizing histiocytic intervillositis/perivillous fibrin deposition

Tissue-type plasminogen activator (t-PA) which has a high affinity for fibrin in the clot, was labeled with 131I by the iodogen method, and its binding to de-endothelialized lesions in the rabbit was measured to assess the detectability of thrombi. The de-endothelialized lesion was induced in the abdominal aorta with a Fogarty 4F balloon catheter. Two hours after the de-endothelialization, 131I-labeled t-PA (125 ± 46 μCi) was injected intravenously. The initial half-life of the agent in blood (n = 12) was 2.9 ± 0.4 min. The degree of binding of 131I-labeled t-PA to the de-endothelialized lesion was evaluated at 15 min (n = 6) or at 30 min (n = 6) after injection of the agent. In spite of the retention of the biochemical properties of 131I-labeled t-PA and the presence of fibrin deposition at the de-endothelialized lesion, the binding of t-PA to the lesion was not sufficiently strong. Lesion-to-control ratios (cpm/g/cpm/g) were 1.65 ± 0.40 (at 15 min) and 1.39 ± 1.31 (at 30 min), and lesion-to-blood ratios were 1.39 ± 0.32 (at 15 min) and 1.36 ± 0.23 (at 30 min). These results suggest that radiolabeled t-PA may be inappropriate as a radiopharmaceutical for the scintigraphic detection of a pre-existing thrombotic lesion.

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Fibrin Derivatives, Plasma Hemoglobin and Glomerular Fibrin Deposition in Experimental Intravascular Coagulation

Thrombosis and Haemostasis ◽

10.1055/s-0038-1647778 ◽

1973 ◽

Vol 29 (02) ◽

pp. 363-374 ◽

Cited By ~ 11

Author(s):

F. K Beller ◽

W Theiss

Keyword(s):

Quantitative Measurement ◽

Plasma Fibrinogen ◽

Moderate Increase ◽

Consumption Coagulopathy ◽

Fibrin Deposition ◽

Intravascular Coagulation ◽

Plasma Hemoglobin ◽

Three Stages ◽

Two Parameters ◽

Gelation Test

SummaryPlasma fibrinogen, circulating fibrinmonomers (as indicated by a positive ethanol gelation test), fibrinolysis breakdown products and plasma hemoglobin were assayed in 122 rats subjected to endotoxin injection or infusion. The results were correlated with the quantitative measurement of glomerular fibrin deposition. Based on these data four groups were determined : consumption coagulopathy and three stages of increasing severity of disseminated intravascular coagulation (DIG).Consumption coagulopathy was defined by a decrease in plasma fibrinogen and a positive ethanol gelation test in the absence of glomerular fibrin deposition. Plasma hemoglobin and fibrinolysis breakdown products were normal or only slightly increased.DIG as characterized by glomerular fibrin deposition was defined as moderate (1 to 20% glomeruli showing fibrin strands), intermediate (21 to 80%), and severe (81 to 100%). Decrease in plasma fibrinogen and frequence of a positive ethanol gelation test in all stages of DIG were only slightly different from the findings in consumption coagulopathy. However, a sharp increase in plasma hemoglobin levels was noted when glomerular fibrin deposition did occur even in small amounts. At this time only a moderate increase was noted in fibrin(ogen) breakdown products. These two parameters increased only slightly in the group of intermediate DIG. Severe DIG was characterized by a massive increase in fibrin (ogen) breakdown products and high levels of plasma hemoglobin.

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Fibrinolysis in Decidual Spiral Arteries in Late Pregnancy

Thrombosis and Haemostasis ◽

10.1055/s-0038-1646752 ◽

1978 ◽

Vol 39 (03) ◽

pp. 751-758 ◽

Cited By ~ 12

Author(s):

B L Sheppard ◽

J Bonnar

Keyword(s):

Electron Microscopy ◽

Endothelial Cells ◽

Fibrinolytic Activity ◽

Physiological Mechanism ◽

Late Pregnancy ◽

Full Term ◽

Fibrin Deposition ◽

Placental Villi ◽

The Media ◽

Slide Technique

SummaryThe fibrinolytic activity of the intimal cells of decidual spiral arteries and the syncytium of placental villi was studied by electron microscopy in ten normal full-term human pregnancies using a modification of the fibrin slide technique. Endothelial cells lining the intima of the decidual spiral arteries showed a considerably greater fibrinolytic activity than intimal cytotrophoblast and the syncytiotrophoblast showed no activity.The replacement of endothelial cells by an intimal lining of cytotrophoblast, and the presence of cytotrophoblast in the media, appears to play an important role in the reduction of the fibrinolytic activity of the vessel. This inhibition of fibrinolytic activity in the utero-placental arteries may be the physiological mechanism which controls fibrin deposition in these vessels and on the placental villi.

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Anti-thrombotic Effect of a PAI-1 Inhibitor in Rats Given Endotoxin

Thrombosis and Haemostasis ◽

10.1055/s-0038-1650231 ◽

1996 ◽

Vol 75 (01) ◽

pp. 118-126 ◽

Cited By ~ 27

Author(s):

T Abrahamsson ◽

V Nerme ◽

M Strömqvist ◽

B Åkerblom ◽

A Legnehed ◽

...

Keyword(s):

Plasminogen Activator Inhibitor ◽

Rat Plasma ◽

Clot Lysis ◽

Fibrin Deposition ◽

Plasminogen Activator Inhibitor 1 ◽

Fab Fragment ◽

Dose Dependent Decrease ◽

Pai 1

SummaryThe aim of this study was to investigate the anti-thrombotic effects of an inhibitor of the plasminogen activator inhibitor-1 (PAI-1) in rats given endotoxin. In studies in vitro, PRAP-1, a Fab-fragment of a polyclonal antibody against human PAI-1, was shown to inhibit PAI-1 activity in rat plasma as well as to stimulate clot-lysis of the euglobulin fraction derived from rat plasma. Endotoxin administered to anaesthetised rats produced a marked increase in plasma PAI-1 activity. To study fibrin formation and lysis in vivo after intravenous (i. v.) injection of the coagulant enzyme batroxobin, 125I-fibrinogen was administered to the animals. The thrombi formed by batroxobin were rapidly lysed in control animals, while the rate of lysis was markedly attenuated in rats given endotoxin. PRAP-1 was administered i.v. (bolus + infusion) to rats given endotoxin and batroxobin and the PAI-1 inhibitor caused a dose-dependent decrease in the 125I-fibrin deposition in the lungs. An immunohistochemical technique was used to confirm this decrease in density of fibrin clots in the tissue. Furthermore, PRAP-1 decreased plasma PAI-1 activity in the rats and this reduction was correlated to the decrease in lung 125I-fibrin deposition at the corresponding time point. It is concluded that in this experimental model the PAI-1 antibody PRAP-1 may indeed inhibit thrombosis in animals exposed to endotoxin.

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Hypercoagulability and High Lipoprotein(a) Levels in Patients with Central Retinal Vein Occlusion

Thrombosis and Haemostasis ◽

10.1055/s-0038-1648808 ◽

1994 ◽

Vol 72 (01) ◽

pp. 039-043 ◽

Cited By ~ 46

Author(s):

Francesco Bandello ◽

Silvana Vigano’ D’Angelo ◽

Mariella Parlavecchia ◽

Alessandra Tavola ◽

Patrizia Della Valle ◽

...

Keyword(s):

Retinal Vein Occlusion ◽

Central Retinal Vein Occlusion ◽

Specific Treatment ◽

Fibrin Deposition ◽

Heparin Cofactor Ii ◽

Lipoprotein A ◽

Vein Occlusion ◽

Acute Event ◽

D Dimer ◽

Central Retinal Vein

SummaryA series of coagulation parameters and lipoprotein(a) (Lp(a)) were explored in plasma from 40 patients with central retinal vein occlusion (CRVO, non-ischemic type n = 12; ischemic type n = 28) free of local and systemic predisposing factors, 1 to 12 months after the acute event. Forty age- and sex-matched patients with cataract served as controls. Prothrombin fragment 1.2 (FI.2), D-dimer, FVII:C - but not FVII: Ag - were higher and fibrinogen was lower in CRVO patients than in controls. Patients with non-ischemic CRVO had higher FI .2 and FVII:C and lower heparin cofactor II than patients with ischemic CRVO. Lp(a) levels greater than 300 mg/1 were observed in 12 patients with CRVO and in 4 controls (30% vs 10%, p <0.025). Patients with high Lp(a) - consistently associated with the S2 phenotype - had higher FVII:C, FVII:C/Ag ratio, and fibrinogen than the remaining CRVO patients. Plasma FI.2 and D-dimer correlated fairly in controls (r = 0.41) and patients with normal Lp(a) levels (r = 0.55), but they did not in the group of patients with high Lp(a) (r = 0.19), where the latter parameter was negatively related to D-dimer (r = −0.55). There was no dependence of the abnormalities observed on the time elapsed from vein occlusion. The findings of activated FVII and high FI.2, D-dimer, and Lp(a) are not uncommon in patients with CRVO. Increased thrombin formation with fibrin deposition and impaired fibrinolysis may play a role in the pathophysiology of CRVO and require specific treatment

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The Intravascular Generation of Fibrinogen Derivatives and the Blood Vessel Wall in Venous Thrombosis and Disseminated Intravascular Coagulation

Thrombosis and Haemostasis ◽

10.1055/s-0038-1651902 ◽

1977 ◽

Vol 38 (04) ◽

pp. 0831-0849 ◽

Cited By ~ 1

Author(s):

Gwendolyn J. Stewart

Keyword(s):

Blood Vessel ◽

Venous Thrombosis ◽

Vessel Wall ◽

Fluid Phase ◽

Primary Site ◽

Blood Vessel Wall ◽

Fibrin Deposition ◽

Tissue Destruction ◽

Fibrin Formation ◽

Rich Material

SummaryBoth deep venous thrombosis and DIC are intermediate mechanisms of disease – both are a consequence of the deposition of fibrin-rich material in blood vessels some distance from the primary site of tissue destruction. The great difference in the sites of fibrin deposition may depend on the extent and site of activation of the clotting mechanism. DIC likely occurs in the fluid phase of the blood as a consequence of massive fibrin formation while thrombosis results from limited fibrin formation at the interface between blood and vessel wall. Leukocytes may be essential for attaching thrombi to the vessel wall in many places.

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Abnormal Haemostasis and Blood Viscosity in Malignant Hypertension

Thrombosis and Haemostasis ◽

10.1055/s-0038-1661190 ◽

1984 ◽

Vol 52 (03) ◽

pp. 253-255 ◽

Cited By ~ 11

Author(s):

C Isles ◽

G D O Lowe ◽

B M Rankin ◽

C D Forbes ◽

N Lucie ◽

...

Keyword(s):

Blood Pressure ◽

Blood Viscosity ◽

Renal Damage ◽

Antithrombin Iii ◽

Plasma Viscosity ◽

Malignant Hypertension ◽

Fibrin Deposition ◽

Group 3 ◽

Group 2 ◽

Group 1

SummaryWe have previously shown abnormalities of haemostasis suggestive of intravascular coagulation in patients with malignant hypertension, a condition associated with retinopathy and renal fibrin deposition. To determine whether such abnormalities are specific to malignant hypertension, we have measured several haemostatic and haemorheological variables in 18 patients with malignant hypertension (Group 1), 18 matched healthy controls (Group 2), and 18 patients with non-malignant hypertension (Group 3) matched for renal pathology, blood pressure and serum creatinine with Group 1. Both Groups 1 and 3 had increased mean levels of fibrinogen, factor VIIIc, beta-thrombo- globulin, plasma viscosity and blood viscosity (corrected for haematocrit); and decreased mean levels of haematocrit, antithrombin III and platelet count. Mean levels of fast antiplasmin and alpha2-macroglobulin were elevated in Group 1 but not in Group 3. We conclude that most blood abnormalities are not specific to malignant hypertension; are also present in patients with non-malignant hypertension who have similar levels of blood pressure and renal damage; and might result from renal damage as well as promoting further renal damage by enhancing fibrin deposition. However increased levels of fibrinolytic inhibitors in malignant hypertension merit further investigation in relation to removal of renal fibrin.

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