Localization of Fibrinolytic Activity in Myocardial Infarcts in Rats

1964 ◽  
Vol 12 (02) ◽  
pp. 407-417 ◽  
Author(s):  
H. C Kwaan ◽  
T Astrup
Keyword(s):  
Blood Vessels ◽  
Plasminogen Activator ◽  
Normal Tissue ◽  
Fibrinolytic Activity ◽  
Tissue Repair ◽  
Left Coronary Artery ◽  
Repair Process ◽  
Ventricular Wall ◽  
Heat Treated

SummaryAcute myocardial infarction was produced in rats by ligation of the left coronary artery. Different phases of healing, up to 6 weeks, were studied in order to compare its normal histology with the appearance and localization of fibrinolytic activity.The fibrinolytic activity was studied by the histochemical method using plasminogen rich fibrin substrate for demonstration of plasminogen activator, and a plasminogen free fibrin substrate (heat treated) for protease estimation. In all the specimens studied only plasminogen activator was detected.The usual morphological features were essentially the same as those described by previous authors. The fibrinolytic activity in the normal ventricular wall was sparsely distributed and was localized to the small blood vessels. In the early infarct fibrinolytic activity had disappeared, but it reappeared in the thrombosed small blood vessels as organization and recanalization took place. It was present in increased amounts in the newly formed blood vessels growing into the infarcted area and persisted in these vessels after healing was complete though slowly decreasing in frequency of distribution and in concentration. The results show that healing of myocardial infarcts follows the pattern of a normal tissue repair process, and they substantiate the role of the fibrinolytic system in wound healing.

Persistence of Fibrinolytic Activity in Fragments of Human Veins Cultured in Vitro

1970 ◽  
Vol 24 (01/02) ◽  
pp. 043-047 ◽  
Author(s):  
M Pandolfi
Keyword(s):  
Blood Vessels ◽  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Vasa Vasorum ◽  
Adult Human ◽  
Slide Technique

SummaryExplants from 5 adult human veins were cultured in a fibrinolytically inactive medium for 3 weeks and assayed for the presence of plasminogen activator by the fibrin slide technique. The explants from 3 veins showed fibrinolytic activity confined to their vasa vasorum for the whole duration of the culture; no decrease of activity was seen. The finding suggests that small blood vessels are able to synthesize plasminogen activator.

scholarly journals The Lysis of Early Fibrin by Eosinophils

1977 ◽  
Author(s):  
Hau C. Kwaan ◽  
Ali A. Hatem
Keyword(s):  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Cell Membranes ◽  
Red Cell ◽  
Platelet Thrombus ◽  
Platelet Aggregates ◽  
Platelet Thrombi ◽  
Arteries And Veins ◽  
Morphologic Changes

This study examins the role of leukocytes within a thrombus by demonstrating the morphologic detail of their activities, the chemotactic properties of thrombi and the presence of plasminogen and possible plasminogen activator within eosinophils. A model which produces discrete, reproducible platelet thrombi in arteries and veins of dogs allowed timed studies of their early evolution. In this model, the growth of the thrombus was constantly monitored by a flowmeter and the thrombus could thus be removed at a selected period in its formation. It was then studied histologically for fibrin activity and also ultrastructually. Little fibrinolytic activity was found. In contrast to neutrophils which are concerned particularly with the phagocytosis and disruption of platelet aggregates, we observed that eosinophils participate in the lysis and disruption of the fibrin within these aggregates. The fibrin is rarely phagocytosed but is acted on at the surfaces of the eosinophils, usually in shallow invaginations of the cell membranes. The fibrin shows morphologic changes of lysis. It appears that eosinophils and neutrophils are concerned with the transformation of the early fibrin and platelet thrombus, rather than with the resolution of the formed, mainly fibrin and red cell thrombus.

P5374Genetic deletion of IL-22 increased cardiac rupture after myocardial infarction in mice

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Yamamoto ◽  
H Yasukawa ◽  
J Takahashi ◽  
S Nohara ◽  
T Sasak ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Real Time ◽  
Real Time Pcr ◽  
Tissue Repair ◽  
Repair Process ◽  
Cardiac Rupture ◽  
Blue Dye ◽  
Border Area ◽  
Infarct Area

Abstract Background Interleukin-22 (IL-22) is a member of the IL-10 cytokine family, which mainly targets epithelial cells and does not target immune cells. Recently, it has been reported that IL-22 play roles in tissue repair in the skin and the liver; however, role of IL-22 in the process of tissue repair after myocardial infarction (MI) is unknown. Here, we investigated the role of IL-22 in tissue repair process after MI. Methods and results First, we examined the expression of IL-22 and its receptor IL-22RA1 in the wild type (WT) mice by real-time PCR. The expression of IL-22 and IL-22RA1 in the hearts were significantly increased 3 days after MI (p<0.05). To clarify the role of IL-22 in the heart after MI, we produced MI model in the WT mice and IL-22 knockout (KO) mice. We found that the IL-22 KO mice had significantly higher mortality than the WT mice after MI (p<0.05). Approximately 80% of the IL-22 KO mice died with cardiac rupture after MI. The infarct size which was estimated by evans blue dye and triphenyltetrazolium chloride staining at 3 days after MI was comparable between the IL-22 KO mice and the WT mice. Next, we performed real time PCR and PCR array analysis for tissue fibrosis and repair genes. We found that alpha-smooth muscle actin (aSMA), NF-kB, TNF-a and MMP13 (also known as collagenase-3) were significantly increased in the infarct area of IL-22 KO mice compared to WT mice. Immunostaining showed that the myofibroblast marker aSMA positive cells in the border area after MI were markedly higher in the IL-22 KO mice compared with the WT mice (p<0.05). Approximately 70% of cardiac rupture after MI in the IL-22 KO mice were occurred in the infarct area adjacent to the border area. Furthermore, we found aSMA positive cells and MMP13 positive cells around the ruptured site of the heart. Conclusion Thus, IL-22 KO mice exhibit high mortality and increased cardiac rupture after MI. And expression of aSMA and MMP13 were highly expressed in the ruptured site after MI in the IL-22 KO mice. These results suggest that IL-22 may play an important role in the tissue repair process after MI.

Endothelial and Smooth Muscle Cells as Antagonists in Vascular Fibrinoysis

1975 ◽  
Author(s):  
V. Noordhoek Hegt
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Vascular System ◽  
Muscle Cells ◽  
Vascular Wall ◽  
Vasa Vasorum ◽  
Slide Technique

Endothelial plasminogen activator activity in different types of human blood vessels obtained from fifty necropsies and thirty-five biopsies was detected and localized by means of plasminogen-rich fibrin slides. Great differences in endothelial activator activity were found along and across (vasa vasorum) the wall of the human vascular system.The same blood vessels were simultaneously investigated by a modified fibrin slide technique using plasminogen-free fibrin slides covered by plasmin to detect and localize inhibition of fibrinolysis in the vascular wall. The great variation in plasmin inhibition in different vessels revealed by this “fibrin slide sandwich technique” appeared to be closely associated with the localization and number of smooth muscle cells present in the walls of the vascular system. Strong plasmin inhibition was generally found at sites which showed no activator activity with the regular fibrin slide technique, while areas with a high endothelial fibrinolytic activity mostly revealed no inhibitory capacity.These results indicate that much of the variation in endothelial fibrinolytic activity on fibrin slides is due to inhibitory effects from the surrounding smooth muscle cells rather than to variability in the plasminogen activator content of the endothelium itself.

The Disappearance of Fibrin from the Pulmonary Vessels in Experimental Fat Embolism

1969 ◽  
Vol 22 (02) ◽  
pp. 360-371 ◽  
Author(s):  
T Saldeen
Keyword(s):  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Early Stage ◽  
Fat Embolism ◽  
Plasminogen Activation ◽  
Activator Concentration ◽  
Embolism Syndrome ◽  
Local Fibrinolysis ◽  
Reticulo Endothelial System

SummaryThe background mechanism for the disappearance of intravascular fibrin from the lungs in connection with pulmonary fat embolism in the rat was studied.The reticulo-endothelial system did not appear to play an important role in the disappearance of fibrin. Premedication of the animals with trypan blue had only slight influence on this disappearance, and the capacity of RES for phagocytizing 131I-denatured albumin was not diminished.Treatment of the rats with a plasminogen activation inhibitor (EACA) resulted in a protracted presence of intravascular fibrin deposits, indicating a role of fibrinolysis in the elimination of the fibrin.In connection with experimental fat embolism induced by fracture, an increase was observed in the plasminogen activator concentration in the blood, but when the fat embolism was induced by intravenous injection of homogenized adipose tissue, this activator decreased. At an early stage following intravascular coagulation in the lungs there was an increased fibrinolytic activity in the lung. These results indicated that the disappearance of fibrin is caused by local fibrinolysis in the lung.Twenty-four hrs after the induction of the fat embolism an increase in the plasminogen activator inhibitors in the blood and a decrease in the fibrinolytic activity in the lung was observed. The significance of this inhibition of the fibrinolytic system for the understanding of the fat embolism syndrome is discussed.

On the Role of the Stable Plasminogen Activator of the Venous Wall in Occlusion Induced Fibrinolytic State

1969 ◽  
Vol 22 (03) ◽  
pp. 544-551 ◽  
Author(s):  
R Constantini ◽  
F Spöttl ◽  
F Holzknecht ◽  
H Braunsteiner
Keyword(s):  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Venous Blood ◽  
Venous Occlusion ◽  
Histochemical Method ◽  
Before And After ◽  
Venous Wall

SummaryThe fibrinolytic activity respectively the PA activity of normal veins before and after venous occlusion is measured by the histochemical method of Todd. The results show marked decreases of PA of the adventitia and an increase of PA of the endothelial type, after venous occlusion. This suggests a transfer of PA through the venous wall into the intravascular lumen, and may be the cause of increased fibrinolytic activity in venous blood after occlusion. Contrary assumptions are discussed.

Targeting vessels to treat hepatocellular carcinoma

2008 ◽  
Vol 114 (7) ◽  
pp. 467-477 ◽  
Author(s):  
Pamela Romanque ◽  
Anne-Christine Piguet ◽  
Jean-François Dufour
Keyword(s):  
Hepatocellular Carcinoma ◽  
Wound Healing ◽  
Embryonic Development ◽  
Blood Vessel ◽  
Corpus Luteum ◽  
Normal Tissue ◽  
Tissue Repair ◽  
Adult Life ◽  
Cyclical Growth

The process of blood vessel proliferation, known as angiogenesis, is essential during embryonic development and organogenesis. In adult life, it participates in normal tissue repair, wound healing, and cyclical growth of the corpus luteum and the endometrium. Crucial as it is, angiogenesis can become pathological, and abnormal angiogenesis contributes to the pathogenesis of inflammatory and neoplasic diseases. The present review highlights the evidence for the role of angiogenesis in HCC (hepatocellular carcinoma) and discusses the increasing importance of inhibitors of angiogenesis in HCC therapy.

scholarly journals Plasminogen activator inhibitor-1 in the evolution of stroke

2004 ◽  
Vol 132 (5-6) ◽  
pp. 143-147 ◽  
Author(s):  
Zagorka Jovanovic ◽  
Mirka Ilic ◽  
Jasna Zidverc-Trajkovic ◽  
Aleksandra Pavlovic ◽  
Milija Mijajlovic ◽  
...  
Keyword(s):  
Acute Stroke ◽  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Plasminogen Activator Inhibitor ◽  
Control Group ◽  
Plasminogen Activator Inhibitor 1 ◽  
Computed Tomography Scanning ◽  
Activator Inhibitor ◽  
Pai 1

Fibrinolytic activity in the acute stroke was examined by monitoring the level of plasminogen activator inhibitor-1 (PAI-1), as one of the indicators of fibrinolytic activity. Given the role of PAI-1 in the processes of atherogenesis and thrombogenesis, plasma PAI-1 level was measured in 59 patients (up to 50 years of age) with atherothrombotic stroke (verified by computed tomography scanning or magnetic resonance imaging of brain) in the period from 12 to 24 hours (I analysis) and 30 days after the onset of stroke (II analysis); then, it was correlated with plasma PAI-1 level in the control group (57 healthy subjects), which was 2.86?0.70 U/ml. It was found that PAI-1 level was significantly higher in the acute stroke (I analysis: PAI-1 =4.10?1.40 U/ml, p<0.001; II analysis: PAI-1 =3.64+0.90 U/ml, p<0.001), while fibrinolytic activity was lower, especially on the first day from the stroke that was not completely increased even after 30 days. There was no difference in PAI-1 levels between the subgroups of patients with infarction and lacunar cerebral ischemia (p>0.05), as well as between females and males (p>0.05). Along with significantly increased fibrinogen level (4.65?1 g/l, in the controls - 2.83?0.64 g/l, p<0.001), significantly higher triglycerides (2.04?0.76 mmol/l, in the controls - 1.38+0.54 mmol/l, p<0.001) and lipoproteins(a) (0.405?0.29 g/l, in the controls -0.172?0.14 g/l, p<0.001) were found, correlating with higher plasma PAI-1 level in these patients. The increased plasma level of PAI-1 pointed to possibility of decreased fibrinolytic activity in pathogenesis of ischemie stroke, as well as, risk of reinsult, which had been the greatest after the onset of stroke and declined gradually within several weeks.

Increased Fibrinolytic Activity in the Inflamed Gingiva of Beagle Dogs

1977 ◽  
Vol 56 (12) ◽  
pp. 1533-1538 ◽  
Author(s):  
Oscar N. Lucas
Keyword(s):  
Blood Vessels ◽  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Beagle Dogs ◽  
Beagle Dog

The fibrinolytic activity originated by activation of plasminogen was found to be greater in the inflamed gingiva than in the normal gingiva. The activator of plasminogen present in the normal and inflamed gingiva of the beagle dog was demonstrated histochemically. Plasminogen activator was found adjacent to the crevicular epithelium and blood vessels.

Tissue Plasminogen Activator in Human Megakaryocytes and Platelets: Immunocytochemical Localization, Immunoblotting and Zymographic Analysis

1988 ◽  
Vol 59 (03) ◽  
pp. 529-534 ◽  
Author(s):  
C Jeanneau ◽  
Y Sultan
Keyword(s):  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Blood Platelets ◽  
Fibrinolytic System ◽  
Plasminogen Activation ◽  
Sds Page ◽  
Tissue Plasminogen ◽  
Zymographic Analysis

SummaryTwo approaches were used to identify and characterize the presence of tissue plasminogen activator (t-PA) in megakaryocytes and platelets. We investigated the fibrinolytic activity of human megakaryocytes (MK) and platelets. The presence of t-PA antigen in megakaryocytes and platelets was demonstrated using immunocytochemical techniques and polyclonal or monoclonal antibodies specific for t-PA. When cells were applied to fibrin plates, lysis zones developed around isolated human megakaryocytes, whereas no fibrinolytic activity appeared when either intact washed platelets or platelet lysate were deposited. After SDS-PAGE of platelet and MK extracts (Triton X-100) immunoblotting and peroxidase staining identified t-PA antigen in several bands. Zymographic analysis of SDS-PAGE carried out on fibrin film overlays identified one or two zones corresponding to free or complexed t-PA. These results indicate that t-PA is present in platelets as well as in the precursor cells, however, in platelets, t-PA may not be immediately available for plasminogen activation and fibrin degradation. From our findings and from previous work of others, it appears that platelets may either activate or inhibit the fibrinolytic system. Therefore the conditions of plasminogen activation by platelet t-PA and plasmin inhibition by platelet α2-antiplasmin or other inhibitors have to be precised before the role of platelets in clot dissolution is understood.The physiological role of platelets in fibrinolysis and clot dissolution remains unclear. In 1953, the antifibrinolytic activity of blood platelets was demonstrated (1) and in the early 1960’s a fibrinolytic activity, increasing with platelet concentration in the experimental system, was shown (2, 3). In 1979, it was demonstrated that metabolically active platelets were necessary for platelets to play a role in the fibrinolytic system (4). More recently it was established by Plow and Collen (5) that the specific plasmin inhibitor, α2-antiplasmin is a constituent of platelet α-granules.In the present study, we investigated the fibrinolytic components and activity of human megakaryocytes and platelets, using zymographic and immunochemical techniques. We report here our observations that human megakaryocytes and platelets contain tissue plasminogen (t-PA) which possesses fibrinolytic activity.

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