Problems of fibrin adhesion of the nerves

1988 ◽  
Vol 11 (3-4) ◽  
pp. 249-258 ◽  
Author(s):  
Thomas Herter
Keyword(s):  
1985 ◽  
Vol 5 (3) ◽  
pp. 180-181 ◽  
Author(s):  
Jannis Vlachojannis ◽  
Ivar Boettcher ◽  
Lothar Brandt ◽  
Wilhelm Schoeppe

A 46-year-old woman undergoing CAPD developed a recurring right sided hydrothorax. Instillation of tetracycline HCI and triamcinolone acetonide did not correct the condition. However application of a fibrin adhesive (Tissucol) made it possible to achieve permanent adhesion of the pleural layers. This paper descrubes the method in detail. The development of pleural effusions in patients undergoing peritoneal dialysis, although a rare complication, can lead to the interruption of CAPD (2,3). As treatment, several workers have provoked the adhesion of parietal and visceral pleura by instillation tetracycline HCI or triamcinolone acetonide into the pleural space (6). As this report shows, these approaches failed in one patient and we achieved pennanent correction of this hydrothorax by employing a non-invasive, fibrin-adhesion technique.


Blood ◽  
1967 ◽  
Vol 29 (3) ◽  
pp. 385-400 ◽  
Author(s):  
ROBERT B. ERICHSON ◽  
ALFRED J. KATZ ◽  
JOSE R. CINTRON

Abstract The morphology of platelet-fibrin interaction in retracting clots and following exposure of platelets to preformed fibrin particles has been studied with the electron microscope. The interaction involved close conformity of the structures at a finite distance, usually 100 to 200 angstroms, and platelet engulfment of fibrin. The morphology closely resembles other platelet adhesion reactions, and it is suggested that the interaction described here is the ultrastructural representation of platelet-fibrin adhesion.


Author(s):  
Th. Herter ◽  
W. Walter ◽  
M. Brandt ◽  
U. Szuwart
Keyword(s):  

2019 ◽  
Vol 317 (1) ◽  
pp. H63-H72
Author(s):  
Jiqiu Chen ◽  
Benjamin Strauss ◽  
Lifan Liang ◽  
Roger J. Hajjar

The aim of the present study was to develop and study a new model of left atrial thrombus (LAT) in rat with congestive heart failure (CHF). CHF was induced by aortic banding for 2 mo, followed by ischemia-reperfusion (I/R) and subsequent aortic debanding for 1 mo. Cardiac function and the presence of LAT were assessed by echocardiography. Masson’s staining was performed for histological analysis. All CHF rats presented with significantly decreased cardiac function, fibrosis in remote myocardium, and pulmonary edema. The incidence rate of LAT was 18.8% in the rats. LAT was associated with severity of aortic constriction, aortic pressure gradient, aortic blood flow velocity, and pulmonary edema but not myocardial infarction or a degree of left ventricular depression. The progressive process of thrombogenesis was characterized by myocyte hypertrophy, fibrosis, and inflammation in the left atrial wall. Fibrin adhesion and clot formation were observed, whereas most LAT presented as a relatively hard “mass,” likely attributable to significant fibrosis in the middle and outer layers. Some LAT mass showed focal necrosis as well as fibrin bulging. Most LAT occurred at the upper anterior wall of the left atrial appendage. Aortic debanding had no significant impact on large LATs (>5 mm2) that had formed, whereas small LATs (<5 mm2) regressed 1 mo after aortic release. LAT is found in a rat model of aortic banding plus I/R followed by aortic debanding. The model provides a platform to study molecular mechanisms and potential new pathways for LAT treatment. NEW & NOTEWORTHY It is critically important to have a rodent model to study the molecular mechanism of thrombogenesis in the left atrium. Left atrial thrombus (LAT) is not a simple fibrin clot like those seen in peripheral veins or arteries. Rather, LAT is a cellular mass that likely develops in conjunction with blood clotting. Studying this phenomenon will help us understand congestive heart failure and promote new therapies for LAT.


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