Measurement of the Platelet Response to Laserinduced Microvascular Injury

1974 ◽  
Vol 32 (02/03) ◽  
pp. 695-703 ◽  
Author(s):  
T Hovig ◽  
F. N McKenzie ◽  
K.-E Arfors

SummaryMicrovascular injury was produced in rabbit mesentery and ear chamber preparations using a biolaser. Ultrastructural studies of the injury sites revealed damage to the endothelium which showed cytoplasmic swelling and flocculation. Complete destruction of the endothelium was not observed, indicating that sub endothelial structures were not exposed to blood flow. Microvascular thrombi which occurred at the sites of injury were composed of platelets which in general were loosely packed and showed minor alterations in shape and internal structure. Erythrocytes appeared to be heavily damaged by the laser injury. Fibrin was not observed. It is concluded that ADP may be released from red blood cells, and possibly from other sources, as a result of the laser injury, and that the platelet thrombus formation is induced by ADP.

Author(s):  
E. Kucukal ◽  
Y. Man ◽  
U. A. Gurkan ◽  
B. E. Schmidt

Abstract This article describes novel measurements of the velocity of whole blood flow in a microchannel during coagulation. The blood is imaged volumetrically using a simple optical setup involving a white light source and a microscope camera. The images are processed using PIV and wavelet-based optical flow velocimetry (wOFV), both of which use images of individual blood cells as flow tracers. Measurements of several clinically relevant parameters such as the clotting time, decay rate, and blockage ratio are computed. The high-resolution wOFV results yield highly detailed information regarding thrombus formation and corresponding flow evolution that is the first of its kind.


Author(s):  
A. Tokarev ◽  
I. Sirakov ◽  
G. Panasenko ◽  
V. Volpert ◽  
E. Shnol ◽  
...  

Author(s):  
Koichiro Yano ◽  
Daisuke Mori ◽  
Ken-ichi Tsubota ◽  
Takuji Ishikawa ◽  
Shigeo Wada ◽  
...  

It has been pointed out that some mechanical factors play important roles in a series of physiological or biochemical processes during the thrombus formation. Recently, many studies including the authors’ work qualitatively demonstrated how the thrombus is regulated under the influences of the blood flow and the intercellular molecular bridge using computational fluid dynamics techniques[1–4]. They verified the importance of the balance of them in the process of the thrombus formation. However, few studies have taken into account the existence of the other cell constituents than the platelet such as red blood cell (RBC).


2021 ◽  
Vol 10 (22) ◽  
pp. 5349
Author(s):  
Lydie Crescence ◽  
Markus Kramberg ◽  
Martine Baumann ◽  
Markus Rey ◽  
Sebastien Roux ◽  
...  

Selatogrel, a potent and reversible antagonist of the P2Y12 receptor, inhibited FeCl3-induced thrombosis in rats. Here, we report the anti-thrombotic effect of selatogrel after subcutaneous applications in guinea pigs and mice. Selatogrel inhibited platelet function only 10 min after subcutaneous application in mice. In addition, in a modified Folts thrombosis model in guinea pigs, selatogrel prevented a decrease in blood-flow, indicative of the inhibition of ongoing thrombosis, approximately 10 min after subcutaneous injection. Selatogrel fully normalised blood flow; therefore, we speculate that it may not only prevent, but also dissolve, platelet thrombi. Thrombus dissolution was investigated using real-time intravital microscopy in mice. The infusion of selatogrel during ongoing platelet thrombus formation stopped growth and induced the dissolution of the preformed platelet thrombus. In addition, platelet-rich thrombi were given 30 min to consolidate in vivo. The infusion of selatogrel dissolved the preformed and consolidated platelet thrombi. Dissolution was limited to the disintegration of the occluding part of the platelet thrombi, leaving small mural platelet aggregates to seal the blood vessel. Therefore, our experiments uncovered a novel advantage of selatogrel: the dissolution of pre-formed thrombi without the disintegration of haemostatic seals, suggesting a bipartite benefit of the early application of selatogrel in patients with acute thrombosis.


2001 ◽  
Vol 85 (06) ◽  
pp. 1097-1103 ◽  
Author(s):  
Kjell Sakariassen ◽  
Hélène Grandjean ◽  
Claire Thalamas ◽  
Bernard Boneu ◽  
Pierre Sié ◽  
...  

SummaryA number of studies have reported conflicting data on the association of the PlA1/PlA2 polymorphism of the GPIIIa gene and coronary syndromes. We have investigated the effect of this polymorphism on experimental platelet thrombus formation in man. Forty healthy male volunteers were genotyped for the PlA1/PlA2 polymorphism. Thrombus formation was induced ex vivo by exposing a tissue factor (TF) or a collagencoated coverslip in a parallel plate perfusion chamber to native blood for 2 and 4 min. The shear rates at these surfaces were 650 and 2,600 s–1. Platelet and fibrin deposition was quantified by immunoenzymatic methods. The frequencies of PlA1/PlA1 and PlA1/PlA2 genotypes were 52.5% and 47.5%, respectively. Ex vivo deposition of fibrin on TF was not affected by the PlA1/PlA2 polymorphism. However, the ex vivo platelet deposition at 650 s–1 was higher in blood from PlA1/PlA1 individuals than in PlA1/PlA2 individuals (P = 0.008 at 4 min). On collagen, neither fibrin nor platelet deposition was significantly affected by the PlA1/PlA2 polymorphism. Platelet thrombus formation is significantly influenced by genetic variations in the GPIIIa platelet receptor. This effect depends on the blood flow properties and the nature of the thrombogenic stimulus.


Sign in / Sign up

Export Citation Format

Share Document