Adrenaline-Induced Platelet Aggregation in Depressed Patients and Control Subjects

1993 ◽  
Vol 27 (1) ◽  
pp. 21-25 ◽  
Author(s):  
Félicien Karege ◽  
Philippe Bovier ◽  
Henriette Hilleret ◽  
Jean-Michel Gaillard ◽  
René Tissot
Blood ◽  
1987 ◽  
Vol 70 (1) ◽  
pp. 221-226 ◽  
Author(s):  
M Cattaneo ◽  
RL Kinlough-Rathbone ◽  
A Lecchi ◽  
C Bevilacqua ◽  
MA Packham ◽  
...  

Abstract Platelets from two afibrinogenemic patients were used to determine whether fibrinogen is essential for platelet aggregation and to examine whether released fibrinogen contributes to the stabilization of platelet aggregates when platelets have been induced to aggregate and release their granule contents by stimulation with thrombin. The addition of adenosine diphosphate (ADP) to platelet-rich plasma (PRP) or to suspensions of washed platelets from the afibrinogenemic patients caused the formation of small aggregates, which was either not inhibited or only slightly inhibited by the F(ab')2 fragments of an antibody to fibrinogen but was inhibited by an antibody (10E5) to glycoprotein IIb/IIIa. Thus there is a component of ADP-induced platelet aggregation that is not dependent on fibrinogen or other plasma proteins but is dependent on glycoprotein IIb/IIIa. There was little difference in the extent of aggregation and the release of granule contents of normal and afibrinogenemic platelets in response to the release-inducing agents collagen, platelet-activating factor (PAF), sodium arachidonate, or thrombin. With normal or afibrinogenemic platelets, aggregation by thrombin (0.2 U/mL or higher) was not inhibited by the F(ab')2 fragments of an antibody to human fibrinogen. Deaggregation by combinations of inhibitors of platelets aggregated by 1 U/mL thrombin showed no difference between platelets from afibrinogenemic and control subjects, indicating that released fibrinogen does not make a major contribution to the stabilization of platelet aggregates formed by thrombin stimulation.


1988 ◽  
Vol 24 (6) ◽  
pp. 710-712 ◽  
Author(s):  
Kenneth L. Davis ◽  
Michael Davidson ◽  
Ren-Kui Yang ◽  
Bonnie M. Davis ◽  
Larry J. Siever ◽  
...  

2003 ◽  
Vol 17 (5) ◽  
pp. 365-372 ◽  
Author(s):  
Michael Irwin ◽  
Camellia Clark ◽  
Brian Kennedy ◽  
J Christian Gillin ◽  
Michael Ziegler

2001 ◽  
Vol 50 (12) ◽  
pp. 960-964 ◽  
Author(s):  
Brett D Rusch ◽  
Heather C Abercrombie ◽  
Terrence R Oakes ◽  
Stacey M Schaefer ◽  
Richard J Davidson

1992 ◽  
Vol 22 (4) ◽  
pp. 1045-1050 ◽  
Author(s):  
Michael Irwin ◽  
Ute Lacher ◽  
Cindy Caldwell

SynopsisCross-sectional studies have demonstrated that natural killer (NK) cell activity is reduced in depression. To extend these observations and examine further the association between severity of depressive symptoms and values of NK activity, this study used a longitudinal case control design and assessed NK cytotoxicity at intake and at follow-up 6 months after discharge from the hospital in depressed patients and control subjects. From acute hospitalization to follow-up, depression scores significantly (P < 0·01) decreased following treatment in the depressed patients but did not change in the control subjects. NK activity significantly (P < 0·05) increased from intake to follow-up in the depressives while lytic activity did not change in the controls. At intake NK activity was significantly (P < 0·01) reduced in the depressed patients as compared to values in the controls, while at follow-up cytotoxicity was similar between the two groups. These longitudinal data suggest that a reduction of NK cytotoxicity is temporally associated with the state of acute depression.


2000 ◽  
Vol 8 (1) ◽  
pp. 57-65 ◽  
Author(s):  
Sandra S. Kindermann ◽  
Balu Kalayam ◽  
Gregory G. Brown ◽  
Katherine E. Burdick ◽  
George S. Alexopoulos

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