Effect of Tricyclic Antidepressants on Cerebral Capillary Permeability: An Action on a Fundamental Cerebral Homeostatic Mechanism

2015 ◽  
pp. 111-129
Author(s):  
Boyd K. Hartman
Keyword(s):  
Tricyclic Antidepressants ◽  
Capillary Permeability ◽  
Homeostatic Mechanism ◽  
Cerebral Capillary

Long-term antidepressant treatment: Alterations in cerebral capillary permeability

1980 ◽  
Vol 70 (1) ◽  
pp. 1-4 ◽  
Author(s):  
Sheldon H. Preskorn ◽  
Boyd K. Hartman ◽  
H. Brent Clark
Keyword(s):  
Capillary Permeability ◽  
Antidepressant Treatment ◽  
Cerebral Capillary

Effect of Vasopressin on Ependymal and Cerebral Capillary Permeability to Tritiated Water in Cat

1986 ◽  
Vol 481 (1 The Neuronal) ◽  
pp. 383-385 ◽  
Author(s):  
G. A. ROSENBERG ◽  
W. T. KYNER ◽  
E. ESTRADA ◽  
C. S. PATLAK
Keyword(s):  
Capillary Permeability ◽  
Tritiated Water ◽  
Cerebral Capillary

Review of Living With Tricyclic Antidepressants.

1997 ◽  
Vol 42 (1) ◽  
pp. 84-84
Author(s):  
Terri Gullickson
Keyword(s):  
Tricyclic Antidepressants

Fibrin Formation: The Role of the Fibrinogen-Fibrin Monomer Complex

1976 ◽  
Vol 36 (01) ◽  
pp. 037-048 ◽  
Author(s):  
Eric P. Brass ◽  
Walter B. Forman ◽  
Robert V. Edwards ◽  
Olgierd Lindan
Keyword(s):  
Particle Size ◽  
Induction Period ◽  
Fibrin Clot ◽  
Clot Formation ◽  
Appreciable Amount ◽  
Buffer System ◽  
Homeostatic Mechanism ◽  
Fibrin Formation ◽  
Fibrin Monomer

SummaryThe process of fibrin formation using highly purified fibrinogen and thrombin was studied using laser fluctuation spectroscopy, a method that rapidly determines particle size in a solution. Two periods in fibrin clot formation were noted: an induction period during which no fibrin polymerization occurred and a period of rapid increase in particle size. Direct measurement of fibrin monomer polymerization and fibrinopeptide release showed no evidence of an induction period. These observations were best explained by a kinetic model for fibrin clot formation incorporating a reversible fibrinogen-fibrin monomer complex. In this model, the complex serves as a buffer system during the earliest phase of fibrin formation. This prevents the accumulation of free polymerizable fibrin monomer until an appreciable amount of fibrinogen has reacted with thrombin, at which point the fibrin monomer level rises rapidly and polymerization proceeds. Clinically, the complex may be a homeostatic mechanism preventing pathological clotting during periods of elevated fibrinogen.

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