Comprehensive Physiology Wiley Online Library

Platelet‐Blood Vessel Interactions

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Morphological Models of Capillary Endothelium
2 Transport Across Endothelium
3 Cell Turnover
4 Endothelial Cell Culture
5 Endothelial Function
6 Endothelial Injury
7 Platelets
7.1 Morphology and Content
7.2 Platelet Function
7.3 Platelet‐Derived Growth Factor
8 Endothelium‐Smooth Muscle Interactions
9 Platelet‐Endothelial Cell Interactions
10 Summary
Figure 1. Figure 1.

Mechanisms of permeation across endothelium. A, passage through cell junctions; B, passage through fenestrae; C, direct passage through cell across plasmalemma; D, passage through connected chains of vesicles; E, vesicular transport; and F, high‐affinity endocytosis.

Figure 2. Figure 2.

Region of endothelial desquamation in thoracic aorta of a 2‐yr‐old pigtail monkey fed a hypercholesterolemic diet for 2 yr. Platelets have adhered to exposed subendothelial collagen. Top, intact endothelium. × 2,040.

Figure 3. Figure 3.

Hemostatic plug formation. Platelets are normally nonreactive to intact vascular endothelium. Vessel injury initiates platelet adherence with von Willebrand's factor (vWF) as essential plasma co‐factor. Adherent platelets release densegranule contents, including ADP, and α‐granule contents, including platelet factor 4 (PF4), β‐thromboglobulin (βTG), and platelet‐derived growth factor (PDGF). Thrombin is generated locally through tissue factor (XIIα) and platelet procoagulant activity. Thromboxane A2 (TXA2) is synthesized from arachidonic acid liberated by membrane phospholipases. Released ADP, TXA2, and thrombin recruit additional circulating platelets to the enlarging platelet mass. Thrombin‐generated fibrin stabilizes the platelet mass. Prostacyclin (PGI2) released by the vessel wall in response to thrombin limits thrombus formation by inhibiting further platelet aggregation.

From Harlan and Harker


Figure 1.

Mechanisms of permeation across endothelium. A, passage through cell junctions; B, passage through fenestrae; C, direct passage through cell across plasmalemma; D, passage through connected chains of vesicles; E, vesicular transport; and F, high‐affinity endocytosis.



Figure 2.

Region of endothelial desquamation in thoracic aorta of a 2‐yr‐old pigtail monkey fed a hypercholesterolemic diet for 2 yr. Platelets have adhered to exposed subendothelial collagen. Top, intact endothelium. × 2,040.



Figure 3.

Hemostatic plug formation. Platelets are normally nonreactive to intact vascular endothelium. Vessel injury initiates platelet adherence with von Willebrand's factor (vWF) as essential plasma co‐factor. Adherent platelets release densegranule contents, including ADP, and α‐granule contents, including platelet factor 4 (PF4), β‐thromboglobulin (βTG), and platelet‐derived growth factor (PDGF). Thrombin is generated locally through tissue factor (XIIα) and platelet procoagulant activity. Thromboxane A2 (TXA2) is synthesized from arachidonic acid liberated by membrane phospholipases. Released ADP, TXA2, and thrombin recruit additional circulating platelets to the enlarging platelet mass. Thrombin‐generated fibrin stabilizes the platelet mass. Prostacyclin (PGI2) released by the vessel wall in response to thrombin limits thrombus formation by inhibiting further platelet aggregation.

From Harlan and Harker
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Russell Ross, Stephen M. Schwartz. Platelet‐Blood Vessel Interactions. Compr Physiol 2011, Supplement 10: Handbook of Physiology, The Respiratory System, Circulation and Nonrespiratory Functions: 545-558. First published in print 1985. doi: 10.1002/cphy.cp030117