1. Reperfusion therapy—What’s with the obstructed, leaky and broken capillaries? 
D. Neil Granger, Peter R. Kvietys 
Pathophysiology 
Volume 24, Issue 4, Pages (December 2017)
DOI: /j.pathophys
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2. Fig. 1
Mechanisms proposed to explain the endothelial barrier failure and haemorrhage that are manifested in tissues exposed to ischemia and reperfusion (I/R). Panel A. Normal capillary (surrounded by macrophages and mast cells) with an intact endothelial barrier that limits the extravasation of both macromolecules (albumin) and red blood cells (RBC). Panel B. The inflammatory response to I/R at the peri-infarct zone leading to neutrophil-dependent endothelial barrier dysfunction that allows for enhanced leakage of albumin (increased vascular permeability) without RBC extravasation. Products of macrophage and mast cell activation contribute to the neutrophil dependent response. Panel C. An extension of the mechanisms and responses depicted in panel B, but with increased severity and showing wider inter-endothelial gaps and disrupted basement membrane, which allows for RBC extravasation and haemorrhage. Panel D. Direct (neutrophil-independent) endothelial cell injury and necrosis as a result of hypoxia/anoxia within the infarct zone that allows for enhanced permeation of albumin through swollen and dying endothelial cells with disrupted plasma membrane. Panel E. An extension of the events of panel D with eventual loss of the endothelial cells and fragmentation of the basement membrane, which allows for the extravasation of both albumin and RBCs. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
Pathophysiology  , DOI: ( /j.pathophys )
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3. Fig. 2
Events occurring in the different segments of the microvasculature that have been implicated in the development of the “no-reflow” phenomenon following reperfusion of ischemic tissues.
Pathophysiology  , DOI: ( /j.pathophys )
Copyright © 2017 Elsevier B.V. Terms and Conditions

4. Fig. 3
The generation of reactive oxygen species (ROS) in post-ischemic tissues has largely been attributed to four sources, xanthine oxidase, mitochondria, NADPH oxidase, and nitric oxide synthase.
Pathophysiology  , DOI: ( /j.pathophys )
Copyright © 2017 Elsevier B.V. Terms and Conditions

5. Fig. 4
Domain structure of the major MMPs that have been implicated in the microvascular dysfunction induced by ischemia/reperfusion in the heart and brain. MMP-3 and – 8 contain the basic domain structure of MMPs, MMP-14 is a furin-activated, membrane-anchored MMP, and MMP-2 and – 9 containing the fibronectin II module are gelatin-binding MMPs.
Pathophysiology  , DOI: ( /j.pathophys )
Copyright © 2017 Elsevier B.V. Terms and Conditions