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Review
, 2 (4), 171-187
eCollection

Tissue Conservation for Transplantation

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Review

Tissue Conservation for Transplantation

Nicco Krezdorn et al. Innov Surg Sci.

Abstract

Pathophysiological changes that occur during ischemia and subsequent reperfusion cause damage to tissues procured for transplantation and also affect long-term allograft function and survival. The proper preservation of organs before transplantation is a must to limit these injuries as much as possible. For decades, static cold storage has been the gold standard for organ preservation, with mechanical perfusion developing as a promising alternative only recently. The current literature points to the need of developing dedicated preservation protocols for every organ, which in combination with other interventions such as ischemic preconditioning and therapeutic additives offer the possibility of improving organ preservation and extending it to multiple times its current duration. This review strives to present an overview of the current body of knowledge with regard to the preservation of organs and tissues destined for transplantation.

Keywords: allograft preservation; graft preservation; machine perfusion; organ conditioning; organ preservation; static cold storage.

Figures

Figure 1:
Figure 1:
Overview of the pathophysiology of ischemia and IRI. (A) Under normal conditions, oxygen and glucose are delivered to the cells and used for oxidative ATP production in the mitochondria (see Supplemental Figure 4). (B) Under ischemic conditions, energy production switches to anaerobic metabolism and cellular changes occur (for more details, see Supplemental Figure 5) that lead to the creation of ROS and subsequent cellular damages, which can lead to cell death. These changes start to attract local resident immune cells and after local inflammatory responses. On an endothelial level, ischemic stress leads to increased expression of membrane adhesion molecules and reduced cAMP leads to decreased barrier function and increased vascular permeability. (C) Restitution of oxygen and glucose upon reperfusion leads to injuries on the cellular, local, and even systemic levels. The details of the cellular changes during reperfusion are depicted in Supplemental Figure 6. Increased rates of cell swelling and injuries with expression of cell surface adhesion molecules as well as increased numbers of necrotic and apoptotic cells trigger strong local immune responses and attract even more immune cells from the bloodstream. On the vascular level, the binding of natural IgM to the adhesion molecules leads to the activation of the complement cascade through factors C3a and C5a. ROS decrease NO, which triggers more expression of adhesion molecules and negatively affects vascular tone. The release of DNA from damaged endothelial cells as well as DAMPs attract and activate both innate and adaptive immune cells. The combination of increased immune cell attraction, swelling, and activation of coagulation cascade can lead to a “clogging” of the microvasculature resulting in a so-called “no reflow” phenomenon.
Figure 2:
Figure 2:
Tissue preservation methods for transplantation.
Figure 3:
Figure 3:
Basic schematic of a machine perfusion system.

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