Attenuating ischemia-reperfusion injury with polymerized albumin.

J Appl Physiol (1985)

William G. Lowrie Department of Chemical and Biomolecular Engineering, The Ohio State University, Columbus, Ohio.

Published: February 2022

Ischemia-reperfusion injury increased vascular permeability, resulting in fluid extravasation from the intravascular compartment into the tissue space. Fluid and small protein extravasation lead to increased interstitial fluid pressure and capillary collapse, impairing capillary exchange. Polymerized human serum albumin (PolyHSA) has an increased molecular weight (MW) compared with unpolymerized human serum albumin (HSA) and can improve intravascular fluid retention and recovery from ischemia-reperfusion injury. To test the hypothesis that polymerization of HSA can improve recovery from ischemia-reperfusion injury, we studied how exchange transfusion of 20% of the blood volume with HSA or PolyHSA immediately before reperfusion can affect local ischemic tissue microhemodynamics, vascular integrity, and tissue viability in a hamster dorsal window chamber model. Microvascular flow and functional capillary density were maintained in animals exchanged with PolyHSA compared with HSA. Likewise, exchange transfusion with PolyHSA preserved vascular permeability measured with extravasation of fluorescently labeled dextran. The intravascular retention time of the exchanged PolyHSA was significantly longer compared with the intravascular retention time of HSA. Lastly, the viability of tissue subjected to ischemia-reperfusion injury increased in animals exchanged with PolyHSA compared with HSA. Therefore maintenance of microvascular perfusion, improvement in vascular integrity, and reduction in tissue damage resulting from reperfusion with PolyHSA suggest that PolyHSA is a promising fluid therapy to improve outcomes of ischemia-reperfusion injury. Polymerized human serum albumin reduced reperfusion injury and preservers microvascular hemodynamics. Polymerized human serum albumin reduces fluid extravasation and prevents fluid extravasation. Consequently, the tissue viability of ischemic tissue is preserved by polymerized human serum.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8816619PMC
http://dx.doi.org/10.1152/japplphysiol.00117.2021DOI Listing

Publication Analysis

Top Keywords

ischemia-reperfusion injury
24
human serum
20
polymerized human
16
serum albumin
16
fluid extravasation
12
exchanged polyhsa
12
injury polymerized
8
injury increased
8
vascular permeability
8
polyhsa
8

Similar Publications

Dysregulation of long non-coding RNAs (lncRNAs) is implicated in the pathophysiology of ischemic stroke (IS). However, the molecular mechanism of the lncRNA SERPINB9P1 in IS remains unclear. Our study aimed to explore the role and molecular mechanism of the lncRNA SERPINB9P1 in IS.

View Article and Find Full Text PDF

Stroke is the second-leading global cause of death. The damage attributed to the immune storm triggered by ischemia-reperfusion injury (IRI) post-stroke is substantial. However, data on the transcriptomic dynamics of pyroptosis in IRI are limited.

View Article and Find Full Text PDF

Hypothermic oxygenated machine perfusion (HOPE) has emerged as a critical innovation in liver transplantation (LTx), offering significant protection against ischemia-reperfusion injury (IRI). This study focuses on quantifying and characterizing immune cells flushed out during HOPE to explore its effects on graft function and post-transplant outcomes. Fifty liver grafts underwent end-ischemic HOPE.

View Article and Find Full Text PDF

This narrative review explores the benefits and risks of cannabinoids in kidney health, particularly in individuals with pre-existing renal conditions. It discusses the roles of cannabinoid receptor ligands (phytocannabinoids, synthetic cannabinoids, and endocannabinoids) in kidney physiology. The metabolism and excretion of these substances are also highlighted, with partial elimination occurring via the kidneys.

View Article and Find Full Text PDF

Brain-derived neurotropic factor (BDNF) is expressed by skeletal muscle as a myokine. Our previous work showed that the active precursor, proBDNF, is the predominant form of BDNF expressed in skeletal muscle, and that following skeletal muscle injury, proBDNF levels are significantly increased. However, the function of the muscle-derived proBDNF in injury-induced inflammation has yet to be fully understood.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!