Mechanisms and Implications of Capillary Endotheloal Swelling and Luminal Narrowing in Low-Flow Ischemias

Mazzoni, Michelle C.; Borgström, Per; Warnke, K. C.; Skalak, Thomas C.; Intaglietta, Marcos; Arfors, K. E.

doi:10.1159/000179028

Cited by 45 publications

(29 citation statements)

References 13 publications

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“…39,40 Liver intravital microscopy has probably yielded the most exciting findings to date about EC-PMN interactions following the differential fluid resuscitation of hemorrhagic shock. Indeed, several studies report decreases in capillary and sinusoidal luminal narrowing and improved flow parameters, 25,[41][42][43] as well as diminished EC-PMN interactions (sinusoids and postsinusoidal venules) in animals resuscitated with hypertonic fluids. 24 -26 Because none of these studies evaluated the effects of HTS alone, but rather used HTS-sugar resuscitation regimens, it is difficult to reach a conclusion on the individual effect of HTS.…”

Section: Discussionmentioning

confidence: 99%

Hypertonic Saline Resuscitation of Hemorrhagic Shock Diminishes Neutrophil Rolling and Adherence to Endothelium and Reduces In Vivo Vascular Leakage

Pascual

Ferri²,

Seely³

et al. 2002

Annals of Surgery

119

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ObjectiveTo evaluate the in vivo effects of hypertonic saline (HTS) resuscitation on the interactions of endothelial cells (ECs) and polymorphonuclear neutrophils (PMNs) and vascular permeability after hemorrhagic shock. Summary Background DataThe PMN has been implicated in the pathogenesis of EC damage and organ injury following hemorrhagic shock. Compared to Ringer's lactate (RL), HTS resuscitation diminishes PMN and EC adhesion molecule expression and organ sequestration of PMNs. MethodsIn a murine model of hemorrhagic shock (50 mmHg for 45 minutes followed by resuscitation) using intravital microscopy on cremaster muscle, the authors studied PMN-EC interactions and vascular leakage (epifluorescence after 50 mg/kg fluorescent albumin) in three resuscitation groups: HTS (shed blood ϩ 4 cc/kg 7.5% HTS, n ϭ 12), RL (shed blood ϩ RL [2ϫ shed blood volume], n ϭ 12), and sham (no hemorrhage or resuscitation, n ϭ 9). EC ICAM-1 expression was evaluated by immunohistochemistry. Data, presented as mean Ϯ SEM, were evaluated by analysis of variance with Bonferroni correction. ResultsThere were no differences between groups in flow mechanics. Compared to RL, HTS animals (t ϭ 90 minutes) displayed diminished PMN rolling and PMN adhesion to EC at time intervals beyond t ϭ 0. There were no differences between the sham and HTS groups. Vascular leakage was 45% lower in HTS than in RL-resuscitated animals. Cremaster EC ICAM-1 expression was similar in the two groups. ConclusionsUsing HTS instead of RL to resuscitate hemorrhagic shock diminishes vascular permeability in vivo by altering PMN-EC interactions. HTS could serve as a novel means of immunomodulation in hemorrhagic shock victims, potentially reducing PMN-mediated tissue injury.Over 30 years ago, the Vietnam War established the current standard use of isotonic crystalloid fluids (normal saline [NS] and Ringer's lactate [RL]) for the resuscitation of hemorrhagic shock. Subsequent studies have demonstrated that crystalloids represent an effective and inexpensive means to restore intravascular volume and additionally offer a survival advantage over colloids in the resuscitation of traumatic hemorrhagic shock. 1More recently, "small volume resuscitation" 2 with 4 mL of 7.5% NaCl per kilogram of body weight of hypertonic saline (HTS) has been proposed in the treatment of hemorrhagic shock. Whereas isotonic fluid administration requires large volumes, hypertonic resuscitation offers the advantages of ease of transport, speed of administration, and

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Section: Discussionmentioning

confidence: 99%

Hypertonic Saline Resuscitation of Hemorrhagic Shock Diminishes Neutrophil Rolling and Adherence to Endothelium and Reduces In Vivo Vascular Leakage

Pascual

Ferri²,

Seely³

et al. 2002

Annals of Surgery

119

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“…A low-flow ischemia causes a decrease of the FCD, which persists after reperfusion. Due to endothelial swelling the capillary width decreases clearly [23,30]. A barrier for perfusion opposes to stored red blood cells with impaired viscosity so that the described recruitment of the capillary network fails.…”

Section: Influence Of Morphology Of Erythrocytes On the Gas Exchange mentioning

confidence: 99%

Massive Transfusion and Its Influence on Oxygen Transport and Electrolyte Balance

Schmitt¹,

Lackes²

2000

Transfus Med Hemother

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During the process of storing erythrocyte-containing blood products, components of the preservatives and modifications of the erythrocyte function cause disorders of the electrolyte and acid-base balance as well as a deficiency of 2,3-diphosphoglycerate (2,3-DPG). Thereby transitory hyperkalemias may occur in the course of a massive transfusion, if the patient has a shock or another disturbance of the regulating mechanisms caused by diabetes mellitus or a treatment with β-blockers or ACE inhibitors. During the treatment with blood components, hypocalcemia and hypomagnesemia may develop after a dose of more than 12 fresh frozen plasms (FFP) per hour, if the metabolism of citrate, which binds bivalent cations as a chelate, is disturbed by hypothermia, shock or during the anhepatic stage of a liver transplantation. As a consequence, a low-output syndrome as well as tachyarrhythmias and torsades de pointes may develop. Whether the decrease of the 2,3-DPG level with the accompanying leftward shift of the oxyhemoglobin dissociation curve brings about a deficiency of the oxygen supply of the organs, has not yet been verified by experiment. The studies presented rather point at morphological changes of the erythrocytes due to the storage as the cause of the disturbances of capillary perfusion. For this reason patients with impending organ failure or marked disturbances of the coronary or cerebral perfusion should be transfused with packed red blood cells (RBCs) not older than 14 days.

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“…During reperfusion when the organ is warmed up and reoxygenated, oxygen-free radicals are produced and superoxides are formed by hypoxanthine. This all results in microvascular damage and perfusion failure, known as the no-reflow phenomenon (Vollmar et al 1994, Mazzoni et al 1995. These processes, among others, can be studied in an isolated rat liver reperfusion model.…”

Section: ) and Synthesis Of Proteinsmentioning

confidence: 99%

The isolated perfused rat liver: standardization of a time-honoured model

Hart²,

et al. 2006

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SummaryFor many years, the isolated perfused rat liver (IPRL) model has been used to investigate the physiology and pathophysiology of the rat liver. This in vitro model provides the opportunity to assess cellular injury and liver function in an isolated setting. This review offers an update of recent developments regarding the IPRL set-up as well as the viability parameters that are used, with regards to liver preservation and ischaemia and reperfusion mechanisms.A review of the literature was performed into studies regarding liver preservation or liver ischaemia and reperfusion. An overview of the literature is given with particular emphasis on perfusate type and volume, reperfusion pressure, flow, temperature, duration of perfusion, oxygenation and on applicable viability parameters (liver damage and function).The choice of IPRL set-up depends on the question examined and on the parameters of interest. A standard technique is cannulation of the portal vein, bile duct and caval vein with pressure-controlled perfusion at 20 cm H 2 O (15 mmHg) to reach a perfusion flow of approximately 3 mL/min/g liver weight. The preferred perfusion solution is Krebs-Henseleit buffer, without albumin. The usual volume is 150-300 cm 3 , oxygenated to a pO 2 of more than 500 mmHg. The temperature of the perfusate is maintained at 371C. Standardized markers should be used to allow comparison with other experiments.Keywords Isolated perfused rat liver (IPRL); liver preservation; parameters; liver function; liver damage For many years, the isolated perfused rat liver (IPRL) model has been used to investigate the physiology and pathophysiology of the rat liver. This in vitro model provides the opportunity to assess cellular injury and liver function in an isolated setting.The IPRL model was first reported by Claude Bernard in 1855 (Gores et al. 1986).In the review about the IPRL written by Gores et al. in 1986, the authors stated that the model remained a valuable reperfusion model, although other methods such as the assessment of liver slices, cell cultures, cell suspensions and isolated organelles had emerged. To date, the IPRL provides valuable data in studies regarding liver physiology using new techniques in the field of molecular biology and genetics.In the field of liver preservation, the IPRL model has been used for, among others, assessment of ischaemia-reperfusion injury, metabolism of perfusate compounds, metabolism of ammonium and amino acids (Haussinger 1987), endothelial function using hyaluronic acid uptake (Reinders et al. 1996), oxygen consumption (Dahn et al.

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Mechanisms and Implications of Capillary Endotheloal Swelling and Luminal Narrowing in Low-Flow Ischemias

Cited by 45 publications

References 13 publications

Hypertonic Saline Resuscitation of Hemorrhagic Shock Diminishes Neutrophil Rolling and Adherence to Endothelium and Reduces In Vivo Vascular Leakage

Hypertonic Saline Resuscitation of Hemorrhagic Shock Diminishes Neutrophil Rolling and Adherence to Endothelium and Reduces In Vivo Vascular Leakage

Massive Transfusion and Its Influence on Oxygen Transport and Electrolyte Balance

The isolated perfused rat liver: standardization of a time-honoured model

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