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. 2011 Jun;54(3):194-200.
doi: 10.1503/cjs.048309.

Compartment syndrome-induced microvascular dysfunction: an experimental rodent model

Abdel-Rahman Lawendy  1 , David W Sanders, Aurelia Bihari, Neil Parry, Daryl Gray, Amit Badhwar
Affiliations

Compartment syndrome-induced microvascular dysfunction: an experimental rodent model

Abdel-Rahman Lawendy et al. Can J Surg. 2011 Jun.

Abstract
in English, French

Background: Acute compartment syndrome (CS) is a limb-threatening disease that results from increased intracompartmental pressure. The pathophysiologic mechanisms by which this occurs are poorly understood. This study was designed to measure the effects of increased intracompartmental pressure on skeletal muscle microcirculation, inflammation and cellular injury using intravital videomicroscopy (IVVM) in a clinically relevant small animal model.

Methods: We induced CS in 10 male Wistar rats (175-250 g), using a saline infusion technique. Intracompartmental pressure was controlled between 30 and 40 mm Hg and maintained for 45 minutes. After fasciotomy, the extensor digitorum longus muscle was visualized using IVVM, and perfusion was quantified. We quantified leukocyte recruitment to measure the inflammatory response. We measured muscle cellular injury using a differential fluorescent staining technique.

Results: The number of nonperfused capillaries increased from 12.7 (standard error of the mean [SEM] 1.4 ) per mm in the control group to 30.0 (SEM 6.7) per mm following 45 minutes of elevated intracompartmental pressure (CS group; p = 0.031). The mean number of continuously perfused capillaries (and SEM) decreased from 78.4 (3.2) per mm in the control group to 41.4 (6.9) per mm in the CS group (p = 0.001). The proportion of injured cells increased from 5.0% (SEM 2.1%) in the control group to 16.3% (SEM 6.8%) in the CS group (p = 0.006). The mean number of activated leukocytes increased from 3.6 (SEM 0.7) per 100 μm(2) in the control group to 8.6 (SEM 1.8) per 100 μm(2) in the CS group (p = 0.033).

Conclusion: Early CS-induced microvascular dysfunction resulted in a decrease in nutritive capillary perfusion and an increase in cellular injury and was associated with a severe acute inflammatory component.

Contexte: Le syndrome compartimental aigu (SC) est une affection qui met en danger un membre et résulte d’une élévation de la pression intracompartimentale. Les mécanismes physiopathologiques à l’origine du syndrome sont mal compris. Cette étude visait à mesurer les effets de l’élévation de la pression intracompartimentale sur la microcirculation dans les muscles de l’appareil locomoteur, l’inflammation et les lésions cellulaires au moyen de la vidéomicroscopie intravitale (VMIV) dans un modèle d’animal de petite taille pertinent sur le plan clinique.

Méthodes: Nous avons provoqué un SC chez 10 rats Wistar mâles (175–250 g) en utilisant une technique de perfusion de solution physiologique. La pression intracompartimentale a été maintenue entre 30 et 40 mm Hg pendant 45 minutes. Après une fasciotomie, nous avons visualisé le muscle extenseur commun des orteils par VMIV et quantifié la perfusion. Nous avons quantifié la mobilisation des leucocytes afin de mesurer la réaction inflammatoire. Nous avons mesuré les lésions des cellules des muscles en utilisant une technique de coloration fluorescente différentielle.

Résultats: Le nombre de capillaires non perfusés est passé de 12,7 (erreur type de la moyenne [ETM] 1,4 ) par mm chez les sujets témoins à 30,0 (ETM 6,7) par mm après 45 minutes de pression intracompartimentale élevée (groupe SC; p = 0,031). Le nombre de capillaires perfusés continuellement (et ETM) est passé de 78,4 (3,2) par mm chez les sujets témoins à 41,4 (6,9) par mm chez les sujets du groupe SC (p = 0,001). La proportion de cellules traumatisées est passée de 5,0 % (ETM 2,1 %) chez les sujets témoins à 16,3 % (ETM 6,8 %) chez ceux du groupe SC (p = 0,006). Le nombre moyen de leucocytes activés est passé de 3,6 (ETM 0,7) par 100 μm2 chez les sujets témoins à 8,6 (ETM 1,8) par 100 μm2 chez ceux du groupe SC (p = 0,033).

Conclusion: Le SC a provoqué rapidement une dysfonction microvasculaire entraînant une baisse de la perfusion capillaire nutritive et une élévation des lésions cellulaires, et a été associé à une composante inflammatoire aiguë sévère.

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Figures

Fig. 1
Fig. 1
The effect of elevated intracompartmental pressure on microvascular perfusion measured using intravital videomicroscopy. The graph represents the overall surface microvascular perfusion within the extensor digitorum longus muscle when subject to elevated pressure as a function of time. *Continuous and intermittently perfused capillaries after 45 minutes (compartment syndrome [CS] group) are significantly different than that in the control group (p = 0.001 and p = 0.021, respectively). *The number of nonperfused capillaries increased (p = 0.031) in the CS group compared with the control group.
Fig. 2
Fig. 2
Leukocyte adherence and rolling in postcapillary venules observed in the control group and after 45 minutes of elevated intracompartmental pressure (compartment syndrome group). *An early and significant (p = 0.022) difference in leukocyte adherence was noted. In inflamed tissue, leukocyte rolling leads to a stationary state in which the leukocyte remains firmly attached to the endothelial cell surface without motion. This high-affinity adhesive interaction (leukocyte sticking or adherence) denotes the absence of movement of the leukocyte along the length of the venule.
Fig. 3
Fig. 3
The effect of elevated intracompartmental pressure on parenchymal tissue injury within the extensor digitorum longus muscle. Sham muscles (0 min) have a low baseline level of parenchymal injury, indexed by the number of ethidium bromide (EB)–labelled nuclei relative to the bisbenzimide (BB)-labelled nuclei. *After 45 minutes of elevated intracompartmental pressure (compartment syndrome CS group) a significant increase (p = 0.006) in muscle cellular injury was noted.
Fig. 4
Fig. 4
Proposed conceptual model of compartment syndrome (CS)–induced microvascular dysfunction. Oxygenated blood flows from the arteriole through the capillary, unloading oxygen to cells. With elevated compartmental pressure, nonperfused and intermittently perfused capillaries become visible within capillary beds and are ineffective at gas exchange (X), contributing to cellular injury (darkened cells). Furthermore, maintenance of capillary perfusion during CS allows oxygenated blood into the compromised compartment, which may lead to reactive oxygen metabolites contributing to the chemotactic stimuli for the expression and activation of leukocytes. In the postcapillary venule, activated leukocytes that may contribute further to tissue injury can be observed.
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