Mikrovaskuläre Effekte des Verbrennungsplasma­transfers und therapeutische Optionen im Tiermodell

Zusammenfassung

Einleitung:

Thermische Verletzungen mit mehr als 20% verbrannter Körperoberfläche (vKOF) führen zusätzlich zu den lokalen Gewebezerstörungen zu einem systemischen Schock mit generalisierter Ödembildung. Dieser als Verbrennungskrankheit bezeichnete Zustand wird durch immunmodulative Mediatoren hervorgerufen, deren individuelle Bedeutung aber noch nicht abschließend beurteilt werden kann. Wir stellen ein experimentelles Modell vor, bei dem Plasma verbrannter Tiere (Verbrennungsplasma) in gesunde Tiere übertragen wird, um hier eine Verbrennungskrankheit auszulösen.

Material und Methoden:

Die systemische Ödem­bildung wird mittels Extravasation von fluore­szenzmarkiertem Albumin in Mesenterialvenolen von Wistarratten gemessen. Zusätzlich werden Leukozyten-Endothel Interaktionen („Leukozyten-Rolling und Sticking“) untersucht.

Ergebnisse:

Das systemische Kapillarleck wird ebenso durch ein direktes thermisches Trauma wie durch die Infusion von Verbrennungsplasma induziert. Dies ist auch noch nach deutlicher Plasmaverdünnung (1% in Ringerlaktat) der Fall. Zusätzlich bewirkt eine topische Therapie der verbrannten Spendertiere mit Ceriumnitrat eine signifikante Reduktion der Plasmaextravasation im Empfänger. Außerdem kann die systemische antioxidative Therapie des Empfängers mit hochdosiertem Vitamin C die Ausprägung des Kapillarlecks reduzieren. Leukozyten-Endothel-Interaktionen werden jeweils nicht signifikant beeinflusst.

Schlussfolgerung:

Zusammengefasst wurde erstmals ein verlässliches Modell der Verbrennungskrankheit etabliert, das mediator-unabhängige Effekte eliminiert. Zusätzlich wurde für die antioxidative Therapie mit hochdosiertem Vitamin C und für die topische Therapie mit Ceriumnitrat gezeigt, dass beide das systemische ­Kapillarleck positiv beeinflussen und daher bereits kurzfristig in die Therapiealgorithmen integriert werden könnten.

Abstract

Introduction:

Thermal injuries with more than 20% of burned body surface area (BSA) lead to systemic shock with generalised oedema in addition to local tissue destruction. This condition, known as burn injury, is caused by immunmodulative mediators whose individual significance is not known in detail. We present an experimental model where plasma of burned animals (burn plasma) is transmitted to healthy animals, to trigger burn iniury without performing direct burn trauma.

Material and Methods:

The systemic oedema is measured by extravasation of fluorescent albumin in mesenterial venules of Wistar rats. In addition, leukocyte-endothelial interactions (“leukocyte rolling and sticking”) is examined.

Results:

The systemic capillary leak is induced by both direct thermal trauma as well as by infusion of burn plasma. This is evident even after plasma dilution (1% in Ringer’s lactate) of the burn plasma. In addition, topical therapy for burned animals (donors) with cerium nitrate led to a significant reduction of plasma extravasation in receiver animals. In addition, systemic antioxidant therapy with high-dose vitamin C of receiver animals, led to a significant reduction of the capillary leak. Leukocyte-endothelial interactions are not significantly affected in either case.

Conclusion:

In summary, for the first time a reliable model of burn injury has been established, which eliminates mediator-independent effects. In addition, our studies show that antioxidant therapy with high doses of vitamin C and topical treatment with cerium nitrate both reduce the systemic capillary leak in receiver animals. Their positive influence could therefore soon be integrated in clinical treatment algorithms.

Schlüsselwörter

Mikrozirkulation - Verbrennungsintensiv­medizin - Tiermodell - Verbrennungsplasmatransfer

Key words

microcirculation - burn intensive care - animal model - burn plasma transfer

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