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internist (), @12/29/2005 9:56:58 AM
Morgen alle Pharmers, jullie geduld zal beloond worden!
Volgende maand wordt een AMC onderzoek gepubliceerd in: Clin Exp Immunol 2006 Jan;143(1):15-23.
Onderzoek met C1-INH bij ratten blijkt (wederom) schade aan de lever te voorkomen na afsluiting en weer openen van een bloedvat. Denk aan potenti�le toepassingen van rhC1-INH bij hartinfarcten e.d.
Inhibition of classical complement activation attenuates liver ischaemia and reperfusion injury in a rat model.
Heijnen BH, Straatsburg IH, Padilla ND, Van Mierlo GJ, Hack CE, Van Gulik TM.
Department of Surgery, Surgical Laboratory, Academic Medical Centre, Amsterdam, the Netherlands.
Activation of the complement system contributes to the pathogenesis of ischaemia/reperfusion (I/R) injury. We evaluated inhibition of the classical pathway of complement using C1-inhibitor (C1-inh) in a model of 70% partial liver I/R injury in male Wistar rats (n = 35). C1-inh was administered at 100, 200 or 400 IU/kg bodyweight, 5 min before 60 min ischaemia (pre-I) or 5 min before 24 h reperfusion (end-I). One hundred IU/kg bodyweight significantly reduced the increase of plasma levels of activated C4 as compared to albumin-treated control rats and attenuated the increase of alanine aminotransferase (ALT). These effects were not better with higher doses of C1-inh. Administration of C1-inh pre-I resulted in lower ALT levels and higher bile secretion after 24 h of reperfusion than administration at end-I. Immunohistochemical assessment indicated that activated C3, the membrane attack complex C5b9 and C-reactive protein (CRP) colocalized in hepatocytes within midzonal areas, suggesting CRP is a mediator of I/R-induced, classical complement activation in rats. Pre-ischaemic administration of C1-inh is an effective pharmacological intervention to protect against liver I/R injury.
Goed uiteinde!