Sedat KALAYCIOĞLU, Eser OZ, Yıldırım IMREN, Gulbin AYGENCEL, Timothy P. MARTENS, Ariel A. BENSON, Mustafa ARSLAN

Complement-1 inhibitor attenuates myocardial ischemia reperfusion injury in a guinea pig model

Endojen olarak üretilen Kompleman 1 Esteraz İnhibtörü ( C1-INH ), kompleman sisteminin regülasyonunda rol oynayan anahtar mediyatörlerden biridir. Bu çalışmada, miyokardial iskemi-reperfüzyon hasarı oluşturulmuş deneklerde C1-INH’ın koruyucu özelliği olup olmadığı araştırılmıştır. Kobay kalpleri ( 20 ), modifiye Langendorff perfüzyon cihazıyla perfüze edilmek üzere hazırlanmış, 10 tanesi çalışma, 10 tanesi de deneysel olarak çalışmaya dahil edilmiştir. Kontrol grubu, pre-iskemi ve reperfüzyon dönemleri esnasında, Krebs-Henseleit solusyonu ile perfüze edilirken, deney grubunda bu perfüzata reperfüzyon aşamasında C1-INH eklenmiştir. Her iki grupta, kalp hızı ( atım / dk. ), kontraktilite ( mm ) ve aortik basınç ( mmHg ) ölçümleri, pre-iskemi, post-iskemi ve reperfüzyon aşamasında kaydedilmiştir. Dokuda ve perfüzatta Glutatyon, Malenildialdehid ( MDA ) seviyeleriyle birlikte, perfüzat Nitrik Oksit ölçümleri de yapılmıştır. Aortik basınç ve kalp kontraktilitesinin yanı sıra deney grubunda doku Glutatyon ve MDA seviyeleri reperfüzyon aşamasında yüksek bulunmuştur. Ancak bu iki parametrenin perfüzat seviyeleri değişmemiştir. Sonuç olarak C1-INH’nün kardiyak kontraktiliteyi arttırıcı ve iskemireperfüzyon hasarı üzerine koruyucu etkileri olabileceği sonucuna varılmıştır

Kompleman 1 inhibitörünün miyokardiyal iskemi-reperfüzyon hasarındaki koruyucu özelliğinin kobaylar üzerinde gösterilmesi

Complement-1 esterase inhibitor (C1-INH), an endogenously derived compound, is a key mediator providing regulation of the complement system. In this study, the protective role of C1-INH was investigated in the setting of myocardial ischemia reperfusion injury. Guinea pig hearts (n=20) were studied in control (n=10) and experimental (n=10) groups, using a modified Langendorff perfusion apparatus. Control hearts were perfused with Krebs Henseleit solution during pre-ischemia and reperfusion periods while C1-INH was added to the perfusates of experimental hearts during the reperfusion period. Heart rate (pulse/ minute), contractility (mm), and aortic pressure (mmHg) values were recorded at the end of pre-ischemia, post-ischemia, and reperfusion periods. Perfusate and tissue analysis for glutathione and malondialdehyde levels and perfusate analysis for nitric oxide levels were obtained at the end of each experimental period. Both increased aortic pressure and cardiac contractility as well as elevated levels of tissue glutathione and MDA were observed in the experimental group during reperfusion. Perfusate levels of glutathione and MDA remained unchanged. As a result, it was concluded that C1 esterase inhibitor preserved cardiac contractility and protected against ischemia reperfusion injury.

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