M. Ertuğrul KAFALI, Ayşegül BAYIR, Mustafa ŞAHİN, AHMET AK

Hemorajik şokta ringer laktat, HAES % 10 ve HAES % 10+Dimetilsülfoksitin serbest oksijen radikalleri düzeyine etkileri

Amaç: Bu çalışmada amaç hemorajik şok sırasında kullanılan resussitasyon sıvılarının ve bunlara antioksidan eklenmesinin doku iskemisi üzerine etkilerini araştırmaktır. Yöntem: Hemorajik şok geliştirdiğimiz 40 adet Yeni Zelanda tipi tavşan Kontrol (K), ringer laktat (RL), % 10 hidroksi etil nişasta (HAES) (H) ve % 10 HAES +Dimetilsülfoksit (DMSO) olarak 4 gruba ayrıldı. Tavşanlar karotid arter yoluyla kanatıldılar. 30 dk. şoktan sonra K grubuna sıvı ressusitasyonu yapılmazken, RL grubuna kanama miktarının 1.5 katı sıvı verildi. Diğer 2 gruba ise kanama miktarı kadar HAES ve HAES+DMSO verildi. Sıvıların ve DMSO’nun etkisini değerlendirmek için kan, karaciğer ve ince barsak TBARS (Thiobarbitürik asit reaktif maddeleri) ve laktat düzeyleri çalışıldı. Sonuçlar karşılaştırıldı. Bulgular: Grupların doku ve plazma TBARS ve Laktat seviyeleri kıyaslandığında istatistiksel olarak anlamlı bir fark görülmedi. Diğer taraftan (hemorajik şokun neden olduğu oksidatif stresin ortadan kaldırılmasında plazma ve eritrositler üzerinde) % 10 HAES + DMSO, ringer laktat ve % 10 HAES’den daha üstün bulundu. Sonuç: Replasman sıvılarının hemorajik şokta gelişen doku iskemisini azaltmada birbirlerine belirgin bir üstünlüğü yoktur. Diğer taraftan resusitasyonda antioksidanların eklenmesinin serbest oksijen radikali oluşumunu azaltarak doku hasarı ve organ fonksiyon bozukluğunu önlediği düşünülmüştür.

Effects of ringer lactate, HAES 10% and HAES 10%+dimethylsulphoxide on free oxygen radicals in hemorrhagic shock

Objective: The aim of this study was to investigate the effects of antioxidant and resuscitation fluids which were used during hemorrhagic shock on tissue ischemia. Methods: Forty New Zealand type rabbits were divided into four groups as C (control), R (Ringer Lactate), H (Hydroxyethyl starch) (HAES) and D (Dymethylsulphdxide-DMSO)+H (HAES). Hemorrhagic shock was induced by bleeding from carotid artery. Thirty minutes after shock, Group C was not resuscitated while Group R was resuscitated with Ringer Lactate, Group H with 10% HAES and Group D with HAES 10% and DMSO. Thiobarbituric acid reactive substances (TBARS) and lactate levels in blood, liver and small bowel samples were measured. Results: There were no significant differences among the groups tissue and plasma TBARS and lactate levels. There were significant differences with D Group and other groups. Conclusion: Resuscitation fluids do not have any superiority over each other to prevent tissue ischemic insult in hemorrhagic shock. But addition of antioxidants to the resuscitation fluids give positively results.

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