Ratlarda Oluşturulan Hemorajik Şok Ardından Verilen Farklı Sıvı Tedavileri Sonrası Glikokaliks Dökülme Düzeyleri Açısından Sindekan-1 Düzeyinin Karşılaştırılması
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Date
2023Author
Özkan, Seda
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Acute hemorrhage can be defined as rapid blood loss that accompanies
various medical or surgical events. Hemorrhagic shock occurs when there is a significant
loss of blood to the extent that it jeopardizes normal physiological compensatory
responses, tissue perfusion, and oxygenation. This is a circulatory system failure
requiring urgent resuscitation due to inadequate organ perfusion leading to systemic
inflammation, organ dysfunction and ultimately death. In treatment, the two primary
goals are to achieve hemorrhage control and promptly replace the lost blood with
appropriate fluids. In addition to shock-related morbidity, resuscitation fluids can lead
to cardiac and pulmonary complications, a systemic inflammatory response, edema,
coagulation and electrolyte/acid-base abnormalities. Vascular walls have an adhesive
layer on their inner surface known as the endothelial glycocalyx (EG), which is
composed of proteoglycans (such as syndecan-1) and glycosaminoglycans (including
heparan sulfate, chondroitin sulfate, and hyaluronan). The EG barrier can be a
significant determinant in vascular homeostasis. Endothelial cell dysfunction plays a
significant role in the microcirculation, including leukocyte adhesion to endothelium,
red blood cell (RBC) disorders, and changes in vascular smooth muscle cells. The
inadequacy of inflammatory activation due to endothelial dysfunction can enhance and
prolong the inflammatory process. Therefore, the impairment of its components has
been associated with endothelial damage, tissue dysfunction, and mortality in trauma
patients. In this study, a rodent hemorrhagic shock model was established, and
commonly used resuscitation fluids were administered. To assess the effects on the
endothelial glycocalyx (EG) in vivo after resuscitation, syndecan-1 levels were measured
in the blood at 0 minutes, 30 minutes, 60 minutes, and 120 minutes. In this
experimental rat study utilizing a hemorrhagic shock model, our aim was to compare
three different intravenous resuscitation fluids with groups receiving no intravenous
resuscitation fluid, focusing on EG damage. When evaluated over time, a continuous
increase was observed for each of the four groups, with the increase showing statistical
significance between time intervals (p=0.001<0.05). However, when comparing the
data obtained based on groups, no statistically significant difference was found
(p=0.671 >0.05). Upon evaluation of these results, the limitation of our study lies in the
fact that the number of animals in the groups was analyzed with less power than the
minimum number of subjects required by ethical principles of animal experimentation.
Increasing the number of subjects may lead to a closer approach to the statistical
significance value. Although there was no statistically significant difference in terms of
EG damage between colloid, crystalloid, and albumin fluids administered in
hemorrhagic shock, the untreated control group exhibited a significantly slower
increase than the other groups. All fluids caused varying levels of EG damage.