In the Experimental Model of Acute Mesenteric Ischemia, The Correlation of Blood Diagnostic Parameters with the Duration of Ischemia and their Effects on Choice of Treatment.

Purpose/Aim: Acute mesenteric ischemia is a syndrome characterized by sudden onset abdominal pain followed by intestinal necrosis. Morbidity and mortality increase with delayed diagnosis. Even with the latest radiological diagnostic methods, early diagnosis and initiation of treatment can be delayed. Using an experimental model, here we aim to determine the relationship between the laboratory parameters used to detect acute mesenteric ischemia and the duration of irreversible ischemia. Materials and Methods: A total of 30 male Wistar albino rats were divided into five groups, all of which underwent general anesthesia: (i) Superior mesenteric artery (SMA) dissection with laparotomy was performed, and blood samples and intestinal segment samples were taken after 2 hr (Sham group); (ii) volvulus of one-third of the small intestines was performed manually by laparotomy, and blood samples and intestinal segment samples were taken after 2 hr (Volvulus group); (iii) SMA was ligated with laparotomy, and blood samples and intestinal segment samples were taken after 2 hr (SMA+ligated 2-hr group); (iv) SMA was ligated with laparotomy, and blood samples and intestinal segment samples were taken after 4 hr (SMA+ligated 4-hr group); and (v) SMA was ligated with laparotomy, and blood samples and intestinal segment samples were taken after 6 hr (SMA+ligated 6-hr group). Results: The mean lactate dehydrogenase (LDH) activities of the SMA+ligated 2-hr and SMA+ligated 6-hr groups were statistically higher than the control group (p = .004). Compared to the Sham and Volvulus groups, the mean lactate level of the SMA+ligated 6-hr group was significantly higher (p = .004). Compared to the Sham and Volvulus groups, the mean D-dimer levels of the SMA+ligated 4-hr and SMA+ligated 6-hr groups were significantly higher (p = .004 and .003, respectively). By histopathological evaluation, we found that pathological damage increased as the ischemia lengthened. Conclusions: Mesenteric ischemia leads to an irreversible loss of intestinal perfusion and an increase in parameters of ischemia. Irreversible tissue damage occurs after 4 hr of ischemia and peaks after 6 hr, whereas parameters of ischemia (D-dimer, LDH, and L-Lactate levels) are highest at 2 hr after the onset of ischemia.