Morphological Assessment of Vascular Wall in Ischemia Reperfusion Model

  • #VS 01-EP-12
  • Vascular Surgery. E-POSTER (ORAL) SESSION 1
  • E-Poster (oral)

Morphological Assessment of Vascular Wall in Ischemia Reperfusion Model

Igor A. Suchkov 1, Roman E. Kalinin 1, Aleksandr S. Pshennikov 1, Nina D. Mzhavanadze 1, Maksim V. Mnikhovich 2, Roman V. Deev 1

Ryazan State Medical University, Ryazan, Russia; Research Institute of Human Morphology, Moscow, Russia;

Date, time and location: 2018.05.26 08:30, Exhibition area, 1st Floor. Zone – B


Objective: to evaluate morphology of vascular wall in ischemia reperfusion model.

Material and methods: the study was carried out on Wistar rats according to regulations and ethical considerations in animal experiments. Two models of ischemia-reperfusion injury were performed by cross-clamping the aorta (group 1) with following conditioning (group 2). Routine light and electron microscopy were used.

Results. At 1 and 3 days after the cross-clamping of the aorta distinctions in pathohistological and ultrastructural changes were subtle. Light microscopy revealed dystrophic and necrobiotic changes. A collection of interstitial fluid was detected in vascular wall. Endothelium was heteromorphic and was characterized by focal smoothening and thinning or “swelling”. Mosaic desquamation of the inner vascular layer is specific for such time period after ischemia. Endothelial mitochondria had average electronic density and homogenous matrix. Mitochondrial cristae were absent, i.e. smoothened or destroyed. Separate mitochondria contained totally lysed cristae, matrix had fibrillar content. Severe destructive changes occured at 5 and 7 days after ischemia induction. At 1 day after the induction of ischemia-reperfusion pathohistological findings did not differ from those in group 1. However, at 3 days pathological alterations were accompanied by the adaptive process in vascular wall, i.e. changes in endothelial cells organelles and enlargement of vascular lumen. At 7 days ultrasctructure of all vascular layers was impaired. Endothelial cells presented with severe dystrophy and necrosis with partial protruding into the vascular lumen. Heterogeneity in thickness of the basement membrane with average electronic density was among the findings. The structure of basement membrane was characterized by the presence of vacuole-like bodies extending beyond the membrane itself. Focal destructive lesions in basement membrane were also detected.

Conclusions: there were no significant structural or ultrastructural differences between the ischemia and ischemia-reperfusion groups. Pathomorphogenesis of these two conditions should be assessed using high-resolution methods.

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