Fig. 8: Macroscopic and histological postmortem examination.
From: COVID-19 pathophysiology may be driven by an imbalance in the renin-angiotensin-aldosterone system

a Model lungs. Image of posterior aspect with discoloring. b Coronal cut through the posterior aspect of the model lung. c Control lungs. Image of posterior aspect. d Similar coronal cut of a control lung. e The dominating microscopic image in the model lungs was blood stasis in vessels of all sizes. This corresponded to areas with stasis perfusion as illustrated by a parametric max enhancement map from the same model animal (yellow is higher contrast enhancement). f High power magnification (x40) with fluids in the alveolar sacs and sloughing of pneumocytes into the alveolar space (marked by arrows), consistent with early diffuse alveolar damage (scale bar 100 µm). g Parametric relative contrast enhancement, with same color lookup table setting as in e, of control animal. h High power magnification showing a fluid collection in control lung (marked by arrow) in the alveolar sacs (scale bar 100 µm). i The macroscopic texture of the model lung was rubbery. Large areas of the model lungs were fully consolidated (scale bar 2.5 mm). j Fluids and cells in bronchi in a fully consolidated model lung (scale bar 100 µm). k In small areas in the most posterior aspects of the model lungs we could also identify fully consolidated lung (arrow, scale bar 2.5 mm). l Ventilated bronchi in fully consolidated control lungs (scale bar 100 µm). m Model kidney. n Histological sample from model kidney with narrowing of proximal tubule wall thickness and sloughing of epithelial cells (arrows), consistent with acute tubular necrosis (scale bar 100 µm). o Control kidney. p Control kidney without signs of acute tubular necrosis (scale bar 100 µm). q Model liver without histological damage (scale bar 250 µm). r Model small bowel (scale bar 500 µm). s Control liver (scale bar 250 µm). t Control small bowel (scale bar 500 µm).