Structural alterations of pancreatic microvasculature in cerulein-induced pancreatitis in the rat

Abstract

Pancreatic microvasculature in cerulein-induced pancreatitis was studied at the electron and light microscopic level. Using a modified model of in situ india ink perfusion, focally a marked reduction of the number of india-ink-filled microvessels was found. The numerical density (NA) of filled microvessels was reduced by 66.7% in pancreatitis. The morphological correlate for this extreme numeric reduction might be a collapse of the lumen of pancreatic microvessels. In the presence of cerulein pancreatitis 42% of pancreatic capillaries had a collapsed lumen as shown by electron microscopy. The endothelium of capillaries in acute pancreatitis demonstrated surface blebbing, the formation of cytoplasmatic vacuoles, edema, and swollen mitochondria. Some capillaries had irregularities at the interendothelial junction, and the majority of examined vessels were surrounded by marked perivascular edema. No strict correspondence between histological signs of pancreatitis and light microscopic and/or ultrastructural microvascular alterations could be demonstrated. Our study emphasizes that alterations of microvasculature are present early in experimental edematous pancreatitis. Therefore, alterations of pancreatic microcirculation seem to be of great importance in the pathogenesis of pancreatic inflammation, and should be the subject of further studies.

Effects of the bradykinin antagonist, icatibant (Hoe 140), on pancreas and liver functions during and after caerulein-induced pancreatitis in rats

“…It has been reported that blood flow within the pancreas is already drastically reduced very early during acute pancreatitis (Gress et al 1990;McEntee and Kelly 1991) so that adverse effects on the physiological functions of the gland might be expected. Prevention of the oedema by icatibant could thus be expected to be beneficial also in this aspect.…”

Pancreatic capillary blood flow during caerulein-induced pancreatitis evaluated by a laser-doppler flowmeter in rats

“…Enclosure of intracellular organelles within autophagic vacuoles with subsequent lysosomal degradation appears to contribute to the destruction of the acinar cells in this model of acute pancreatitis 12,13 . During caerulein-induced pancreatitis there is a collapse in the pancreatic capillaries and surface blebbing, formation of cytoplasmatic vacuoles, edema, and swollen mitochondria in the 14,15,16 . These structural alterations were present early in the experimental edematous pancreatitis 14 .…”

“…During caerulein-induced pancreatitis there is a collapse in the pancreatic capillaries and surface blebbing, formation of cytoplasmatic vacuoles, edema, and swollen mitochondria in the 14,15,16 . These structural alterations were present early in the experimental edematous pancreatitis 14 . Overall, experimental 17 and clinical 5 studies have found that during acute pancreatitis there is a decrease in the blood flow to the pancreas.…”

“…Electron microscopy showed endothelial injury such as vascular degeneration, disorganized intracellular junctions, perivascular edema and vascular occlusion during caerulein-incuced AP. Early edema formation is due to increased capillary permeability in caerulein-induced AP 14 .…”

“…In that study, there was a volemic replacement with a crystalloid infusion rate three times higher than our study. Besides, normovolemia does not represent the AP natural clinical evolution where there is intravascular fluid depletion due to increased capillary permeability 14 .…”