Microangiography of the Pancreas in Experimental Oedemic and Haemorrhagic Pancreatitis

Abstract

Nuutinen P, Kivisaari L, Standertskjold-Nordenstam C-G, Lempinen M, Schroder T. Microangiography of the pancreas in experimental oedemic and haemorrhagic pancreatitis. Scand J Gastroenterol 1986, 21 (suppl 126). 12-17Microangiography of the pancreas was performed in five normal piglets and in 10 piglets with oedemic and haemorrhagic pancreatitis in order to evaluate the role of microcirculatory changes in experimental pancreatitis. Acute haemorrhagic pancreatitis was induced by intraductal infusion of trypsin-taurocholate and oedematous pancreatitis correspondingly by infusion of autologous diluted bile. Both types of pancreatitis were confirmed by histological examination. Microangiography of the control animals revealed well-filled arteries, arterioles and capillaries, which formed a dense capillary network. In the areas of histologically documented haemorrhagic pancreatitis, unfilled capillary nets were observed as empty areas in the microangiography. Other areas of focal extravasation of the contrast material could be seen.Arteries and arterioles were well filled. In oedematous pancreatitis, the microangiography was unchanged compared with the control. Conclusion: Acute experimental haemorrhagic pancreatitis is associated with severe disturbances in the capillary circulation of the pancreas, whereas in oedematous pancreatitis the microangiography of the pancreas is normal.

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

“…Vascular alterations in several models of hemorrhagic pancreatitis have been documented by different techniques [2,7,20,22,27,28,41]. Using microangiographic techniques in a model of hemorrhagic pancreatitis, Nuutinen [28] and Kivisaari [22] showed severe alterations of the capillary network, consisting in a large number of unfilled capillaries and extravasations of contrast material.…”

“…Using microangiographic techniques in a model of hemorrhagic pancreatitis, Nuutinen [28] and Kivisaari [22] showed severe alterations of the capillary network, consisting in a large number of unfilled capillaries and extravasations of contrast material. They saw no alterations of the capillary system in edematous pancreatitis using the same techniques.…”

“…There is evidence from different experimental models to show that pancreatitis is associated with reduced pancreatic blood flow [11,23,24,44], increased Offprint requests to: G. Adler capillary permeability [20,21,39], vascular leakage [2,7,22,25,41], poor capillary filling [22,27,28,41,46], dilatation of capillaries [4], congestion and stasis in the capillary circulation [4,24], and microthrombosis [2]. It is a matter of controversy whether these alterations in pancreatic circulation cause pancreatitis [8,10,37] or occur as a consequence of pancreatitis [4,42].…”

Octreotide and Pancreatic Perfusion on the Outcome of Experimental Acute Pancreatitis

“…In contrast, Jenkins et al [30,31], working in a bile duct ligation plus caerulein infusion model and using microspheres, revealed that the somatostatin analogue significantly reduces pancreatic blood flow at 4 h, but maintains it compared to a further reduction observed in controls at 16 h. Based on these findings they concluded that somatostatin prevents early hypoperfusion and late hyperperfusion during the development of acute pancre atitis in rats. However, according to McEntee et al [4] and others [32][33][34][35][36], precapillary sphincters identified in the pancreas of cats and dogs could explain the paradoxical finding of an increase in pancreatic blood flow in the cae rulein model, due to local arteriovenous shunting, despite a reduction in the number of perfused capillaries. In addi tion Kelly et al [32] commented that caerulein produces a mild edematous and reversible pancreatitis, thus the ob servation of Jenkins et al [30,31] at 16 h may be in the healing or regeneration phase [37], Murayama and Joehl [13] hypothesized that caerulein administration induced acute pancreatitis by specific stimulation of choiecystokinin receptors and thus the inhibition of pancreatic secre tion by somatostatin would also prevent or ameliorate the pancreatic reaction produced by caerulein.…”

Peritoneal Lavage Efficiently Eliminates Protease-Alpha-2-Macroglobulin Complexes and Components of the Contact System from the Peritoneal Cavity in Patients with Severe Acute Pancreatitis

“…Even if the doses of protease inhibitor added to the lavage fluid are strongly in creased, it will be a problem to achieve suffi cient concentration within the most severely affected areas threatened by formation of necrosis. Because of reduced blood flow, the intravenous route of protease inhibitor ther apy also faces the same problems in obtain ing sufficient concentrations in these areas where additional protease inhibitor activity is most strongly needed [24], Therefore, it is of imminent importance to reevaluate treat ment regimens of protease inhibitors in acute pancreatitis and try to establish the most efficient way to improve control of pro teolysis in this state.…”