Experimental pancreatitis in the rat. Light and electron microscopical observations on early pancreatic lesions induced by intraductal injection of trypsin, phospholipase A2, lysolecithin and non-ionic detergent

Aho, Heikki; Nevalainen, Timo J.

doi:10.1007/bf02932876

Cited by 24 publications

(1 citation statement)

References 26 publications

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“…Lesions caused by similar injections of lysolecithin are morphologically identical, which indicates that the phospholipase A 2 -induced tissue injury is mediated by lysolecithin. The tissue destruction is most probably due to the detergent action of lysolecithin [3].…”

Section: Phospholipase A2mentioning

confidence: 99%

Phospholipase A2 in Acute Pancreatitis

Nevalainen

Aho

1987

Acute Pancreatitis

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Section: Phospholipase A2mentioning

confidence: 99%

Phospholipase A2 in Acute Pancreatitis

Nevalainen

Aho

1987

Acute Pancreatitis

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Pancreatic ischaemia in experimental acute pancreatitis: Mechanism, significance and therapy

Klar

Meßmer

Warshaw

et al. 1990

Journal of British Surgery

246

123

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Much clinical and experimental evidence suggests that pancreatic ischaemia in the early phase of acute pancreatitis is important in the development of pancreatic necrosis. While depletion of intravascular volume has often been assumed to be the main circulatory defect, an additional disturbance of pancreatic microcirculation has been demonstrated experimentally. Possible contributory mechanisms include chemical-induced vasoconstriction, direct injury of vessel wall, intravascular coagulation and increased endothelial permeability resulting in pancreatic oedema, haemoconcentration and impaired venous drainage. Pancreatic ischaemia as a consequence of these local effects seems to be responsible for the transition of mild pancreatitis to parenchymal necrosis. In experimental models the beneficial effect of various drugs and of sympathetic blockade has been ascribed to an improvement in pancreatic perfusion. Although effective volume therapy is generally accepted as the mainstay of conservative treatment in acute pancreatitis, the efficacy of different fluid preparations is still controversial, and simple fluid resuscitation has not been shown to prevent the development of parenchymal necrosis. The specific impairment of pancreatic microcirculation cannot be prevented merely by replenishment of intravascular volume with crystalloids, albumin or plasma despite normalization of macrohaemodynamics. In contrast, partial replacement of blood by dextran preparations has been shown to increase pancreatic perfusion by improving blood fluidity. Isovolaemic haemodilution in conjunction with conventional fluid therapy may provide a new and effective means of protecting the pancreas from secondary injury due to the early ischaemic phase of acute pancreatitis.

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Pancreatic Blood Flow with Special Emphasis on Blood Perfusion of the Islets of Langerhans

Jansson

Carlsson

2019

Comprehensive Physiology

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The pancreatic islets are more richly vascularized than the exocrine pancreas, and possess a 5‐ to 10‐fold higher basal and stimulated blood flow, which is separately regulated. This is reflected in the vascular anatomy of the pancreas where islets have separate arterioles. There is also an insulo‐acinar portal system, where numerous venules connect each islet to the acinar capillaries. Both islets and acini possess strong metabolic regulation of their blood perfusion. Of particular importance, especially in the islets, is adenosine and ATP/ADP. Basal and stimulated blood flow is modified by local endothelial mediators, the nervous system as well as gastrointestinal hormones. Normally the responses to the nervous system, especially the parasympathetic and sympathetic nerves, are fairly similar in endocrine and exocrine parts. The islets seem to be more sensitive to the effects of endothelial mediators, especially nitric oxide, which is a permissive factor to maintain the high basal islet blood flow. The gastrointestinal hormones with pancreatic effects mainly influence the exocrine pancreatic blood flow, whereas islets are less affected. A notable exception is incretin hormones and adipokines, which preferentially affect islet vasculature. Islet hormones can influence both exocrine and endocrine blood vessels, and these complex effects are discussed. Secondary changes in pancreatic and islet blood flow occur during several conditions. To what extent changes in blood perfusion may affect the pathogenesis of pancreatic diseases is discussed. Both type 2 diabetes mellitus and acute pancreatitis are conditions where we think there is evidence that blood flow may contribute to disease manifestations. © 2019 American Physiological Society. Compr Physiol 9:799‐837, 2019.

show abstract

Experimental pancreatitis in the rat. Light and electron microscopical observations on early pancreatic lesions induced by intraductal injection of trypsin, phospholipase A2, lysolecithin and non-ionic detergent

Cited by 24 publications

References 26 publications

Phospholipase A2 in Acute Pancreatitis

Phospholipase A2 in Acute Pancreatitis

Pancreatic ischaemia in experimental acute pancreatitis: Mechanism, significance and therapy

Pancreatic Blood Flow with Special Emphasis on Blood Perfusion of the Islets of Langerhans

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