Low molecular weight dextran in experimental pancreatitis: Effects on pancreatic microcirculation

Knol, James A.; Edgcomb, Leslie P.; Inman, Mark G.; Eckhäuser, Frederic E.

doi:10.1016/0022-4804(83)90128-2

Cited by 36 publications

(16 citation statements)

References 16 publications

(11 reference statements)

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“…Intravascular fluid replacement for stabilizing cardiac and urinary output on the one hand and edema formation due to fluid leaking from the vessels on the other hand is a clinically relevant problem. Attempts to overcome this dilemma include plasma expanders, small volume resuscitation and isovolemic hemodilution [26,27]. However, since capillary leakage per se is not affected, the efficacy of these methods is limited.…”

Section: Discussionmentioning

confidence: 99%

Effect of Fluid Resuscitation with and without Endothelin A Receptor Blockade on Hemoconcentration and Organ Function in Experimental Pancreatitis

Forgács

Eibl²,

Faulhaber³

et al. 2000

Eur Surg Res

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Background: Intravascular fluid loss contributes to pancreatitis-associated multiple organ dysfunction and is thus a major target for therapy in this life-threatening disease. Aim: To evaluate intravascular fluid loss and extravascular fluid sequestration together with cardiorespiratory and renal function in a well-established rat model of severe acute pancreatitis (AP) and to investigate the effect of fluid resuscitation with and without endothelin receptor A blockade on these parameters. Method: Induction of AP in rats by a standardized bile salt infusion into the pancreatic duct and intravenous cerulein hyperstimulation. Six hours after AP induction, animals were randomized into 4 groups to receive (1) no therapy; (2) 4 ml/kg/h Ringer’s lactate (RL) i.v.; (3) 8 ml/kg/h RL i.v., or (4) 4 ml/kg/h RL plus an endothelin receptor antagonist. Target parameters measured before and after AP induction and during the 24-hour observation period included: mean arterial blood pressure, heart rate, hematocrit, arterial blood gases, urine production, ascites and pleural effusions. Results: After 6 h, all animals presented with severe hemoconcentration (hematocrit >57%) and oliguria (<0.5 ml/6 h). Cardiorespiratory parameters were within the normal range. Up to 12 h after AP induction, animals without therapy had an increased hematocrit and oliguria and developed metabolic acidosis. Animals receiving fluid resuscitation had a significant drop in hematocrit and maintained compensated blood gas values. A significant increase in urine production was only observed in animals given 8 mg/kg/h RL. Between 12 and 24 h, urine production significantly increased with fluid resuscitation and respiratory parameters stabilized except for animals treated with 8 ml/kg/h RL which developed arterial hypoxia and hypercapnia. Conclusions: Intravascular fluid loss and extravascular fluid sequestration together with decreased urine production characterize the early phase of this model of severe AP. Massive fluid resuscitation necessary for increasing urine output may lead to respiratory distress. Reduction of intravascular fluid loss by endothelin receptor blockade is associated with improved renal and respiratory function.

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Section: Discussionmentioning

confidence: 99%

Effect of Fluid Resuscitation with and without Endothelin A Receptor Blockade on Hemoconcentration and Organ Function in Experimental Pancreatitis

Forgács

Eibl²,

Faulhaber³

et al. 2000

Eur Surg Res

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“…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].…”

Section: Introductionmentioning

confidence: 99%

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

1990

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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.

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“…The early hours of experimental hemorrhagic pancreatitis are characterized by low cardiac output, reduced pancreatic blood flow, and hypovolemia due to plasma loss of up to 30% of the circulating blood volume (19). Pancreatic blood flow, as shown by the microsphere technique, is reduced by 43-60% of the initial value (16,20).…”

Section: Discussionmentioning

confidence: 99%

Hypovolemic Shock and Contrast-Enhanced Computed Tomography of the Pancreas

Nuutinen¹,

Kivisaari²,

Lehtola³

et al. 1986

Scandinavian Journal of Gastroenterology

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The effect of profound hemorrhagic hypovolemia on cardiac output and pancreatic blood flow was studied in pigs with the thermodilution method and microsphere technique. Approximately 30-40% of the circulating blood volume was withdrawn slowly during 5 h. Cardiac output and pancreatic blood flow decreased by 35% and 32%, respectively. The animals underwent contrast-enhanced computed tomography (CT) before hypovolemia and at 5 h after its onset. The changes in systemic and local blood flow were related to the contrast enhancement of the pancreas. In spite of profound hypovolemia and a significant decrease in pancreatic blood flow (p less than 0.005), the contrast enhancement remained normal. The results of the present study indicate that pancreatic hypoperfusion caused by hypovolemia does not affect the contrast enhancement of the pancreas in CT.

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Low molecular weight dextran in experimental pancreatitis: Effects on pancreatic microcirculation

Cited by 36 publications

References 16 publications

Effect of Fluid Resuscitation with and without Endothelin A Receptor Blockade on Hemoconcentration and Organ Function in Experimental Pancreatitis

Effect of Fluid Resuscitation with and without Endothelin A Receptor Blockade on Hemoconcentration and Organ Function in Experimental Pancreatitis

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

Hypovolemic Shock and Contrast-Enhanced Computed Tomography of the Pancreas

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