Improvement of impaired microcirculation and tissue oxygenation by hemodilution with hydroxyethyl starch plus cell-free hemoglobin in acute porcine pancreatitis

Freitag, M.; Standl, Thomas; Kleinhans, Helge; Gottschalk, André; Mann, Oliver; Rempf, Christian; Bachmann, Kai; Gocht, Andreas; Petri, Susan; Izbicki, Jakob R.; Strate, Tim

doi:10.1159/000091962

Cited by 33 publications

(27 citation statements)

References 28 publications

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“…Inhibition of certain coagulatory steps, for example by applying anticoagulant substances, is well known to improve the outcome in acute pancreatitis (Freitag et al 2006;Yamaguchi et al 1997). Coagulation and hemostasis consist of two interacting pathways: (1) humoral factors that lead to the activation of fibrinogen as the final step in the coagulation cascade, and (2) cellular factors that are represented by activated platelets.…”

Section: Discussionmentioning

confidence: 99%

Pathophysiological role of platelets in acute experimental pancreatitis: influence of endothelin A receptor blockade

et al. 2006

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The potential pathophysiological role of platelet-endothelium interactions was investigated during ischemia/reperfusion (I/R), and the effect of a selective endothelin(A) receptor antagonist (ET(A)-RA) was evaluated in an acute pancreatitis model. Acute pancreatitis was induced by warm ischemia (60 min) in Wistar rats, and its effects with and without antagonist treatment were investigated. Equivalent sham-operated animals were also studied. Microcirculatory changes were assessed by in vivo microscopy, and serum levels for lipase/amylase and histological specimens were investigated. Capillary constriction to 83.7 +/- 6.7% of sham-operated diameters was observed after 60 min of ischemia. A capillary density of 56.8 +/- 9.3% of the sham-operated group (396.3 +/- 15.8 mm(-1)) was measured after reperfusion. Stagnant leukocytes (329.5 +/- 30.4%) and platelets (337.5 +/- 32.3%) increased in postcapillary venules (P < 0.05). Administration of the ET(A)-RA significantly reduced I/R injury. Capillary diameters were maintained (101.4 +/- 4.5%), and capillary density was improved to 73.3 +/- 7.6% of sham-operated animals (P < 0.05). Stagnant leukocytes (152.3 +/- 10.6%) and platelets (207.1 +/- 19.8%) in sinusoids and postcapillary venules were reduced (P < 0.05). The extent of acute pancreatitis was reduced in the therapy group as indicated by serum lipase/amylase values and histological tissue damage (P < 0.05). Thus, ET(A)-RA therapy was effective in reducing I/R-induced pancreatitis in this experimental model.

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Section: Discussionmentioning

confidence: 99%

Pathophysiological role of platelets in acute experimental pancreatitis: influence of endothelin A receptor blockade

et al. 2006

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“…59,60 Furthermore, a combination of isovolemic hemodilution with hydroxyethyl starch and addition of a plasmatic oxygen carrier (like cell-free bovine hemoglobin HBOC-301) preserved pancreatic microcirculation, reduced mortality, and improved pancreatic tissue oxygenation. 58 This beneficial effect of additional oxygen supply does not lead to enhanced lipid peroxidation as feared. 61 In the future, a combination of rheologic and O 2 -delivering therapy may represent a novel therapeutic option for the treatment of AP.…”

Section: Type Of Fluidvcrystalloid Versus Colloidsmentioning

confidence: 99%

“…57 It is well known that the disturbance of the pancreatic microcirculation and the consequent tissue hypoxia perpetuate progression from mild to severe pancreatitis. 58 A cell-free hemoglobin-based oxygen carrier (HBOC-301) improves fluidity because of its colloid effects and delivers cell-free oxygen to oxygen-deprived tissue, thus improving pancreatic microcirculation and pancreatic oxygen tension. This was assessed by leukocyte adherence and decreased tissue damage as compared with normal saline in a rodent model.…”

Section: Type Of Fluidvcrystalloid Versus Colloidsmentioning

confidence: 99%

Current Controversies in Fluid Resuscitation in Acute Pancreatitis

Trikudanathan¹,

Navaneethan²,

Vege³

2012

Pancreas

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Acute pancreatitis (AP) is a common inflammatory disorder of the pancreas resulting in considerable morbidity and mortality. Aggressive intravenous fluid resuscitation generally is recommended in all patients with AP and remains the cornerstone of management of these patients. However, the optimal rate, type, and the goal of resuscitation remain unclear. The purpose of this review was to give an insight about the pathophysiologic alterations in the pancreatic microcirculation that occur in AP, the markers for early recognition of severity of pancreatitis, the optimal fluid, and timing and extent of fluid resuscitation. An early elevated hematocrit, blood urea nitrogen, or creatinine should prompt clinicians to institute more intensive early resuscitation measures. Crystalloids are the currently recommended fluids for management of these patients. Current studies are underway to determine the optimal end points of fluid resuscitation that determine outcome.

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“…This alteration in microcirculation significantly increases the degree of pancreatic ischemia, irrespective of etiology, thus exacerbating the systemic inflammatory response syndrome [6,7] and leading to multisystem organ failure. Inflammatory mediators cause an increase in vascular permeability [8][9][10][11][12][13], and a decrease in endothelial tone causes significant extravasation of both interstitial fluid, leading to acute edematous changes around the acinus, and inflammatory cells [14]. In addition, hypercoagulability leading to microthrombi formation also contributes to pancreatic ischemia and subsequent pancreatic tissue necrosis [15].…”

Section: Microcirculatory Derangementmentioning

confidence: 99%

“…Experimental studies have shown that isovolemic hemodilution with hydroxyethyl starch or without plasmatic hemoglobin reduce mortality and preserves pancreatic microcirculation [8,26,27]. Studies in humans are not conclusive because based on a small number of patients [28].…”

Section: Future Developmentsmentioning

confidence: 99%

Fluid Replacement Strategy in Severe Acute Pancreatitis

Pezzilli¹

2013

Pancreat Disorders Ther

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Improvement of impaired microcirculation and tissue oxygenation by hemodilution with hydroxyethyl starch plus cell-free hemoglobin in acute porcine pancreatitis

Cited by 33 publications

References 28 publications

Pathophysiological role of platelets in acute experimental pancreatitis: influence of endothelin A receptor blockade

Pathophysiological role of platelets in acute experimental pancreatitis: influence of endothelin A receptor blockade

Current Controversies in Fluid Resuscitation in Acute Pancreatitis

Fluid Replacement Strategy in Severe Acute Pancreatitis

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