Capillary Perfusion of the Pancreas in Acute Pancreatitis and Effects of Isovolemic Hemodilution

Author(s):  
E. Klar ◽  
K. Messmer
1993 ◽  
Vol 217 (4) ◽  
pp. 369-374 ◽  
Author(s):  
Ernst Klar ◽  
Thomas Foitzik ◽  
Heinz Buhr ◽  
Konrad Messmer ◽  
Christian Herfarth

Gut ◽  
1998 ◽  
Vol 43 (3) ◽  
pp. 401-407 ◽  
Author(s):  
J Werner ◽  
C Fernández-del Castillo ◽  
J A Rivera ◽  
N Kollias ◽  
K B Lewandrowski ◽  
...  

Background—Ectopic protease activation, microcirculatory changes, and leucocyte activation are the main events in the pathogenesis of acute pancreatitis. Nitric oxide (NO) is known to be a key mediator in the normal and inflamed pancreas.Aims—To investigate the targets on which NO exerts its effect in caerulein induced pancreatitis.Methods—Acute pancreatitis was induced in rats which additionally received either the NO synthase substrate, l-arginine; the NO donor, sodium nitroprusside; or the NO synthase inhibitor, N-nitro-l-arginine methyl ester (l-NAME). At six hours, pancreatic injury (oedema, leucocyte content, ectopic trypsinogen activation) was analysed and pancreatic oxygenation and perfusion were determined. A direct influence of NO on amylase secretion and trypsinogen activation was evaluated separately in vitro.Results—Both NO donors reduced the grade of inflammation. l-NAME increased the severity of inflammation, while decreasing pancreatic tissue oxygenation. Although neither amylase secretion nor intracellular trypsinogen activation in caerulein stimulated pancreatic acini was influenced by either NO donors or inhibitors, both NO donors decreased intrapancreatic trypsinogen activation peptide (TAP) and pancreatic oedema in vivo, andl-NAME increased TAP.Conclusions—NO protects against injury caused by pancreatitis in the intact animal but has no discernible effect on isolated acini. It is likely that in pancreatitis NO acts indirectly via microcirculatory changes, including inhibition of leucocyte activation and preservation of capillary perfusion.


2007 ◽  
Vol 293 (2) ◽  
pp. H1206-H1215 ◽  
Author(s):  
Pedro Cabrales

Responses to exchange transfusion using red blood cells (RBCs) with normal and reduced flexibility were studied in the hamster window chamber model during acute moderate isovolemic hemodilution to determine the role of RBC membrane stiffness in microvascular perfusion and tissue oxygenation. Erythrocyte stiffness was increased by 30-min incubation in 0.02% glutaraldehyde solution, and unreacted glutaraldehyde was completely removed. Filtration pressure through 5-μm pore size filters was used to quantify stiffness of the RBCs. Anemic conditions were induced by two isovolemic hemodilution steps using 6% 70-kDa dextran to a hematocrit (Hct) of 18% (moderate hemodilution). The protocol continued with an exchange transfusion to reduce native RBCs to 75% of baseline (11% Hct) with either fresh RBCs (RBC group) or reduced-flexibility RBCs (GRBC group) suspended in 5% albumin at 18% Hct; a plasma expander (6% 70-kDa dextran; Dex70 group) was used as control. Systemic parameters, microvascular perfusion, capillary perfusion [functional capillary density (FCD)], and oxygen levels across the microvascular network were measured by noninvasive methods. RBC deformability for GRBCs was significantly decreased compared with RBCs and moderate hemodilution conditions. The GRBC group had a greater mean arterial blood pressure (MAP) than the RBC and Dex70 groups. FCD was substantially higher for RBC (0.81 ± 0.07 of baseline) vs. GRBC (0.32 ± 0.10 of baseline) and Dex70 (0.38 ± 0.10 of baseline) groups. Microvascular tissue Po2 was significantly lower for Dex70 and GRBC vs. RBC groups and the moderate hemodilution condition. Results were attributed to decreased oxygen uploading in the lungs and obstruction of tissue capillaries by rigidified RBCs, indicating that the effects impairing RBC flexibility are magnified at the microvascular level, where perfusion and oxygenation may define transfusion outcome.


2006 ◽  
Vol 105 (2) ◽  
pp. 354-359 ◽  
Author(s):  
Hendrik Freise ◽  
Stefan Lauer ◽  
Soeren Anthonsen ◽  
Verena Hlouschek ◽  
Evgeny Minin ◽  
...  

Background Acute pancreatitis has been linked to intestinal barrier dysfunction and systemic inflammatory response with high mortality. Thoracic epidural analgesia improves intestinal perfusion. The authors hypothesized that thoracic epidural analgesia influences microcirculation injury, inflammatory response, and outcome of acute pancreatitis in rats. Methods Control groups underwent a sham procedure or untreated pancreatitis induced by intraductal taurocholate injection. In the treatment groups, epidural analgesia was commenced immediately or after a 7-h delay. Fifteen hours after injury, the ileal mucosal perfusion was assessed by intravital microscopy. Thereby, the intercapillary area between all perfused capillaries and between continuously perfused capillaries only was used to differentially quantify total and continuous capillary mucosal perfusion. Villus blood flow and serum levels of amylase, lactate, and interleukin 6 were determined, and pancreatic injury was scored histologically. Seven-day survival was recorded in an additional 30 rats undergoing untreated pancreatitis or pancreatitis with epidural analgesia. Results In untreated pancreatitis, decreased total capillary perfusion increased the total intercapillary area by 24%. Furthermore, loss of continuous perfusion increased continuous intercapillary area to 228%. After immediate and delayed epidural analgesia, continuous perfusion was restored (P < 0.05). Blood flow decreased 50% in untreated pancreatitis but was preserved by epidural analgesia (P < 0.05). Biochemical and histologic signs of pancreatitis were not affected by epidural analgesia. Lactate and interleukin-6 levels increased in untreated pancreatitis, which was prevented in the treatment groups (P < 0.05). Epidural analgesia increased 7-day survival from 33% to 73% (P < 0.05). Conclusion Thoracic epidural analgesia attenuated systemic response and improved survival in severe acute pancreatitis. These effects might be explained by improved mucosal perfusion.


2005 ◽  
Vol 289 (6) ◽  
pp. H2392-H2400 ◽  
Author(s):  
Pedro Cabrales ◽  
Amy G. Tsai ◽  
Robert M. Winslow ◽  
Marcos Intaglietta

Isovolemic hemodilution to 11% systemic hematocrit was performed in the hamster window chamber model using 6% dextran 70 kDa (Dx 70) and 5% human serum albumin (HSA). Systemic and microvascular effects of these solutions were compared with polyethylene glycol (PEG)-conjugated 5% albumin (MPA) and PEG-conjugated 4.2% Hb (MP4). These studies were performed for the purpose of comparing systemic and microvascular responses of PEG vs. non-PEG plasma expanders and similar oxygen-carrying vs. noncarrying blood replacement fluids. Mean arterial blood pressure was statistically significantly reduced for all groups compared with baseline ( P < 0.05), HSA, MPA, and MP4 higher than Dx 70 ( P < 0.05). MP4 and MPA had a significantly higher cardiac index than HSA and Dx 70, in addition to a positive base excess. Microvascular blood flow and capillary perfusion were significantly higher for the PEG compounds compared with HSA and Dx 70. Intravascular Po2 for MP4 and MPA was higher in arterioles ( P < 0.05) compared with HSA and Dx 70, but there was no difference in either tissue or venular Po2 between groups. Total Hb in the MP4 group was 4.8 ± 0.4 g/dl, whereas the remaining groups had a range of 3.6–3.8 g/dl. The hemodilution results showed that PEG compounds maintained microvascular conditions with lower concentrations than conventional plasma expanders. Furthermore, microvascular oxygen delivery and extraction in the window chamber tissue were significantly higher for the PEG compounds. MP4 was significantly higher than MPA ( P < 0.05) and was not statistically different from baseline, an effect due to the additional oxygen release to the tissue by the Hb MP4.


Author(s):  
Murat Sarikaya ◽  
Nesibe Taser ◽  
Zeynal Dogan ◽  
Bilal Ergul ◽  
F. Irsel Tezer ◽  
...  

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