Impairment Of Pancreatic Microcirculation Research Articles

Impairment of pancreatic microcirculation in the early reperfusion period correlates with degree of organ damage in clinical pancreas transplantation

Impairment of pancreatic microcirculation in the early reperfusion period correlates with degree of organ damage in clinical pancreas transplantation

Impairment of pancreatic microcirculation in the early reperfusion period during simultaneous pancreas-kidney transplantation.

The most likely cause of graft pancreatitis is the ischemia/reperfusion injury which can be a major problem in simultaneous pancreas-kidney transplantation. Animal experiments suggest the important role in this process of an impaired microcirculation after reperfusion. We have investigated pancreatic microcirculation in the early reperfusion period during clinical pancreas-kidney transplantation. Tissue PO2 (PO2ti) was monitored by a PO2-sensitive electrode. After reperfusion (a.r.) samples were taken from the venous effluent of the pancreas and simultaneously from the radial artery. After an initial peak a transient fall of PO2 was found. Total blood flow and hemoglobin oxygen saturation (sHbO2) in the venous effluent increased until 90 min a.r. (107 ml/min, 97.1%) High venous sHbO2 and high PO2ti correlated with good graft outcome. These findings can be explained by an impairment of capillary perfusion (no reflow) and concomitant shunt perfusion. The data suggest the considerable relevance of pancreatic microcirculation in the early reperfusion period during clinical pancreas transplantation.

Impairment of pancreatic microcirculation in the early reperfusion period during simultaneous pancreas-kidney transplantation

Abstract The most likely cause of graft pancreatitis is the ischemia/reperfusion injury which can be a major problem in simultaneous pancreas-kidney transplantation. Animal experiments suggest the important role in this process of an impaired microcirculation after reperfusion. We have investigated pancreatic microcirculation in the early reperfusion period during clinical pancreas-kidney transplantation. Tissue PO2 (PO2ti) was monitored by a PO2-sensitive electrode. After reperfusion (a. r.) samples were taken from the venous effluent of the pancreas and simultaneously from the radial artery. After an initial peak a transient fall of PO2 was found. Total blood flow and hemoglobin oxygen saturation (sHbO2) in the venous effluent increased until 90 min a. r. (107 ml/min, 97.1%) High venous sHbO2 and high PO2ti correlated with good graft outcome. These findings can be explained by an impairment of capillary perfusion (no reflow) and concomitant shunt perfusion. The data suggest the considerable relevance of pancreatic microcirculation in the early reperfusion period during clinical pancreas transplantation.

Pancreatic microcirculation in acute pancreatitis.

We present a review of the microvascular morphology of the pancreas and microstructure of the pancreatic lobule, and report our experimental results of the investigation of pancreatic microcirculation following acute pancreatitis. Impairment of pancreatic microcirculation in the early phase of acute pancreatitis may play a key role in the progression of this disease. Possible contributory mechanisms include increased vascular permeability, reduced blood flow, leukocyte-endothelial cell interaction and intravascular thrombus formation. Using an in-vivo microscope system and off-line computer analysis, we achieved direct visualization and quantification of changes in microvascular permeability and leukocyte behavior in pancreas with acute pancreatitis. Bradykinin and oxygen radicals have been demonstrated to be involved in the increase of vascular permeability in the early stage of caerulein pancreatitis. Leukocyte adherence to the vessels in the pancreatic microcirculation is a secondary event following permeability changes in acute pancreatitis. Leukocyte infiltration during exacerbation of acute pancreatitis is mediated by leukocyte-endothelial cell interaction via leukocyte integrin CD11b/18.

Analysis of the derangement of the pancreatic microcirculation in a rat caerulein pancreatitis model using an intravital microscope system.

In order to clarify the derangement of the pancreatic microcirculation in acute pancreatitis, the pancreatic microcirculation in caerulein pancreatitis was monitored intravitally and the roles of bradykinin and nitric oxide were examined using bradkykinin B2 receptor antagonist, HOE140. Under an intravital microscope, the pancreatic microcirculation was observed 2 or 6 hr after the induction of acute pancreatitis. HOE140 was administered 30 min before the induction of acute pancreatitis. The videoimages were taken into the computer, and the value of grayscale was measured with imaging software to quantify the degree of extravasation. Extravasation in the postcapillary venules was remarkable and the velocity in pancreatic terminal arterioles decreased significantly. However, the adherence of leukocytes was not observed until 6 hr after the induction. Both the extension of extravasation and the decrease of velocity were prevented by HOE140. The levels of nitric oxides in the pancreatic tissue declined and this decline was not influenced by HOE140. Bradykinin participates mainly in the regulation of vascular permeability in the early stage of caerulein pancreatitis. Further, the impairment of pancreatic microcirculation may play a key role in the onset and development of acute pancreatitis.

Impact of microcirculatory flow pattern changes on the development of acute edematous and necrotizing pancreatitis in rabbit pancreas.

Impairment of pancreatic microcirculation has often been advocated as one pathogenic mechanism in necrotizing pancreatitis. In contrast, data on pancreatic capillary perfusion in edematous pancreatitis are scarce. It was the aim of this experimental study to compare changes in pancreatic microcirculation in edematous and necrotizing pancreatitis. Twelve rabbits were allocated to two groups. Two different models of acute pancreatitis were used. Edematous pancreatitis was elicited by intravenous administration of cerulein (25 micrograms/kg/hr) (N = 6). Necrotizing pancreatitis of the biliary type was induced by pressure-controlled intraductal infusion of a mixture of taurocholate, trypsin, and blood (N = 6). Pancreatic microcirculation was quantified by means of intravital microscopy assessing functional capillary density, blood cell velocity, and distribution of the plasma marker FITC-dextran 70. Systemic hemodynamics were maintained at baseline values by fluid administration. Regardless of edema or necrosis, pronounced extravasation of FITC-dextran was recorded in the early stage of pancreatitis. In cerulein-induced pancreatitis, hyperemia developed as indicated by an increase in blood cell velocity in the presence of homogeneous capillary perfusion. In contrast, a progressive reduction of the number of perfused capillaries was detected in necrotizing pancreatitis. In conclusion, pancreatic microvascular perfusion may be regarded as an important pathogenetic factor for the determination of acute pancreatitis.

Therapeutic Effect of Isovolemic Hemodilution with Dextran 60 on the Impairment of Pancreatic Microcirculation in Acute Biliary Pancreatitis

Dextran of different molecular weight (Dx 40, Dx 60/70) has often been evaluated as adjunct treatment of experimental acute pancreatitis. A beneficial effect has been documented by a decrease in its lethality. However, the mechanism of action is poorly understood. A specific effect on the pancreatic microcirculation generally has not been documented and differentiation from unspecific improvement of pancreatic blood flow due to volume expansion has been difficult. This investigation was designed to quantify the effect of dextran on the impairment of pancreatic microcirculation during acute biliary pancreatitis by means of intravital microscopy. Dextran 60 (Dx 60, molecular weight 60,000) was chosen in light of the increase in vascular permeability in the early stage of pancreatitis as demonstrated previously in the same model. Isovolemic hemodilution, i.e., exchange of whole blood for Dx 60 was used as a mode of administration to achieve instantaneous onset of therapy without changes in intravascular volume. In the control group a progressive reduction of pancreatic capillary perfusion commenced 30 minutes after induction of acute pancreatitis, resulting in cessation of nutritive tissue perfusion after 3 hours. In the animals subjected to hemodilution, stabilization of the pancreatic microcirculation was accomplished throughout the observation period of 6 hours. Because volume-related effects could be excluded by the protocol and by monitoring central venous pressure and hematocrit, a specific effect of hemodilution with DX 60 on the pancreatic microcirculation is indicated by our results.