Microcirculatory changes in sodium taurocholate-induced pancreatitis in rats

Abstract

Using an in vivo microscopy technique, we studied the microcirculatory changes in sodium taurocholate-induced pancreatitis in rats. With a computerized image analyzer system, blood flow, vascular permeability changes, and capillary densities were measured. Intraductal infusion of 0.4 ml saline had only minor effects on the microcirculation. Various concentrations and volumes of sodium taurocholate solutions were infused into the pancreatic duct. Sodium taurocholate (0.4 ml, 4%) led to increased vascular permeability preceding stasis within 232 +/- 47 s, followed by hemorrhagic necrosis in the head of the pancreas. In the corpus close to the tail of the pancreas capillary blood flow was maintained. In conclusion, this study shows that the microcirculation of the pancreas can be excellently investigated with in vivo microscopy. With this method, tremendous distribution disturbances of the microcirculation in the pancreas can be seen in the course of acute pancreatitis. Vascular permeability changes and stasis of the microcirculation represent the primary microcirculatory events in acute pancreatitis induced by sodium taurocholate in the areas where hemorrhagic necrosis occurs.

Ischemia/Reperfusion-Induced Pancreatitis

“…Breakdown of the microcirculation induced by ischemia/reperfusion plays a central role in the pathogenesis of the early stages of AP [11, 14, 26, 30, 36, 90, 91, 92]. Impairment of the microcirculation correlates with the severity of AP, as evidenced by the diminished numbers of perfused capillaries and hemoglobin desaturation, the extent of which depends on the duration of both ischemia and reperfusion [50, 88, 93].…”

Is the pancreas affected in patients with septic shock? — a prospective study

“…[9,10] In addition, microvascular perfusion failure is a characteristic hallmark of pancreatitis. [10][11][12] Since Panum [13] presented the first report, other researchers have reported that the pancreas is highly sensitive to ischemia. [14][15][16][17][18] In humans, acute pancreatitis may develop after embolic closure of the vessels supplying the pancreas, [19] after hypoperfusion of the pancreas during cardiac surgery [20,21] and surgery for thoraco-abdominal aneurysms, [22] after splanchnic hypoperfusion, [23] or after pancreatic transplantation.…”

Therapeutic Small-Volume Resuscitation Preserves Pancreatic Microcirculation in Acute Experimental Pancreatitis of Graded Severity in Rats

“…The extent of pancreatic and peripancreatic necrosis appears to be the main determinant of lethal septic complications [18,25] . Among other factors, microcirculatory impairment has been reported to play an important role in the initiation of the pathophysiologic cascade leading to acute pancreatitis [2,4,11,[26][27][28] . Furthermore, ischemia and hypoperfusion can convert an edematous pancreatitis into a hemorrhagic necrotizing pancreatitis [29,30] .…”

“…Acridine Orange (1%, 1.2 ml kg -1 BW; injection within 20-30 s; Sigma Chemicals, St. Louis, Mo., USA) was injected intravenously to label leukocytes (figs. 4,5). The experiments were recorded on an S-VHS videotape with an attached video camera (Sony 3CCD, Tokyo, Japan).…”