The etiology and pathogenesis of acute necrotizing hemorrhagic pancreatitis remain controversial. Recent work has suggested that an early fall in pancreatic blood flow, causing ischemia, may be the initiating factor. Using an established rat model of hemorrhagic pancreatitis and the fractional indicator distribution technique with86RbCl, pancreatic blood flow and tissue perfusion have been measured at various times in the condition. Six groups of ten rats were studied; control sham operation and pancreatitis groups were sacrificed at 1,6, and 24 hr. Pancreatic blood flow ( of cardiac output) and perfusion (blood flow/g tissue) were measured. Blood flow was increased by a maximum of 53 at 1 hr (P<0.001) and remained elevated for 24 hr, and perfusion was increased by a maximum of 70 (P<0.001) at 1 hr and remained elevated at 6 hr. Pancreatic perfusion declines after 6 hr due to increasing gland edema. The results demonstrate a significant increase in pancreatic blood flow and perfusion in experimentally induced acute pancreatitis, suggesting a primary inflammatory response, and refute the ischemic etiological theory.
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