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  • Title: Nutritive perfusion of pancreatic endocrine tissue during hemorrhagic hypotension: how differ islets in situ from islet isografts?
    Author: Vollmar B, Franke K, Menger MD.
    Journal: Shock; 2008 Oct; 30(4):428-33. PubMed ID: 18799999.
    Abstract:
    Although the exocrine gland frequently has I/R-associated complications such as posttransplant pancreatitis, hypoxia-induced dysfunction of pancreatic endocrine tissue is rarely observed. However, sympathetic hypersensitivity is accused of impaired endocrine function observed in human pancreatic grafts. These tissue-confined differences in susceptibility might be attributed to a distinct islet-specific regulatory control of blood flow (BF). To investigate this hypothesis, intravital microscopy was used for visualization of islets in situ and revascularized islet isografts in Syrian golden hamsters. Blood withdrawal was performed to induce sympathetic stimulation and to evoke an appropriate stress response of the tissue under investigation. Hypotension resulted in a perfusion pressure-dependent reduction of perfusion in both islets in situ and islet isografts. This was associated with comparable microhemodynamics of the tissues in direct vicinity, that is, pancreatic exocrine and host muscle tissue. There was a progressive decrease in functional capillary density of islets in situ and islet isografts that significantly correlated with the stepwise reduction of arterial blood pressure and did not differ in the hypotension-induced perfusion pattern in the neighboring exocrine and host skeletal muscle tissue. Concomitantly, capillary BF in islets in situ and islet isografts and in pancreatic exocrine and host muscle tissue was found to be reduced due to hypotension-associated decreases in capillary diameters and BF velocity. Microvascular perfusion of pancreatic islets and islet isografts is not preserved but strongly parallels perfusion pattern of the neighboring tissue under hemorrhagic stress. This disproves the existence of an individual islet-specific regulatory control of blood flow.
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