These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Islet vasculature in atrophic pancreas: evidence for coexisting parallel and serial (insuloacinar) angioarchitecture.
    Author: Weaver FC, Sorenson RL.
    Journal: Pancreas; 1989; 4(1):10-22. PubMed ID: 2654925.
    Abstract:
    Islet vasculature was studied in rats rendered dietarily copper-deficient, a regimen that effects progressive acinar atrophy while leaving islets and ducts intact. Scanning electron microscopy of corrosion casts produced from Mercox injected rats was used to analyze islet angioarchitecture in the atrophied gland. The results indicate that with the onset of acinar atrophy, the vasculature of islets remained intact despite loss of insuloacinar interconnectivity. With atrophy of the dense acinar vascular matrix, three populations of islets could be distinguished according to their size and vascular structures: (a) All small islets (40-150 microns in diameter) were found to have exclusively serial vasculature since no postcapillary collecting venules were found directly continuous with parallel efferent veins. (b) A second population of intermediate size islets (160-250 microns) was found to have serial vessels in addition to postcapillary collecting venules that were directly continuous with larger interlobular veins indicative of a parallel mode of microcirculation. (c) All larger islets (260-700 microns) were also found to have both serial as well as parallel microcirculatory patterns based upon the coexistence of both types of postcapillary venules within the same islet. In all cases, postcapillary venules, which normally link islet capillaries to peri-insular acinar plexuses, were continuous with veins that extended through lipomatous lobules devoid of acini to link with branches of interlobular veins. It is proposed that the functional integrity of islet blood flow remains in the atrophied pancreas because of preservation of both serial and parallel microcirculation that facilitate normal glucose-stimulated insulin secretion in the atrophied pancreas, as demonstrated in an earlier study. Furthermore, it is suggested that analysis of the atrophied state of the gland provides a valid comparative model with which to study islet angioarchitecture and microcirculation in the normal gland.
    [Abstract] [Full Text] [Related] [New Search]