Superoxide dismutase reduces islet microvascular injury induced by
streptozotocin in the rat.
Enghofer, Michael, Klaus H. Usadel, Otfrid Beck, and Klaus Kusterer.
Department of Medicine I, Johann Wolfgang Goethe University,
Frankfurt am Main, Germany
APStracts 4:0082E, 1997.
Intravenous administration of streptozotocin leads to permanent
diabetes mellitus in rats. We investigated the possible role of islet
microcirculatory changes and free radical formation in this animal
model. In-vivo fluorescence microscopy was performed for 4 hours
after administration of streptozotocin (STZ). Vascular permeability,
capillary blood flow, and endothelial leukocyte adhesion were
measured in endocrine and exocrine pancreatic tissue. The earliest
microcirculatory event was an increase in vascular permeability in
pancreatic islets with a peak 1 h after STZ administration. The
difference between islet and exocrine tissue light intensity was
+15.8 +/- 5.6 % at t = 60 min. Islet blood flow velocity
significantly decreased after 3 h, whereas blood flow in the exocrine
pancreas was not affected. Complete stasis of islet blood flow was
observed only in rats receiving STZ. Neither increased leukocyte
adhesion to islet vascular endothelium, nor ischemia-reperfusion
phenomena were observed. Prophylactic administration of the radical
scavenger superoxide dismutase prevented STZ-induced damage to the
islet microcirculation in the initial phase of this model. We
conclude that streptozotocin leads to severe microcirculatory
disturbances within pancreatic islets in rats. Apparently, these
changes are mediated at least in part by free oxygen radicals.
Received 9 December 1996; accepted in final form 3 April 1997.
APS Manuscript Number E605-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 15 April 1997