1 Departments of Physiology and Anatomy, Harvard Medical School Boston, Massachusetts; Department of Medicine, University of Montreal Montreal, Canada
2 Departments of Physiology and Anatomy, Harvard Medical School Boston, Massachusetts; School of Physiology, University of New South Wales, Kensington, Sydney, Australia
3 Departments of Physiology and Anatomy, Harvard Medical School Boston, Massachusetts; Department of Anatomy, Trinity College, Dublin University, Dublin, Ireland
4 Departments of Physiology and Anatomy, Harvard Medical School Boston, Massachusetts
Renal medullary blood flow was well maintained for several hours after blood loss which produced hypotension. Renal cortical blood flow was altered by trauma and mild hemorrhage even though blood pressure remained normal; rate of blood flow through the subcapsular, peritubular capillaries decreased to the level of that in the outer medulla. With further hemorrhage and the development of hypotension, rate of blood flow in large cortical areas was reduced to that of the outer medulla. With prolonged hypotension, the rate of blood flow in most of the cortex approached outer medullary rate and a single exponential could describe the flow in this combined area. Small regions of even slower flow rate began to appear in the outer cortex; patches of tissue appeared to be completely ischemic. The progression of cortical ischemia noted in these experiments may provide additional evidence for the pathogenesis of the patchy tubular necrosis noted in hemorrhagic shock.
Accepted on January 10, 1966
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