Emboli become lodged in the brains of patients undergoing cardiopulmon
ary, bypass (CPB) and can cause death, stroke, or more subtle neurolog
ical and neuropsychological deficits. Using a specialized vascular sta
in (for alkaline phosphatase) in autopsy, tissues from the brains of p
atients who underwent CPB shortly before death, we found large numbers
of microemboli. All of these microemboli contain lipid some contain s
mall birefringent particles, and some may contain aluminum or silicon.
Within a few weeks after CPB, most of the microemboli had disappeared
front the brain tissues, but some persisted for at least 6 months. Af
ter several days, the endothelial cells of some of the vessels contain
ing microemboli showed subtle damage in the form of Loss of alkaline p
hosphatase reactivity, and some vessels appeared to be degenerating. S
ometimes the surrounding neuropil also showed degeneration. Since shin
and muscle biopsies can be readily obtained before, during, and after
CPB, toe investigated their suitability as surrogate tissues for brai
n; however, they were unsuitable because they had so few microemboli.
By injecting microspheres into dogs at various times during CPB, we ha
ve investigated the timing of the production of microemboli. We are al
so exploring the use of rat brains to trap microemboli from the inject
ed blood of patients undergoing CPB.