PubMed Health⌕ Search

Biomedical subjects

M S Pollanen

Publications and source records attributed to M S Pollanen.

40 records · Page 3Linked to original sources
PubMed1990

The mechanism of embolic watershed infarction: experimental studies.

The mechanism for the preferential distribution of emboli to cerebral arterial borderzone regions, known to cause some watershed infarcts was studied. We hypothesized that emboli of a specific size range are selectively directed to the arterial borderzones due to the tendency of emboli to bypass the small arterial branches which emerge proximal to major borderzones. To test this hypothesis we perfused the brains of cadavers with suspensions of 90-210 microns glass microspheres and chemically extracted the particles from various arterial territories and a watershed zone. Particles in the 150-210 microns size range were found to be preferentially distributed to the watershed zone whereas particles less than 150 microns in size were randomly dispersed in leptomeningeal arteries of all vascular regions. To assess the role of branch size on the concentration of emboli at bifurcations, we perfused artificial analogs of evenly and unevenly branching bifurcations with suspensions of 90-150 microns and 150-210 microns particles. Branching cylinders with symmetrical branches contained the same concentration of particles, independent of particle size. In contrast, when one branch was one-quarter the size of the other, the concentration of 150-210 microns particles in the asymmetric branch was approximately 65% of the main trunk. Particles 90-150 microns in size were evenly distributed despite variation in branch size. These results indicate that emboli, of a limited range of size, may be selectively propagated to the distal ramifications of subarachnoid arteries located in the watershed zone rather than diverging into small calibre branches which arise along the way.

Cerebral Infarction↗
PubMed1990

Fetal globoid cell leukodystrophy.

The early lesions of globoid cell leukodystrophy in a 110-g, 18-week-old fetus were characterized in relation to fetal myelination, and comparisons made to the animal models of this disease. Uninucleated and binucleated periodic acid-Schiff-positive cells were present in the spinal cord but not in ventral roots within regions at very early stages of myelination. These cells stained with the lectin Ricinus communis agglutinin, which preferentially binds to beta-D-galactosyl residues as found in stored metabolites of globoid cell leukodystrophy. Ultrastructural examination of the spinal cord revealed typical tubular spicular cytoplasmic inclusions in cells corresponding to the periodic acid-Schiff-positive cells. The degree and distribution of myelin tubules and myelination glia was similar to that in weight- and size-matched control fetuses. These results indicate that the first appearance of inclusion-bearing cells is closely associated with the onset of myelination in the central nervous system, apparently earlier in the stage of myelination than occurs in the central nervous system of the mouse model. Characteristic tubular inclusions are also present in renal epithelium in animal models but have not been seen in the human kidney. We have since identified noncharacteristic crystalline inclusions in the kidney of this human fetus.

Epithelium↗
PubMed1989

Directed embolization is an alternate cause of cerebral watershed infarction.

Selective embolization of thrombotic material to the borderzone territories between major cerebral arteries was found to be the cause of watershed cerebral infarction in three reported cases. The embolic source was cardiac in two cases and carotid artery in one. The findings in these cases support the hypothesis that small thromboemboli may not be randomly distributed in the cerebral arterial supply but may be preferentially distributed to the small terminal arterial branches in the borderzones between major arterial territories. Previous reports of this phenomenon laid emphasis on the sharp angle at which small penetrating arteries branched from parent arteries as the mechanism underlying this preferential distribution. We propose that the unequal size of the branches at the majority of bifurcations of subarachnoid arteries is a more important anatomic feature leading to this pattern of infarction.

Aged↗