Biomedical subjects

D R Theodore

Publications and source records attributed to D R Theodore.

12 recordsLinked to original sources

PubMed1992

Microvascular morphometry in primate diaschisis.

Focal cerebral ischemia was produced in monkeys by transorbital occlusion of the right middle cerebral artery. Following this, in one group of animals the total microvasculature, including both perfused and nonperfused vessels of the opposite caudate nucleus and insula, was examined by alkaline phosphatase staining of the endothelium. In another group, the patency of the microvascular bed was visualized by india ink perfusion. The number, diameter, and length of visualized vessels were measured by means of a Wild ASBA image analysis system. The perfused patient microvascular bed was significantly reduced in both insula and caudate nucleus in the supposedly normal left side, although the total microvascular volume showed an increase at 4 and 12 hr in the insula and at 48 hr in the caudate nucleus. Reduced perfusion in the hemisphere opposite to the occluded middle cerebral artery provides an anatomical substrate for the phenomenon of "diaschisis."

Animals↗

PubMed1990

The paradox of increased microvascular visualization with decreased perfusion in cerebral focal ischaemia in a primate model.

Microvasculature of the right caudate nucleus and insular cortex of monkeys with their right middle cerebral artery occluded was morphometrically measured with an image analysis system at 1/2, 4, 12, 24, and 48 hr and 2 weeks. A biphasic change in the microvasculature was observed. In the first phase up to 12 hr an increase in the number and length of the total microvasculature, visualized by alkaline phosphatase staining, along with a reduction in the number and length of the perfused part of the microvasculature, visualized by India ink perfusion, was observed. In the second phase after 48 hr, the number and length of the total microvascular bed as well as the perfused functional bed were significantly reduced.

Animals↗

PubMed1989

Changes in noradrenaline and histamine in monkey spinal cords traumatised by weight drop, compression and subsequent decompression.

Levels of noradrenaline (NA) and histamine (H) in the spinal cord of monkeys at 8, 24 and 48 hr following 200 g/cm contusion injury, 50 g of compression injury at 8 hr and decompression for 16 and 40 hr following 8 hr of compression were studied in the traumatised and in an adjacent non-traumatised segment. The NA level doubled in the traumatised and non-traumatised segments at 8 hr contusion injury followed by a slow decline to control values at 24 and 48 hr of contusion injury. There was no change in NA content of the spinal cord segments at 8 hr of compression injury. Decompression for 16 hr following 8 hr of compression increased NA content of the traumatised segment. H levels decreased in the traumatised and non-traumatised segments at 24 and 48 hr of contusion injury. Compression for 8 hr elevated H in the traumatised and non-traumatised segments. On decompression H level was further increased in the traumatised segment.

Animals↗

PubMed1988

Free fatty acids, lipid peroxidation, and lysosomal enzymes in experimental focal cerebral ischemia in primates: loss of lysosomal latency by lipid peroxidation.

Experimental focal cerebral ischemia was produced in monkeys (Macaca radiata) by occlusion of the right middle cerebral artery (MCA). The release of the lysosomal glycosidases, beta-D-hexosaminidase, alpha-L-fucosidase and alpha-D-mannosidase into the soluble fraction in the right basal ganglia of the experimental animals was measured at different periods from 30 min to 12 hr after occlusion and compared with the corresponding sham operated control animals. There was a significant increase in the released lysosomal enzymes in the MCA occluded animals at all periods and particularly at 4 hr after occlusion. The CSF from the experimental animals also showed elevated levels of hexosaminidase and fucosidase. The free fatty acids (FFA) measured in the basal ganglia at 30 min and 2 hr after occlusion showed a 100 fold increase in the experimental animals. The predominant fatty acid released was linoleic acid (18:2) followed by arachidonic acid (20:4). Lipid peroxidation in the basal ganglia measured by the thiobarbituric acid (TBA) reaction in the presence or absence of ascorbic acid also showed a significant increase in the experimental animals at all periods with a maximum at 30 min to 2 hr after occlusion. In order to assess whether lipid peroxidation causes damage to the lysosomes and release of the enzymes, a lysosome enriched P2 fraction from the normal monkey basal ganglia was prepared and the effect of peroxidation studied. Maximum peroxidation in the P2 fraction was observed in the presence of arachidonic acid, ascorbic acid and Fe2+.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Temporal profile of tissue levels of dopamine and its metabolites, HVA and DOPAC following focal cerebral ischaemia in anaesthetized primates.

Occlusion of the middle cerebral artery produced ischaemia and consequent changes in basal ganglia in the primate model of stroke within 0.5 h. Dopamine content was decreased in the right basal ganglia from 0.5 h up to 12 h after occlusion. Homovanillic acid content of the right basal ganglia increased initially at 0.5 h but, was decreased at 12 h. The DOPAC content was increased at 2 h after occlusion in the right basal ganglia, but was decreased significantly at 12 h. In the substantia nigra, there was a significant reduction in the DA content in the right side at 12 h. Minimal changes were observed in the DOPAC and HVA content in the right substantia nigra at 2 h and 4 h, respectively. At other time periods there was no significant change in the content of HVA and DOPAC in substantia nigra.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1985

Spinal cord edema, 5-hydroxytryptamine, lipid peroxidation, and lysosomal enzyme release after acute contusion and compression injury in primates.

Physical and biochemical changes in the spinal cord of monkeys at 1/2, 2, and 4 hours following 200 g cm contusion injury and 50 g of compression injury and 2 hours of decompression following 4 hours of compression were studied. The pathophysiologic changes were milder in compression compared to contusion injury. Following contusion injury, at 1/2 and 2 hours there was significant increase in % water content, lipid peroxidation, and alpha-L-fucosidase. alpha-D-Mannosidase was significantly increased at all time periods, and beta-D-hexosaminidase was increased at 1/2 and 4 hours. At 4 hours following injury, serotonin (5 HT) and 5-hydroxyindole-3-acetic acid (5-HIAA) showed a significant increase. From 10 minutes to 2 hours there was increased platelet aggregation. In compression injury, a significant increase in water content and 5 HT was observed only at 1/2 hour. Lipid peroxidation had increased at all time periods, whereas B-D-hexosaminidase, beta-D-galactosidase, and 5-HIAA were increased at 2 hours. alpha-D-Mannosidase had increased at 1/2 and 2 hours, and alpha-L-fucosidase had increased at 4 hours. After 2 hours decompression following 4 hours compression, water content, beta-D-galactosidase, and alpha-D-Mannosidase were significantly increased. An attempt was made to correlate the findings and to understand the sequential pathophysiologic changes in the first 4 hours following spinal cord trauma, providing a baseline for evaluation of the efficacy of any therapeutic maneuvers.

Acute Disease↗

PubMed1985

Changes in norepinephrine and histamine in monkey spinal cords traumatized by weight drop and compression.

Changes in norepinephrine and histamine levels in the spinal cord of monkeys at 1/2, 2, and 4 hours after 200 g cm of contusion injury, 50 g of compression injury, and 2 hours of decompression following 4 hours of compression were studied in the traumatized and an adjacent nontraumatized segment. Norepinephrine levels were elevated in the traumatized segment at 1/2, 2, and 4 hours after contusion injury and in the adjacent nontraumatized segment at 1/2 hour. Compression of 1/2 and 2 hours caused elevation of norepinephrine in both the traumatized and nontraumatized segments. On decompressing the values of norepinephrine reverted to near normal levels. Histamine content increased in the traumatized segment at 2 and 4 hours after contusion injury and in the adjacent nontraumatized segment at 2 hours. Compression injury did not change histamine levels, but decompression caused an increase. The possible influence of simultaneous changes in norepinephrine and histamine levels on the vessels following injury is discussed.

Animals↗

PubMed1985