Biomedical subjects

S R Ennis

Publications and source records attributed to S R Ennis.

6 recordsLinked to original sources

PubMed1990

Decrease in perfusion of cerebral capillaries during incomplete ischemia and reperfusion.

The effect of unilateral, incomplete cerebral ischemia on CBF, unidirectional flux of alpha-aminoisobutyric acid (AIB) and sodium, and number of perfused capillaries during ischemia and reperfusion was measured in the cortex of gerbils with symptomatic ischemia. Three hours of unilateral carotid occlusion reduced the CBF to the ipsilateral cortex by 81%, with a smaller 30% decrease in the contralateral cortex. Following 11 min of reperfusion, CBF in the ipsilateral cortex returned to the preischemic value, while the contralateral blood flow decreased to 50% of control. The transfer constants for AIB and sodium in the ipsilateral cortex were reduced by 67 and 53%, respectively, after 3 h of ischemia, with no change in the contralateral cortex. The transfer constant for AIB remained decreased by 48% during the first 20 min of reperfusion, while that for sodium returned to its control value. The number of perfused capillaries was reduced 54% by 3 h of ischemia and remained decreased by 20% after 11 min of reperfusion. These data indicate that 3 h of unilateral carotid occlusion reduces the number of perfused capillaries in the ipsilateral cortex during the ischemic period. Further, the early reperfusion phase is characterized by a mismatch between capillary perfusion and CBF. Finally, early in the postischemic phase, sodium transport undergoes a selective stimulation, probably as a result of stimulation of ion transport.

Aminoisobutyric Acids↗

PubMed1990

Permeability of the blood-ocular barrier to mannitol and PAH during experimental diabetes.

The simultaneous uptake of mannitol, a passive permeability marker, and the organic acid, p-aminohippuric acid, was measured in the anterior and posterior vitreous and retina. Uptake was determined in control, probenecid treated and streptozocin diabetic rats. The unidirectional influx, calculated as a 10 minute PS product for these compounds, was not increased by 2, 4, or 12 weeks of diabetes. A clearance value, calculated using an experimental time of 60 minutes was also examined in order to gauge efflux of these compounds from the eye. The 60 minute clearance value for mannitol in the retina increased approximately 75% in 2, 4, and 12 week diabetic rats. This was an unexpected result due to the lack of increase in the unidirectional flux of mannitol during these same periods of diabetes, and may represent a change in the passive efflux out of the retina. The 60 minute clearance value for mannitol was not significantly changed in either the anterior or posterior vitreous. Experimental diabetes increased the 60 minute clearance value for PAH for the retina by 40% to 70%. In contrast, diabetes did not increase influx of PAH into the anterior or posterior vitreous. Because the unidirectional influx of PAH into the retina was not increased during diabetes, a decrease in the active transport for organic acids out of the eye is a likely explanation for the increase in the 60 minute clearance value for PAH during diabetes.

Analysis of Variance↗

PubMed1990

Blood-to-brain sodium transport in ischemic brain edema.

Brain edema is a frequent complication of cerebral ischemia; however, its mechanism of formation is not well understood. Sodium is known to accumulate in brain during the early stages of partial ischemia. Therefore, the present studies were undertaken to determine the relation among BBB sodium transport, integrity of the BBB, and development of brain edema during the first 24 hr after the onset of cerebral ischemia. Partial cerebral ischemia was produced in gerbils by ligation of the left common carotid artery under ether anesthesia. After recovery from the anesthetic, animals were scored for the presence of symptoms, and those with scores greater than 10 of 25 (n = 87) were chosen for this study. Measurements of tissue water, sodium, and potassium contents, and brain uptake of 22Na and 3H-mannitol were made in each group at 1.5, 3, 6, 12, and 24 hr after carotid ligation. Accumulation of sodium and water in the ischemic compared with the nonischemic cerebral cortex was progressive. This edema formation was not of the vasogenic type because the permeability of the BBB to mannitol was unchanged. Blood-to-brain sodium transport was reduced by 30% to 40% at all time points in the ischemic cortex. Nevertheless, the remaining sodium transport activity appeared to play a role in the development of brain edema because Na accumulated in the tissue at a rate that was approximately the same as the rate of 22Na uptake from blood.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Blood-brain barrier sodium transport limits development of brain edema during partial ischemia in gerbils.

Sodium derived from the blood is known to accumulate in brain tissue during the early stages of incomplete ischemia. Our present studies were undertaken to determine the relation between blood-brain barrier sodium transport and the development of ischemic brain edema. Incomplete cerebral ischemia was produced in gerbils by ligation of the left common carotid artery under ether anesthesia. Following recovery from the anesthetic, the gerbis were evaluated for the presence of neurologic symptoms and were divided into symptomatic (n = 77) and asymptomatic (n = 94) groups. Tissue water, sodium, and potassium contents, tissue plasma volume, and brain uptake of 22Na were measured in both groups 1.5, 3, 6, 12, and 24 hours after carotid ligation. There was a progressive accumulation of sodium and water in the ipsilateral cerebral cortex of the symptomatic group compared with either the corresponding contralateral cortex of the same gerbils or with the asymptomatic group. Net changes in brain sodium and potassium concentrations appeared to be the main determinants of fluid accumulation. Brain edema was not due to opening of the blood-brain barrier because the unidirectional transport of 22Na remained low and was even reduced by 35-55% in the ischemic cortex. Nevertheless, this sodium transport activity appeared to be rate-limiting in the development of brain edema during the first 3 hours of ischemia because the rate of sodium accumulation in the tissue was the same as the rate of 22Na transport from the blood to the brain. We conclude that blood-brain barrier sodium transport is an important factor in the formation of ischemic brain edema.

Animals↗

PubMed1986

Sucrose permeability of the blood-retinal and blood-brain barriers. Effects of diabetes, hypertonicity, and iodate.

The permeabilities of the blood-retinal (BRB) and blood-brain (BBB) barriers to sucrose were determined simultaneously using an intravenous injection technique in the rat. The method involved direct sampling of retinal tissue in order to avoid errors caused by sucrose penetration across other components of the blood-ocular barrier. The permeability X surface area (PS) product for the BRB was approximately four times greater than for the BBB. Intracarotid infusion of a hypertonic arabinose solution resulted in a dose-dependent increase in the permeability of both barrier systems. In contrast, 24 hr after treatment of animals with iodate, the PS product for the BRB but not the BBB was increased. The permeability of the blood-retinal barrier to sucrose was measured in normal and 2-, 6-, and 20-week streptozocin diabetic rats. The BRB was unaffected at 2 and 6 weeks of diabetes, and showed only a small increase in permeability at 20 weeks. Our results suggest that alterations in the blood-ocular barrier in early diabetes do not result from an increased passive permeability of the BRB. The method described should permit direct comparison of BRB and BBB permeabilities to a variety of compounds under various conditions.

Animals↗

PubMedDate not supplied

The effects of galactosamine-induced hepatic failure upon blood-brain barrier permeability.

The role of changes in blood-brain barrier permeability in the pathogenesis of hepatic encephalopathy remains uncertain. To test the hypothesis that brain microvessel permeability is nonselectively increased in hepatic encephalopathy we measured the blood-brain barrier permeability-surface area product in rats with acute liver failure induced by intraperitoneal injection of galactosamine. The permeability-surface area products to the diffusion-limited tracers, sucrose and methylaminoisobutyric acid, were determined as a measure of blood-brain barrier permeability. Animals were examined 24, 36 and 42 hr after injection, at times when they were stuporous, but not comatose. No significant elevations of the permeability-surface area products for either compound were detected in clinically affected experimental animals when compared to controls. Our results indicate there is no generalized increase in brain vascular permeability during hepatic insufficiency in precomatose animals.

Animals↗