Critical cerebral blood flow for production of hemiparesis after unilateral carotid occlusion in the gerbil.

Nakai, Kenta; Welch, K. M. A.; Meyer, John Stirling

doi:10.1136/jnnp.40.6.595

Cited by 42 publications

(12 citation statements)

References 12 publications

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“…The observed reduction in CBF is similar to that reported in other studies of unilateral occlusion in gerbils 16 and is in the range that has been reported to cause significant brain edema. 17 There was also a small but significant decrease in flow to the contralateral hemisphere compared with the sham-operated gerbils.…”

Section: Resultssupporting

confidence: 90%

Transport of sodium from blood to brain in ischemic brain edema.

Betz

Schielke³

et al. 1987

Stroke

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Brain water and sodium increase during ischemia, suggesting that the blood-brain barrier permeability to sodium is increased. To test this hypothesis we measured the permeability-surface area products of "Na and [ 3 H]sucrose in gerbils following 3 hours of unilateral ischemia. In animals with neurologic symptoms, unilateral carotid occlusion reduced the cerebral blood flow in the ipsilateral cerebral hemisphere to 13 ± 4 ml/100 g/min (n = 6). The water content of the ischemic hemisphere increased from 79.0 ± 0.6 to 80.8 ± 0.2% (n = 7, p < 0.001) and tissue sodium content increased from 231 ± 17 to 359 ± 23 mEq/kg (p < 0.0001). However, there was a 40% reduction in the sodium permeability-surface area product of the ischemic hemisphere compared with the control side (1.65 ± 0.44 vs 2.79 ± 0.29 //.1/g/mln, a = 6,p< 0.001). The sucrose permeability-surface area product, a measure of blood-brain barrier integrity, was unchanged. Although ischemia was less severe in the diencephalon, the tissue water and sodium contents increased significantly on the ischemic side. In contrast to the cerebral hemisphere, however, the permeability-surface area products for both sodium and sucrose were unchanged in the ischemic diencephalon. These results suggest that the increase in tissue sodium seen in ischemic edema is not due to enhanced sodium uptake; we speculate that it results, in part, from a reduction in sodium and water clearance from the tissue. (Stroke 1987;18:150-157) B RAIN edema is an important clinical complication of cerebral ischemia; however, there are no effective clinical measures to limit its development. This may be due, in part, to an incomplete understanding of the factors that lead to the production of ischemic brain edema. Numerous studies have shown that, in the first several hours following a stroke, brain edema is principally of the cytotoxic type. The blood-brain barrier (BBB) remains intact, and fluid accumulates in response to an increase in tissue osmoles.' While a portion of the increase in tissue osmoles is due to breakdown of cellular constituents, 2 there is also a good correlation between ischemic edema and increases in brain sodium.3 Since the increased sodium content is seen only during incomplete and not during total ischemia, 4 the source of sodium must be the blood. Therefore, some investigators have proposed that during incomplete ischemia, the rate of sodium influx from blood to brain is increased as the result of either diffusion down a concentration gradient 4 or stimulation of specific sodium transport systems in the BBB. 5 To date there have been no direct measurements of the rate of sodium uptake into ischemic brain tissue.In this study, we measured BBB permeability to sodium and sucrose in a model of unilateral cerebral Received March 31, 1986; accepted August 18, 1986. ischemia to test the hypothesis that enhanced uptake of sodium by brain tissue contributes to the formation of ischemic brain edema. Preliminary reports of some of these results have been presented. 67Materials a...

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Section: Resultssupporting

confidence: 90%

Transport of sodium from blood to brain in ischemic brain edema.

Betz

Schielke³

et al. 1987

Stroke

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“…Hemodynamic studies in the same model showed no evidence of ischemia in nonoccluded hemispheres. 22 This finding might be associated with monoamine changes in the contralateral hemisphere or perhaps is secondary to the generalized seizures that occurred more frequently in longer surviving animals. However, the transient increase of brain water content in occluded hemispheres of asymptomatic animals might be explained on the basis of ischemia since hemodynamic shift occurred in this animal group.…”

Section: Cerebral Edemamentioning

confidence: 93%

“…However, the transient increase of brain water content in occluded hemispheres of asymptomatic animals might be explained on the basis of ischemia since hemodynamic shift occurred in this animal group. 22 A direct relationship between disordered monoamine metabolism and the development of cerebral edema cannot be establishedt>y these studies. However, the increased water content that occurred in the occluded hemispheres of both symptomatic and asymptomatic animals, as described above, coincided with reduced dopamine levels.…”

Section: Cerebral Edemamentioning

confidence: 99%

“…Recent experiments have confirmed regional cerebral blood flow (rCBF) decrease in the occluded hemisphere of asymptomatic animals, although the degree of reduction was less than that measured in symptomatic animals. 22 Dopamine metabolism, therefore, may be particularly sensitive to cerebral hemodynamic shifts, even in the absence of clinical signs of ischemia.…”

Section: Biochemical Changesmentioning

confidence: 99%

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Cathecholamine and 5-hydroxytryptamine levels in ischemic brain. Influence of p-chlorophenylalanine.

Welch¹,

Chabi²,

Buckingham³

et al. 1977

Stroke

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The incidence of ischemia induced by carotid occlusion decreased from 44% to 26% in PCPA-treated animals, which also suggests that depletion of 5-HT available for neuronal release prior to the induction of ischemia may reduce stroke incidence by limiting impairment of collateral vasocapacitance. PCPA pretreatment did not influence the development of edema in the occluded hemisphere of ischemic animals once ischemia was established.

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“…Gerbils without neurologic deficits (during ischemia) had minimal amounts of brain edema and brain H202 levels (after reperfusion); gerbils with mild neurologic deficits (during ischemia) had intermediate levels of brain edema and brain H202 (after reperfusion); and gerbils with severe neurologic deficits (during ischemia) had the greatest brain edema and brain H202 levels (after reperfusion). Gerbils were used for these studies because they commonly lack the posterior communicating artery (incomplete Circle of Willis), and therefore, occlusion of one carotid artery provides a model that is similar to human stroke (33)(34)(35)(36)(37)(38). Although the severity of neurologic deficit in each gerbil was not predictable, large groups of gerbils were always tested and the proportions of gerbils that developed either no, mild, or severe neurologic deficits during carotid occlusion (ischemia) were always similar in each test group.…”

Section: Discussionmentioning

confidence: 99%

Xanthine oxidase-derived hydrogen peroxide contributes to ischemia reperfusion-induced edema in gerbil brains.

Patt¹,

Harken²,

Burton³

et al. 1988

J. Clin. Invest.

205

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The contribution of toxic 02 metabolites to cerebral ischemia reperfusion injury has not been determined. We found that gerbils subjected to temporary unilateral carotid artery occlusion (ischemia) consistently developed neurologic deficits during ischemia with severities that correlated with increasing degrees of brain edema and brain H202 levels after reperfusion. In contrast, gerbils treated just before reperfusion (after ischemia) with dimethylthiourea (DMTU), but not urea, had decreased brain edema and brain H202 levels. In addition, gerbils fed a tungsten-rich diet for 4, 5, or 6 wk developed progressive decreases in brain xanthine oxidase (XO) and brain XO + xanthine dehydrogenase (XD) activities, brain edema, and brain H202 levels after temporary unilateral carotid artery occlusion and reperfusion. In contrast to tungsten-treated gerbils, allopurinol-treated gerbils did not have statistically significant decreases in brain XO or XO + XD levels, and reduced brain edema and brain H202 levels occurred only in gerbils developing mild but not severe neurologic deficits during ischemia. Finally, gerbils treated with DMTU or tungsten all survived, while > 60% of gerbils treated with urea, allopurinol, or saline died by 48 h after temporary unilateral carotid artery occlusion and reperfusion. Our findings indicate that H202 from XO contributes to reperfusion-induced edema in brains subjected to temporary ischemia.

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Critical cerebral blood flow for production of hemiparesis after unilateral carotid occlusion in the gerbil.

Cited by 42 publications

References 12 publications

Transport of sodium from blood to brain in ischemic brain edema.

Transport of sodium from blood to brain in ischemic brain edema.

Cathecholamine and 5-hydroxytryptamine levels in ischemic brain. Influence of p-chlorophenylalanine.

Xanthine oxidase-derived hydrogen peroxide contributes to ischemia reperfusion-induced edema in gerbil brains.

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