| 11. |
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| 12. |
- Grøgaard, B, et al.
(författare)
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Delayed hypoperfusion after incomplete forebrain ischemia in the rat. The role of polymorphonuclear leukocytes.
- 1989
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Ingår i: Journal of Cerebral Blood Flow and Metabolism. - : SAGE Publications. - 0271-678X .- 1559-7016. ; 9:4, s. 500-5
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Tidskriftsartikel (refereegranskat)abstract
- The role of polymorphonuclear leukocytes (PMNLs) in postischemic delayed hypoperfusion in the rat brain was investigated. Cerebral ischemia was accomplished by reversible bilateral occlusion of the common carotid arteries for 15 min combined with bleeding to an MABP of 50 mm Hg. The animals of one group were depleted of their circulating. PMNLs by intraperitoneal injections of an antineutrophil serum (ANS) prior to the experiment. All animals included in this group had fewer than 0.2 x 10(9) circulating PMNLs/L at the start of the experiments. In another group ANS was injected intravenously for 5 min starting 2 min after the ischemic insult. After 4 min of recirculation, the number of circulating PMNLs in this group was below 10% of the normal. Control animals were injected with the same amount of normal sheep serum or were not treated at all. Sixty minutes after termination of ischemia, the local blood flow in previously ischemic cerebral structures was 40-50% of the normal as measured with the [14C]iodoantipyrine technique. In animals treated with ANS prior to the ischemic insult, the postischemic blood flow in the frontal, sensorimotor, and parietal cortex as well as caudoputamen and thalamus was significantly higher than that in non-ANS-treated animals. Treatment with ANS immediately after the ischemic period caused no improvement of the local CBF. It is concluded that PMNLs are involved in the cerebral postischemic flow derangements seen in this model. Their effects seem to be exerted during ischemia or immediately upon reinstitution of blood flow.
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| 13. |
- Grøgaard, B, et al.
(författare)
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Forebrain ischemia in the rat. Relation between duration of ischemia, use of adjunctive ganglionic blockade and long-term recovery.
- 1986
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Ingår i: Stroke. - 0039-2499 .- 1524-4628. ; 17:5, s. 1010-5
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Tidskriftsartikel (refereegranskat)abstract
- The relation between duration of ischemia, use of adjunctive ganglionic blockade and long-term recovery was studied in a rat model giving reversible subtotal forebrain ischemia. Ischemia was induced by bilateral carotid artery clamping and controlled hemorrhage to a mean arterial pressure of 50 mm Hg in animals artificially ventilated under 70% N2O. After variable lengths of time, the clamps were removed and the drawn blood was reinfused. In some animals, the ganglion blocker Arfonad was given (group A+) on induction of ischemia to facilitate hypotension. There was a strict dose-response relationship between duration of ischemia and mortality. Mortality was higher among animals not given Arfonad (group A-; 37% after 10 min of ischemia and 100% after 13 min) than in group A+ (about 20% after 12-13 min of ischemia, 50% after 15 min and 80% after 19 min). In group A+ more than half of the animals died later than 24 h after ischemia. All of them were hyperexcitable and 12% died during witnessed epileptic fits. Group A- animals regularly died within the first 24 h, with no indication of central nervous system involvement. Less blood had to be drawn to attain hypotension (mean arterial pressure 50 mm Hg) in group A+ (1.5 +/- 0.3 ml/100 g b.w.) than in group A- (2.5 +/- 0.2 ml/100 g b.w.). Group A+ also had less "washout" acidosis 5 min after reinfusion of the shed blood than group A- (15 min of ischemia: pH 7.24 +/- 0.07 v 6.96 +/- 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)
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| 14. |
- Grøgaard, B, et al.
(författare)
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Inability of flunarizine, lidoflazine or magnesium to counteract delayed hypoperfusion after forebrain ischaemia in the rat.
- 1988
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Ingår i: Acta Neurochirurgica. - 0001-6268 .- 0942-0940. ; 95:3-4, s. 136-42
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Tidskriftsartikel (refereegranskat)abstract
- Local cerebral blood flow (lCBF) was measured autoradiographically 60 min after 15 min of forebrain ischaemia in rats treated with flunarizine (0.1 mg/kg b.w.), lidoflazine (1.0 mg/kg b.w.) or Mg2+ (600 mumol/kg b.w.) before or at the end of the ischaemic period. Incomplete forebrain ischaemia was produced by a combination of common carotid artery occlusion and bleeding to a mean arterial blood pressure of 50 mmHg. During ischaemia lCBFs in cortical areas were less than 1% of preischaemic values. Neither flunarizine, lidoflazine nor Mg2+ influenced lCBF during ischaemia. Sixty minutes after the start of recirculation lCBFs were decreased to between 40 and 60% of the values found in control animals. None of the instituted treatments improved postischaemic cerebral blood flow. The results do not lend support to the view that calcium plays an essential role in the pathogenesis of delayed postischaemic hypoperfusion in the brain in this model.
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| 15. |
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| 16. |
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| 17. |
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| 18. |
- Schürer, L, et al.
(författare)
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Effects of neutrophil depletion and superoxide dismutase on postischemic hypoperfusion of rat brain.
- 1990
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Ingår i: Advances in Neurology. - 0091-3952. ; 52, s. 57-62
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Tidskriftsartikel (refereegranskat)abstract
- In the present investigation, the involvement of PMNLs and oxygen free radicals was explored in rats with postischemic perfusion disturbances of the brain. Reversible forebrain ischemia was induced by bilateral clamping of both carotid arteries in combination with hemorrhagic hypotension. This procedure resulted in a reproducible DPH 1 hr after start of recirculation. Neutropenia was induced by sheep ANS. One group received ANS before and a second group immediately after termination of ischemia. Two additional groups received SOD before or immediately after ischemia. Regional postischemic CBF was determined by [14C]iodoantipyrine autoradiography. It was found that CBF significantly improved in cortical structures of animals treated with ANS before ischemia. Treatment with ANS at the end of ischemia had no effect on the postischemic CBF depression. Neither was injection of SOD effective to influence DPH, irrespective whether given before or after ischemia. It is concluded that PMNLs play a role in the development of DPH of the brain, whereas free radical mechanisms seem to be less relevant.
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| 19. |
- Schürer, L, et al.
(författare)
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Is postischaemic water accumulation related to delayed postischaemic hypoperfusion in rat brain?
- 1988
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Ingår i: Acta Neurochirurgica. - 0001-6268 .- 0942-0940. ; 94:3-4, s. 150-4
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Tidskriftsartikel (refereegranskat)abstract
- The effect of reversible cerebral ischaemia on brain oedema development was studied with a gravimetric method. Cerebral blood flow changes after ischaemia were correlated with alterations in brain specific gravity. Forebrain ischaemia (15 min) was induced in rats by reversible bilateral ligation of both carotid arteries plus induction of controlled hypotension to 50 mm Hg. The specific gravity of different brain structures was determined in a Percoll column up to 24 h after ischaemia. In addition, regional cerebral blood flow was measured by 14C-iodoantipyrine autoradiography. Cerebral ischaemia resulted in reduction of cerebral blood flow to less than 1% of normal in cortical structures and the caudatoputamen. One hour after the end of ischaemia blood flows were still reduced to 30-50% of the control level indicative of delayed postischaemic hypoperfusion. Specific gravity in cortex and hypothalamus reached a maximal decrease 10 min after the end of the ischaemia, and was still significantly reduced at 1 h, while it was normal again 6 hrs later. Regression analysis between regional cerebral blood flows and the corresponding specific gravities were made at various time points, but no significant correlations could be established. Other mechanisms, like vasoconstriction, rheologic or metabolic factors may be causative for the delayed postischaemic hypoperfusion.
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| 20. |
- Schürer, L, et al.
(författare)
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Is postischemic hypoperfusion related to brain edema?
- 1990
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Ingår i: Advances in Neurology. - 0091-3952. ; 52, s. 155-64
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Tidskriftsartikel (refereegranskat)abstract
- The effect of reversible cerebral ischemia on brain edema development was studied with a gravimetric method. CBF changes after ischemia were correlated with alterations in brain SG. Forebrain ischemia (15 min) was induced in rats by reversible bilateral ligation of both carotid arteries plus induction of controlled hypotension to 50 mm Hg. The SG of different brain structures was determined in a Percoll column up to 24 hr after ischemia. In addition, rCBF was measured by [14C]iodoantipyrine autoradiography. Cerebral ischemia resulted in reduction of CBF to less than 1% of normal in cortical structures and the caudatoputamen. One hour after the end of ischemia, blood flows were still reduced to 30% to 50% of the control level indicative of DPH. SG in cortex and hypothalamus reached a maximal decrease 10 min after the end of the ischemia and was still significantly reduced at 1 hr, although it was normal again 6 hr later. Regression analysis revealed a significant correlation between CBF obtained during ischemia and the corresponding SG found at 10-min recirculation, which could also be established at 1-hr recirculation. Therefore, a causal relation between the development of the DPH and the formation of ischemia might be considered.
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