| 1. |
- 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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| 2. |
- 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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| 3. |
- Schürer, L, et al.
(författare)
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Leucocyte depletion does not affect post-ischaemic nerve cell damage in the rat.
- 1991
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Ingår i: Acta Neurochirurgica. - 0001-6268 .- 0942-0940. ; 111:1-2, s. 54-60
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Tidskriftsartikel (refereegranskat)abstract
- Leucocytes play an important role in inflammation and immunologic responses. They might be of special significance under pathophysiological conditions of the brain i.e. ischaemia or stroke. It has been shown that neutropenic animals undergoing reversible ischaemia show higher post-ischaemic blood flow, suggesting improved post-ischaemic perfusion. In this study it was investigated therefore, whether polymorphonuclear leucocytes contribute to the nerve cell loss in the hippocampus after a reversible period of ischaemia. Rats were made neutropenic with a specific anti-serum against rat polymorphonuclear leucocytes yielding leucocyte counts less than 10% of normal. The animals were then subjected to 15 min reversible forebrain ischaemia. Quantitative histology was performed after a survival period of 7 days. Nerve cell counts in the frontal cortex and in the CA1 and CA3 sectors of the hippocampus did not reveal any differences between neutropenic rats and animals with normal leucocyte counts. From the results it might be concluded that neutrophils do not significantly contribute to the selective post-ischaemic nerve cell damage in the rat.
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| 4. |
- Schürer, L, et al.
(författare)
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Superoxide dismutase does not prevent delayed hypoperfusion after incomplete cerebral ischaemia in the rat.
- 1990
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Ingår i: Acta Neurochirurgica. - 0001-6268 .- 0942-0940. ; 103:3-4, s. 163-70
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Tidskriftsartikel (refereegranskat)abstract
- Local cerebral blood flow (1CBF) was measured autoradiographically 60 minutes after 15 minutes of forebrain ischaemia in rats treated with superoxide dismutase (SOD) before (50 mg.kg-1 body weight) or at the end of the ischaemia period (4 mg.kg-1 body weight). 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 the 1CBF values in cortical areas were less than 3% of the preischaemic values and treatment with SOD prior to ischaemia did not influence 1CBF during ischaemia. Sixty minutes after termination of cerebral ischaemia the 1CBF values were decreased to between 40 and 60% of values found in control animals. Neither form of treatment improved the postischaemic cerebral blood flows. The results imply that postischaemic flow disturbances in the brain may not be due to extracellular superoxide production.
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