Die regionale Gehirndurchblutung des Pavians beim ischämischen Hirninfarkt unter Dexamethasonbehandlung*

Hartmann, A.; Menzel, J.; Buttinger, C.; Lange, D; Alberti, E.

doi:10.1055/s-2007-1002342

Cited by 14 publications

(3 citation statements)

References 19 publications

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“…After ischemia the regulatory influence of meta bolic factors on CBF is less conclusive, as experi mental and clinical studies have shown a postisch emic impairment of the cerebrovascular CO2-reac tivity and autoregulation, which was interpreted as a consequence of a postischemic vasoparalysis (Paulson et al, 1970;Hossmann et al, 1973;Ne moto et al, 1975;Hartmann et al, 1981). In accor dance with the postischemic disturbance of the ce rebrovascular CO2 reactivity, a previous study has demonstrated an abolition of the reactivity of pial arteries to H+ (Haller and Kuschinsky, 1981).…”

mentioning

confidence: 99%

Effect of γ-Hydroxybutyrate on the Reactivity of Pial Arteries before and after Ischemia

Haller

Kuschinsky

Reimnitz

1986

J Cereb Blood Flow Metab

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Summary: The effect of "{-hydroxybutyrate (GHB) on the reactivity of pial arteries to local metabolic factors was tested in chloralose-anesthetized cats before or after a pe riod of transient ischemia induced by air embolism. The vascular reactions were determined during the perivas cular microapplication of artificial CSFs with in creasing concentrations of adenosine (10-11_ 10-3 M), H + (pH 5.1-7. 6), or K + (0-JO mM). During nonischemic conditions the pial arterial reactivity to adenosine and H+, but not to K +, was significantly increased by GHB (250 mg/kg i. v. ) when compared with the control reac tivity. After cerebral ischemia the reactivity to adenosine was abolished with and without the administration of GHB prior to air embolism. The reactivity to K + was 'Y-Hydroxybutyrate (GHB) is a naturally occur ring cerebral metabolite (Roth and Giarman, 1970;Walters and Roth, 1977) with an unknown physio logical role. Although the conversion of GHB to 'Y aminobutyrate appears to be possible (Vayer et aI., 1985), the relevance of this step is a matter of dis pute. There is also evidence that GHB fulfills the criteria of a neurotransmitter or -modulator (Hasli and Hasli, 1983;Maitre and Mandel, 1984). The ex ogenous administration of GHB induces a depres sion of consciousness that is reflected by charac teristic changes in the EEG resembling a state of nonconvulsant epilepsy (Winters and Spooner, 1965;Snead et at., 1976) . During the action of GHB, the cerebral glucose utilization is markedly reduced in the awake rat (Kuschinsky et aI., 1985). Address correspondence and reprint requests to Prof. Dr. w.Kuschinsky at Physiologisches Institut der Universitat, Nu f3allee II, D-5300 Bonn I, F.R.G.Abbreviation used: GHB, 'Y-hydroxybutyrate. 658partly preserved but not increased by GHB when com pared with previous results without GHB. In contrast GHB improved the postischemic reactivity to perivas cular H+ that had been found to be abolished in previous experiments without GHB. The perivascular microappli cation of GHB showed no influence of GHB on the vas cular diameter. An important finding of the present study is the demonstration of an increase in cerebrovascular re activity, which may give scope for therapeutic improve ment of the regulation of CBF in pathophysiological conditions. Key Words: Cerebral ischemia-,,{-Hydroxy butyrate -Metabolic factors -Microapplication tech nique-Protection-Vasoreactivity.by pharmacological doses of GHB might be ex plained by an altered reactivity of the cerebral vessels to local metabolic factors. If such an effect also exists at physiological concentrations of GHB, a physiological role of GHB could be to modulate the cerebrovascular reactivity to metabolic stimuli.To test the possibilities of a physiological or phar macological action of GHB on the vascular reac tivity, the responsiveness of pial arteries to adeno sine, H +, and K + was determined during the action of GHB. These three substances play a major role in the local regulation of CBF under physiological conditions (Kusc...

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mentioning

confidence: 99%

Effect of γ-Hydroxybutyrate on the Reactivity of Pial Arteries before and after Ischemia

Haller

Kuschinsky

Reimnitz

1986

J Cereb Blood Flow Metab

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“…Blood flow studies have indicated that this is accompanied by a severe and acute drop of tissue perfusion (6,7). Tissue hypoemia might spread to neighboring areas in the following days, and in some instances even the contralateral hemisphere suffers from decrease of CBF (8).…”

Section: Course Of Cbf In Experimental Ischemiamentioning

confidence: 99%

“…The cause of this secondary CBF drop might be brain edema development, intracellular Ca accumulation, progressive tissue destruction due to metabolic derangement (enzymatic lysis) or rheologic abnormalities as a consequence of the primary ischemia (whole blood viscosity, for instance, depends on actual shear stress and thus on blood flow (9)). Our own studies in baboons have revealed that, at least in the penumbra, the secondary CBF drop and disturbances to autoregulation and CO, reactivity might be partially prevented by antiedematous therapy with early high doses of dexamethasone (7). This seems to be due to reduction of periinfarct water accumulation (10).…”

Section: Course Of Cbf In Experimental Ischemiamentioning

confidence: 99%