Reduction in Brain Dopamine following Experimental Cerebral Ischaemia

Zervas, Nicholas T.; Hori, Hiroshi; Negora, M.; Wurtman, Richard J.; Larin, Frances; Lavyne, Michael H.

doi:10.1038/247283a0

Cited by 123 publications

(32 citation statements)

References 8 publications

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“…Reports from other laboratories using the same model 15 '" indicate a similar inconsistency of norepinephrine results. The significant, although temporary, reduction in norepinephrine levels in the nonoccluded hemispheres of asymptomatic animals is not fully understood, but since norepinephrine is synthesized from dopamine, it might reflect the correspondingly lower dopamine levels in the same hemispheres ( fig.…”

Section: Biochemical Changesmentioning

confidence: 68%

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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Section: Biochemical Changesmentioning

confidence: 68%

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

Welch¹,

Chabi²,

Buckingham³

et al. 1977

Stroke

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“…Since we observed that dopamine, NA and 5-HT decreased almost to a similar extent 28 days after microsphere embolism, the decrease in monoamine levels is severe and irreversible in this model. Several studies have shown a decrease in brain monoamine neurotransmitters in the early stage of cerebral ischaemia in animals (Zervas et al, 1974;Kogure et al, 1975;Welch et al, 1977). In contrast, it has been reported that there were no appreciable changes in monoamine levels during short periods of cerebral ischaemia, and that decreased in the brain monoamines occurred only during prolonged ischaemia (Siesj6, 1978).…”

Section: Discussionmentioning

confidence: 99%

Effects of delayed treatment with nafronyl oxalate on microsphere embolism‐induced changes in monoamine levels of rat brain regions

Takagi

Miyake

Ohiwa

et al. 1996

British J Pharmacology

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1 The present study was undertaken to examine the effects of delayed treatment with nafronyl oxalate (nafronyl), a cerebral vasodilator, on monoamine neurotransmitters of brain regions in the microsphereembolized rat. 2 Microsphere embolism was induced by injecting 900 microspheres with a diameter of 48 gm into the right internal carotid artery of rats. Microsphere-embolized rats were treated with nafronyl, 15 mg kg-, i.p., twice daily from the first to the 5th day. Levels of monoamines and their metabolites in the cerebral cortex, striatum, and hippocampus were measured on days 3 and 5 after the operation by a highperformance liquid chromatograph with electrochemical detection. In vivo tyrosine or tryptophan hydroxylation was estimated by measurement of the accumulation of 3,4-dihydroxyphenylalanine or 5-hydroxy-1-tryptophan after administration of 3-hydroxybenzylhydrazine dihydrochloride, an inhibitor of aromatic L-amino acid decarboxylase. 3 Microsphere embolism induced decreases in dopamine, noradrenaline and 5-hydroxytryptamine in three brain regions of the right hemisphere on days 3 and 5. In the left hemisphere, the monoamines were reduced, but to a lesser degree than in the right hemisphere. On days 3 and 5, the decrease in the monoamines of the right hemisphere was attenuated by nafronyl treatment except for noradrenaline on day 3. The decrease in the monoamines levels in the left hemisphere was almost completely prevented by nafronyl treatment. 4 On day 3 after microsphere embolism, in vivo tyrosine and tryptophan hydroxylation was lower than the pre-embolic value in all three brain regions. Treatment of the embolized rats with nafronyl significantly attenuated the decrease in in vivo tyrosine and tryptophan hydroxylation in the ipsilateral hemisphere, but not hippocampal tryptophan hydroxylation. 5The results suggested that treatment with nafronyl improves or attenuates changes in monoamine neurotransmitter metabolism of the brain regions impaired by microsphere embolism. The mechanisms underlying this effect may be attributed to preservation of the ability to synthesize monoamines when the brain is ischaemic or oligaemic. Keywords: Cerebral ischaemia; microsphere embolism; monoamine neurotransmitters; nafronyl oxalate Introduction Nafronyl oxalate, [2-(diethylamino)ethyltetrahydro-a-(1-naphthylmethyl)-2-furanpropionate ester oxalate](nafronyl), has been shown to increase cerebral blood flow in normal animals (Young et al., 1983;Hiramatsu et al., 1988) and in human subjects (Yamada, 1984;Ohtomo et al., 1986), and thus, has been used clinically to improve cerebral circulation in several European countries (Admani, 1978).Previous studies from our laboratory demonstrated that administration of microspheres into the internal carotid artery induces prolonged cerebral ischaemia and infarction in rats. In these studies, we showed that cerebral embolism with microspheres induced a marked decrease in cerebral blood flow , a pronounced disturbance in brain glucose metabolism (Takeo et al., 1991) and high-ener...

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“…It was suggested that cerebral ischemia could result in the release of vasoactive brain monoamines, which in turn could modify the pattern of vascular reactivity in the ischemic zone, perhaps extending the zone of cerebral infarction. 36 This idea was supported by experimental demonstration of significant (70%) lowering of brain dopamine in the ischemic hemisphere of gerbils. 36 Using H s -dopamine, Lavyne et al 37 then demonstrated that this reduction in dopamine was probably due to liberation of stored catecholamine, and that such release was associated with paradoxical turning behavior indicative of stimulation by endogenous dopamine release.…”

mentioning

confidence: 53%

“…36 This idea was supported by experimental demonstration of significant (70%) lowering of brain dopamine in the ischemic hemisphere of gerbils. 36 Using H s -dopamine, Lavyne et al 37 then demonstrated that this reduction in dopamine was probably due to liberation of stored catecholamine, and that such release was associated with paradoxical turning behavior indicative of stimulation by endogenous dopamine release. 38 More recently, Meyer et al 39 documented release of brain monoamine metabolites or their parent patent compounds in the CSF of patients with cerebral infarction, and Kogure et al <0 demonstrated possible lowering of brain norepinephrine during transient ischemia in rats.…”

mentioning

confidence: 53%

Neurogenic Regulation of Cerebral Blood Flow Following Ischemia

Zervas

Hori

Nagoro

et al. 1976

Stroke

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113The distinction between intracerebral hematoma and cerebral infarction can be made only by CT.Three observations in this study indicate complementary roles for RN brain imaging and CT in evaluation of patients with stroke. (1) While the percentages of abnormalities on both tests were comparable in recent infarction, the results in the same patients were not identical in 55% of the cases.(2) In patients with a recent and an old stroke a positive RN uptake would be the result of the recent insult, while on CT both types of lesions show similar abnormalities. (3) Hemodynamic changes on rapid sequence studies were demonstrated in 38% of 18 patients on whom the test was done.

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Reduction in Brain Dopamine following Experimental Cerebral Ischaemia

Cited by 123 publications

References 8 publications

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

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

Effects of delayed treatment with nafronyl oxalate on microsphere embolism‐induced changes in monoamine levels of rat brain regions

Neurogenic Regulation of Cerebral Blood Flow Following Ischemia

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