Cholinergic Control of Blood Flow in the Cerebral Cortex of the Rat

Scremin, Oscar U.; Rovere, A. A.; Raynald, Augusto C.; Giardini, Adolfo

doi:10.1161/01.str.4.2.232

Cited by 122 publications

(38 citation statements)

References 24 publications

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“…15 It has been shown by direct application to pial vessels as well as by systemic administration of pharmacological agents that inhibit ChE or block ACh receptor sites that the diameter of pial vessels and cortical blood flow were altered as a result of these maneuvers. 6 ' 7 Recent data obtained in this laboratory showed correlation between the development of acute cerebral infarction in the baboon after middle cerebral artery (MCA) occlusion and increased levels of acetylcholinesterase (AChE) and ChE in the infarcted brain tissue which is generally assumed to be associated with increased ACh levels. 8 The intrinsic ability of cerebral vessels to maintain CBF constant despite changes in cerebral perfusion pressure (CPP) has been defined as "autoregulation."…”

Section: Additional Abstract Cerebral Infarctionmentioning

confidence: 99%

Disordered Cholinergic Neurotransmission and Dysautoregulation After Acute Cerebral Infarction

Ott

Abraham

Meyer

et al. 1975

Stroke

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Abstract:Disordered Cholinergic Neurotransmission and Dysautoregulation After Acute Cerebral Infarction• The possible role of displaced neurotransmitter acetylcholine (ACh) in dysautoregulation was examined after experimental regional cerebral infarction was produced by occluding the middle cerebral artery (MCA) in baboons. Regional cerebral blood flow (rCBF) was measured after intracarotid injection of 133 Xenon using the gamma camera. Autoregulation was tested with metaraminol or angiotensin infusion and the autoregulation index (A.I.) was calculated. Acetylcholinesterase (AChE) was measured in brain tissue of noninfarcted and infarcted hemispheres. Cerebral arteriovenous (A-V) differences for cholinesterase (ChE) were also measured. Regional dysautoregulation was found in infarcted gray matter and correlated with increased AChE levels in the same zones of cortex and basal ganglia. The time course of onset of dysautoregulation correlated with increased ChE uptake by the brain. Intravenous infusion of the cholinergic neurotransmitter blocker, scopolamine, restored autoregulation to the ischemic zones. Autoregulation appears to be a myogenic reflex, influenced by neurogenic and metabolic mechanisms. Additional Key Words cerebral infarctionacetylcholine cholinesterase autoregulation regional cerebral blood flow D Apart from the well-known cholinergic neuronal neurotransmitter systems occurring at synapses throughout the central and peripheral nervous system, whereby acetylcholine (ACh) is released from presynaptic vesicles and is inactivated by cholinesterase (ChE), it has been recently confirmed by histochemical methods that there is a rich cholinergic innervation of cerebral vessels accompanying their adrenergic nerves. Nevertheless, there is meager information concerning the functional significance of the cholinergic nerves in controlling cerebral blood flow (CBF).

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Section: Additional Abstract Cerebral Infarctionmentioning

confidence: 99%

Disordered Cholinergic Neurotransmission and Dysautoregulation After Acute Cerebral Infarction

Ott

Abraham

Meyer

et al. 1975

Stroke

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“…Anti-cholinergic drugs decrease the survival time in hypox ic models (9), but the anti-choline esterase drug physostig mine increases cerebral blood flow and has an anti-anoxic effect. Cholinergic mechanisms control the cortical blood flow accompanied by cortical electroencephalogram desyn chronization (18,33,34). These findings support the no tion that the protective effects against cerebral anoxia are closely related to actions in the cholinergic system of the brain.…”

Section: Discussionmentioning

confidence: 99%

Effects of BMY-21502 on Anoxia in Mice

Amano

Goto

Takahashi

et al. 1993

Japanese Journal of Pharmacology

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piperidinyl]methyl]-2-pyrrolidinone) against cerebral anoxia were investigated using various models in mice, in comparison with those of other cerebroactive drugs. Oral administration of BMY-21502 (10-100 mg/kg) significantly prolonged the survival time in KCN (2.4 mg/kg, i.v.)-induced anoxia. Oxiracetam and idebenone exerted similar but weak protection at doses above 100 mg/kg, p.o. and only at a dose of 100 mg/kg, p.o., respectively. Significant protection by BMY-21502 against moderate hypobaric hypoxia was observed at doses of 30 and 100 mg/kg, p.o. Idebenone (100 and 300 mg/kg, p.o.) significantly prolonged the survival time of mice in this model, but oxiracetam (30-300 mg/kg, p.o.) did not. Oral administration of all of these drugs (BMY-21502, 3 300 mg/kg; Oxiracetam, 100-1000 mg/kg; Idebenone, 100-1000 mg/kg) failed to increase the number of gasps and the duration of gasping in the decapitated head of mice as a complete ischemic model. The anti-anoxic effect of BMY-21502 in the KCN-anoxia model was blocked by pretreatment with scopolamine. These findings suggest that BMY-21502 has an anti-anoxic action superior to those of the other cerebroactive drugs used, and activation of the CNS cholinergic system is in volved as one of the causative mechanisms for the anti-anoxic effect of BMY-21502.

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“…Moreover, neuronal activity in general and -neuronal activity of interneurons in particular -appear to influence vascular resistance in a direct, neurotransmitter-mediated way (Mathiesen et al, 1998). Beside glutamate and GABA, dopamine and acetylcholine have been identified as vasoactive neurotransmitters as well (Krimer et al, 1998;Scremin et al, 1973). Another important aspect of neurovascular coordination is based on intramural signalling, which denotes a release of vasoactive substances from upstream endothelial cells in response to increased generalized stress levels due to downstream increases of local CBF (Iadecola, 2004).…”

Section: Physiology and Pathophysiology Of Neurovascular Couplingmentioning

confidence: 99%