Cerebral Vasodilator Nerves and Their Pathway From the Medulla Oblongata

Choróbski, Jerzy; Penfield, Wilder

doi:10.1001/archneurpsyc.1932.02240060016002

Cited by 330 publications

(58 citation statements)

References 32 publications

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“…Cranial nerves have been implicated in cerebral vasodilator responses by a number of investigators who have reported either changes in pial vessel size (Chorobski and Penfield, 1932;Cobb and Fine singer, 1932) or in blood flow of various cerebral structures upon stimulation of selected nerves (James et aI., 1969;D'Alecy and Rose, 1977;Pinard et aI., 1979), or who have observed alteration of the basic regulatory responses of the cerebral vascula ture following ablation of such nerves (James et aI., 1969;Ponte and Purves, 1974). However, this evi dence is counterbalanced by reports showing lack of effects of stimulation (Meyer et aI., 1971;Busija and Heistad, 198 1;Linder, 198 1) or ablation (Bates et aI., 1976;Heistad and Marcus, 1976;Hoff et aI., 1977;Traystman and Fitzgerald, 198 1) of the same cranial nerves on cerebrovascular regulation.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, EEG was routinely monitored during stimulation experiments, and the stimulating conditions that lead to EEG arousal (often associ ated with cerebral vasodilatation) were avoided. An additional point to note is that in some pre vious studies an index of overall CBF was used (Meyer et aI., 1971;D' Alecy and Rose, 1977), whereas in others (Chorobski and Penfield, 1932;Cobb and Finesinger, 1932) cortical circulation was specifically assessed; in only two recent studies (Busija and Heistad, 1981;Linder, 1981) were both measured. The possible variance due to this differ ence in approach was controlled in our experiments by the use of measurement of both ICBF (hemi spheric CBF) and SSBF (cortical CBF), neither of which manifested change in response to nerve stim ulation.…”

Section: Discussionmentioning

confidence: 99%

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Cholinergic Cerebral Vasodilatation: Lack of Involvement of Cranial Parasympathetic Nerves

Scremin¹,

Sonnenschein²,

Rubinstein³

1983

J Cereb Blood Flow Metab

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Cerebral blood flow (CBF) was estimated by measurement of internal carotid blood flow (ICBF) and sagittal sinus blood flow (SSBF) in mechanically ventilated rabbits under 70% N2O/30% O2. Electrical stimulation of cranial nerves III, VII, IX, or X, with stimulus parameters adequate to excite other visceromotor outflows of these nerves, failed to elicit change in CBF. Combined bilateral section of nerves VII, VIII, IX, X, and XI had no effect on the reactivity of CBF to CO2, nor did the sectioning of these nerves affect the increases in CBF induced by physostigmine. Division of the sinus and aortic nerves and of the vagi in the neck failed to change CO2 reactivity, even though normocapnic CBF was reduced. Pentobarbital blocked the increase in CBF produced by physostigmine, but had no effect on that produced by pilocarpine. The results indicate that cranial parasympathetic nerves do not contain cerebral vasodilator fibers, and that they are not the source of acetylcholine which is presumably involved in CBF regulation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cholinergic Cerebral Vasodilatation: Lack of Involvement of Cranial Parasympathetic Nerves

Scremin¹,

Sonnenschein²,

Rubinstein³

1983

J Cereb Blood Flow Metab

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“…Although this is a diffuse system, its pathways parallel those of the INP and for this reason it is the likely source of a cholinergic influence on the INP. Another source of cholinergic nerves is the VlIth cranial nerve, which carries vasodilator fibres to the meningeal blood vessels (Chorobski & Penfield, 1932) and the nucleus of which lies close to the origin of the INP.…”

Section: Discussionmentioning

confidence: 99%

Substance P Increases Hypothalamic Blood Flow via an Indirect Adrenergic‐cholinergic Interaction

Klugman

Lembeck

Markowitz

et al. 1980

British J Pharmacology

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1 Hypothalamic blood flow (HBF) was measured in conscious rabbits by the 133xenon washout technique. 2 Substance P in a dose of 50 or 500 ng increases HBF while 5 ng is without effect. 3 Cholinoceptor blockade, with either atropine or mecamylamine abolishes the vasodilator effect of substance P. 4 Chemical sympathectomy of the hypothalamus with 6-hydroxydopamine, or adrenoceptor blockade with either propranolol or phenoxybenzamine abolishes the effect of substance P on HBF. 5 Destruction of the intracerebral noradrenergic pathway (INP), or blockade of its vasodilator action, with barbiturate or bicarbonate, likewise prevent the vasodilator action of substance P. 6 These results suggest that substance P may cause an increase in HBF via the release of endogenous acetylcholine, which in turn stimulates the INP.

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“…We depend heavily on two papers 25 ' 26 which suggest that the unique origin of the cerebral dilator pathway is the 7th cranial and greater superficial petrosal nerves, the fibers then being distributed with the sympathetic fibers to the major afferent and pial vessels. More recent work has provided further evidence for such a cholinergic pathway.…”

Section: Areas Of Uncertainty Concerning the Neuralmentioning

confidence: 99%