The Influence of Sympathetic Nervous Activity on Cerebral Blood Flow

Harper, A. M.; Deshmukh, Vinod D.; Rowan, J. O.; Jennett, W. B.

doi:10.1001/archneur.1972.00490130003001

Cited by 289 publications

(110 citation statements)

References 12 publications

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“…Thus, to the extent that the renal SNA may also reflect sympathetic activity to the well-innervated circle of Willis and large cerebral arteries, the late CVR increase may be a consequence of increased sympathetic discharge also to these vessels, whereas the initial CVR decrease would reflect the combined effects of 'myogenic' autoregulatory va sodilatation, accumulation of local vasodilatatory substances and reduced sympathetic vasoconstric tor activity. It has been shown by Harper et al (1972) and Fitch et al (1975) that increased SNA to the circle of Willis and large cerebral arteries can shift the lower autoregulatory limit to higher pres sure levels and thereby further decrease CBF, if MABP is already below the lower autoregulatory limit for CBF.…”

Section: Discussionmentioning

confidence: 99%

Relative Cerebral Ischemia in SHR Due to Hypotensive Hemorrhage: Cerebral Function, Blood Flow and Extracellular Levels of Lactate and Purine Catabolites

Skarphedinsson

Sandberg

Hagberg

et al. 1989

J Cereb Blood Flow Metab

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Summary: Cerebral blood flow (CBF, by laser Doppler flowmetry) and extracellular cortical concentrations (by microdialysis) of adenosine, inosine, xanthine, hypoxan thine, and lactate were measured together with somato sensory evoked potentials (SEP) in chloralose-anaes thetized spontaneously hypertensive rats (SHR) during relative cerebral ischemia induced by hypotensive hem orrhage. Reduction of mean arterial blood pressure (MABP) to 40-50 mm Hg, which decreased SEP to about 50% of pre bleeding control level, decreased CBF only to about 75% of control due to cerebrovascular "auto regUlation." A secondary, marked rise in cerebrovascular resistance (CVR) occurred after about 15 min in parallel with a striking increase in heart rate (after initial brady cardia). This late rise in heart rate is probably elicited by relative ischemia in medullary centers. The increase in CVR might indicate increased sympathetic nerve activity Several studies (Hagberg et aI., 1983, Wennberg et aI., 1983, Skarphedinsson et aI., 1986 have indi cated that tissue perfusion is more reduced in spon taneously hypertensive rats (SHR) than in nor motensive Wi star Kyoto rats (WKY) after blood loss, presumably because of the extensive struc tural and functional changes known to be concom itant with arterial hypertension (Folkow, 1982). Ce rebral vessels of SHR thus show a wall hypertrophy associated with some reduction of the inner radius,

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Section: Discussionmentioning

confidence: 99%

Relative Cerebral Ischemia in SHR Due to Hypotensive Hemorrhage: Cerebral Function, Blood Flow and Extracellular Levels of Lactate and Purine Catabolites

Skarphedinsson

Sandberg

Hagberg

et al. 1989

J Cereb Blood Flow Metab

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“…whereas the intraparenchymal vessels constricted initially but then began to dilate and exceeded the control level at the later stage de spite continued stimulation. Harper et al (1972) hypothesized that sympathetic constriction of the extraparenchymal vessels might be compensated for by secondary dilation of the intraparenchymal vessels elicited by a chemical control. Busija et al (19tl2) measured the blood flow velocity of the pial arteries and indicated that constriction of the pial arteries during sympathetic nerve stimulation was accompanied by an increase in the intravascular blood flow velocity.…”

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

“…This controversy seems to depend partly on the method ological limitations of measuring CBF and on the homeostatic mechanism of cerebral circulation. Harper et al (1972) hypothesized that under most circumstances, sympathetic constriction of the ex traparenchymal and pial vessels might be com pen-large pial arteries (173 ± 25 f.Lm, mean ± SEM) remained constricted throughout the stimulation. whereas the in traparenchymal vessels began to dilate after the initial constriction and exceeded the control level at 175 ± 25 s despite continued stimulation.…”

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Comparison between Pial and Intraparenchymal Vascular Responses to Cervical Sympathetic Stimulation in Cats. Part 1. Under Normal Resting Conditions

Gotoh

Fukuuchi

Amano

et al. 1986

J Cereb Blood Flow Metab

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Summary:To investigate the role of sympathetic regula tion in both resistance and capacitance vessels in cerebral circulation, the responses of pial and intraparenchymal vessels to sympathetic nerve stimulation were simulta neously examined in 14 cats by means of a newly devel oped video camera photoelectric system. The system consisted of a video camera system for measurement of pial vascular diameters and a photoelectric apparatus for estimating regional cerebral blood volume in the intrapa renchymal vessels. The ipsilateral superior cervical gan glion was electrically stimulated for 5 min. Initially. both the pial and intraparenchymal vessels constricted. TheIt is well documented that sympathetic nerves derived from the superior cervical ganglion con strict cerebral vessels down to the pial arterioles and venules (Auer et aI. , 1982) and exert a protec tive effect against breakthrough of autoregulation of CBF during acute hypertension (Bill and Linder, 1976). However, the role of the sympathetic nerves in the regulation of the resting CBF is still disputed Purves, 1978). This controversy seems to depend partly on the method ological limitations of measuring CBF and on the homeostatic mechanism of cerebral circulation. Harper et al. (1972) hypothesized that under most circumstances, sympathetic constriction of the ex traparenchymal and pial vessels might be com pen- 342large pial arteries (173 ± 25 f.Lm, mean ± SEM) remained constricted throughout the stimulation. whereas the in traparenchymal vessels began to dilate after the initial constriction and exceeded the control level at 175 ± 25 s despite continued stimulation. In conclusion. such sym pathetic nerve stimulation is considered to exert a con strictive effect on the intraparenchymal as well as the pial vessels at the early stage. The compensatory dilation of the intraparenchymal vessels was delayed 3 min after ini tiation of the stimulation. Key Words: Cerebral blood volume-Escape phenomenon-Pial vessel-Sympa thetic stimulation. sated for by a metabolic dilation of the intraparen chymal vessels and that CBF might be kept con stant. Recently, we developed a video camera photoelectric system that permits simultaneous and continuous measurement of pial vascular diameter and changes in regional cerebral blood volume (CBV). In the present study, to test Harper et al. 's hypothesis, we compared the responses of pial and intraparenchymal vessels to superior cervical gan glion stimulation by using this new method. MATERIALS AND METHODSExperiments were performed on 14 cats weighing from 2.3 to 3.4 kg, anesthetized by intraperitoneal injection of a-chloralose (50 mg/kg) and urethane (5 00 mg/kg). The bilateral femoral arteries and one femoral vein were can nulated for monitoring arterial blood pressure (BP). ana lyzing blood gases. and injection of drugs. The animals were subjected to tracheostomy and were ventilated with a respirator (Harvard 662) after immobilization with al curonium chloride (2 mg i.v.). The animal's head was fixed in a stereotactic head ho...

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“…This means that it may be difficult to consider the cerebrovascular bed as consisting of components in series which are principally regulated by either neural or metabolic factors. 8 Nor is it in dispute that in morphological terms the adrenergic terminals are identical to those seen in other vascular beds and effector organs. They approximate to within 80 9 to 300 nm 1011 of the adventitial border of smooth muscle.…”

Section: Areas Of Uncertainty Concerning the Neuralmentioning

confidence: 99%