The Effect of Sympathetic Denervation on Cerebral CO
            <sub>2</sub>
            Sensitivity

Stone, H. L.; Raichle, Marc; Hernández, M. J.

doi:10.1161/01.str.5.1.13

Cited by 22 publications

(7 citation statements)

References 19 publications

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“…Perhaps norepinephrine failed because it is normally rapidly taken up by sympathetic nerve endings in the area 19 as well as being washed away by the normal flow of CSF. Indeed, the latter may be responsible for the spontaneous reversal of the spasm produced by the various substances tested.…”

Section: Discussionmentioning

confidence: 99%

Experimental Study on the Genesis of Cerebral Vasospasm

White

Hagen

Morgan

et al. 1975

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Experimental Study on the Genesis of Cerebral Vasospasm• The cerebral vasospasm produced by blood, fractions of blood, and blood-borne agents administered intracisternally was studied arteriographically to attain a better understanding of the genesis of vasospasm. The results indicate this phenomenon is multifarious in origin, involving a number of spasmogens. Whole blood, platelets, platelet extracts, some isolated components of platelets, plasma, thrombin, histamine, serotonin and prostaglandins Fi o , E2 and F 2a produced a significant incidence and duration of spasm. Norepinephrine and prostaglandin Ei were inactive. Spasm produced by arachidonic acid and red blood cells was of questionable significance.Compared to whole blood, thrombin usually produced spasm which was more delayed in onset while most other active substances produced a shorter-lived spasm. However, among the pure substances tested, serotonin, prostaglandin E2 and prostaglandin F 2o induced spasm in small doses which most nearly resembled that observed with whole blood.The hypothesis that the course of spasm depends upon synthesis of spasmogens by brain and blood is advanced. Prostaglandin synthesis plays a major role in this concept.

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Section: Discussionmentioning

confidence: 99%

Experimental Study on the Genesis of Cerebral Vasospasm

White

Hagen

Morgan

et al. 1975

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“…Both morphological and physiologi- 1 7 4 KUSCHINSKY, WAHL cal data (5) indicate the existence of sympathetic perivascular nerves at pial arteries, but under what conditions are these nerves activated? From studies using stimulation, denervation, and alphareceptor blockers, it has been suggested that the tone of cerebral arteries may be influenced by sympathetic constrictor nerves under conditions such as changes in arterial Pco 2 (26)(27)(28) or blood pressure (26) or during subarachnoidal hemorrhage or experimental spasm (12,29,30).…”

Section: Discussionmentioning

confidence: 99%

Alpha-receptor stimulation by endogenous and exogenous norepinephrine and blockade by phentolamine in pial arteries of cats.

Kuschinsky¹,

Wahl²

1975

Circulation Research

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The question regarding the existence of an alpha-adrenergic component of pial arterial tone was investigated using a microapplication technique combined with the measurement of vascular diameter. Concentration-response curves for the alpha-receptor blocker, phentolamine, revealed no vascular reaction for a concentration range from 2.5 x 10(-11) to 2.5 x 10(-7) M. At higher concentrations (up to 1.3 x 10(-3) M) concentration-dependent dilations were observed. Constrictions of pial arteries induced by perivascular injection of 2.5 x 10(-6) M norepinephrine could be reduced by 38% and 73% when phentolamine was applied simultaneously in concentrations of 2.5 x 10(-7) and 2.5 x 10(-6) M, respectively, whereas constrictions due to 2.5 x 10(-4) M norepinephrine were not reduced by 2.5 x 10(-6) M phentolamine, indicating a competitive antagonism between norepinephrine and phentolamine for pial arteries. Stimulation of the cervical sympathetic chain (90 seconds, 10 v, 1.4 msec, 20 Hz) induced constrictions of pial arteries (mean 12%) which could be reduced by two-thirds during the simultaneous application of 2.5 x 10(-7) M phentolamine. Since the constriction induced by norepinephrine applied exogenously or released endogenously could be reduced by a concentration of phentolamine which had no vascular effect per se, we conclude that the resting tone of the pial arteries is not influenced by an alpha-adrenergic component under our experimental conditions. The dilations induced by high concentrations of phentolamine are believed to be nonspecific.

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“…9 All of these studies point to a sympathetic vasoconstrictor innervation to the cerebral vessels but this has recently been disputed. Stone, Raichle and Hernandez (1974) 16 using a flowmeter have shown that sympathectomy causes a reduced cerebrovascular dilatation with hypercapnia rather than the enhanced response previously shown. These workers have proposed that the sympathetics are cerebral vasodilators and assist in the reaction to hypercapnia.…”

Section: Discussionmentioning

confidence: 93%

Abnormal cerebrovascular response to altered PaCO2 in baboons with obstructive jaundice.

McCalden¹,

Eidelman²,

Bloom³

1976

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The Effect of Sympathetic Denervation on Cerebral CO ₂ Sensitivity

Abstract: Abstract:The Effect of Sympathetic Denervation on Cerebral C Sensitivitv

Cited by 22 publications

References 19 publications

Experimental Study on the Genesis of Cerebral Vasospasm

Experimental Study on the Genesis of Cerebral Vasospasm

Alpha-receptor stimulation by endogenous and exogenous norepinephrine and blockade by phentolamine in pial arteries of cats.

Abnormal cerebrovascular response to altered PaCO2 in baboons with obstructive jaundice.

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The Effect of Sympathetic Denervation on Cerebral CO 2 Sensitivity

Abstract: Abstract:The Effect of Sympathetic Denervation on Cerebral C Sensitivitv

Cited by 22 publications

References 19 publications

Experimental Study on the Genesis of Cerebral Vasospasm

Experimental Study on the Genesis of Cerebral Vasospasm

Alpha-receptor stimulation by endogenous and exogenous norepinephrine and blockade by phentolamine in pial arteries of cats.

Abnormal cerebrovascular response to altered PaCO2 in baboons with obstructive jaundice.

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Product

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The Effect of Sympathetic Denervation on Cerebral CO ₂ Sensitivity