Parasympathetic cholinergic control of cerebral blood flow in dogs.

DʼAlecy, Louis G.; Rose, Cynthia J.

doi:10.1161/01.res.41.3.324

Cited by 94 publications

(42 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%

“…Cerebral vasodilatation accompanying stimula tion of the facial nerve (VII) was originally de scribed by Cobb and Finesinger (1932) and Cho robski and Penfield (1932), and later confirmed by some (James et aI., 1969;D'Alecy and Rose, 1977;Pinard et aI., 1979) and denied by others (Meyer et aI., 1971;Busija and Heistad, 1981;Linder, 1981), leaving open the question of the role of this nerve in cerebrovascular control. Likewise, evidence has been adduced for the existence of cerebral vasodi lator fibers in cranial nerve III (Klosovskii, 1963;Kameyama, 1980).…”

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confidence: 95%

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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%

mentioning

confidence: 95%

Cholinergic Cerebral Vasodilatation: Lack of Involvement of Cranial Parasympathetic Nerves

Scremin¹,

Sonnenschein²,

Rubinstein³

1983

J Cereb Blood Flow Metab

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“…In light of findings that cortical acetylcholine release increases following cortical arousal (Celesia and Jasper, 1966;Szerb, 1967) and that topically applied atropine can at tenuate the cerebral vasodilatation associated with HV -L V shifts (Scremin et aI., 1973), it is possible that a cholinergic, presumably neurogenic, cerebral vasodilatation occurs concomitantly with cortical arousal. This possibility is strengthened by the well-documented existence of a cerebrovascular dilator innervation whose principal transmitter is presumed to be acetylcholine (Lavrentieva et aI., 1968;Iwayama et aI., 1970;Nielsen et aI., 1971;Nielsen and Owman, 1971;Edvinsson et aI., 1972Edvinsson et aI., , 1976Edvinsson et aI., , 1977Kuschinsky et aI., 1974;Toda, 1974;Matsuda et aI., 1976;Hardebo et aI., 1977;D'Alecy and Rose, 1977;Florence and Bevan, 1979;Burnstock, 1980). …”

Section: Hv-lv Shiftsmentioning

confidence: 99%

The Electroencephalogram, Blood Flow, and Oxygen Uptake in Rabbit Cerebrum

Pearce¹,

Scremin²,

Sonnenschein³

et al. 1981

J Cereb Blood Flow Metab

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Summary: In the present study, the relationships among electroencephalo graphic (EEG) amplitude shifts, cerebral blood flow (CBF), and cerebral oxy gen uptake (CMROz) have been characterized in halothane-anesthetized rab bits. CBF was measured by timed collection of venous effluent from the supe rior sagittal sinus. CMR02 was calculated as the product of CBF and the arteriovenous difference in oxygen content. The depth of anesthesia in the first series of experiments was maintained at a constant level that was characterized by spontaneous EEG shifts from high-to low-voltage states (HV -L V shifts).These shifts were associated with transient decreases in mean arterial pressure (MAP), which averaged 23 ::+:: 2 mm Hg (n = 17). Ninety seconds after spon taneous HV-LV shifts, MAP had returned to its original value, CBF had in creased by 26 ::+:: 7% (11 = 8), and CMROz had increased 22 ::+:: 4% (n = 7). In a second series of experiments, HV-L V shifts were induced by a 90-s application of a standardized nociceptive stimulus (11 = 13). Following these stimulation induced HV-LV shifts, CBF increased 28 ::+:: 5% and CMROz increased 27 ::+:: In a variety of studies, cerebral blood flow (CBF) has increased following sustained decreases in electroencephalographic (EEG) amplitude (HV-LV

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“…11 For this measurement, the entire venous effluent from the anterior cranial fossa was diverted through the left temporal sinus by occluding the occipital emissary veins, both sigmoid sinuses and the right temporal sinus. Cerebral venous outflow from the anterior cranial fossa was then measured by a Doppler flow transducer secured in a fixed position over the left temporal sinus.…”

Section: Measurement Of Cerebral Blood Flowmentioning

confidence: 99%

“…11 In that study, the amount of blood sodium extracted by the contents of the anterior cranial fossa was measured and compared to the amount extracted by noncerebral tissues. Cerebral venous blood samples were taken simultaneously from the dorsal sagittal sinus and the left temporal sinus.…”

Section: Measurement Of Cerebral Blood Flowmentioning

confidence: 99%

Hemorrhage-induced cerebral vasoconstriction in dogs.

Pearce¹,

DʼAlecy²

1980

Stroke

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SUMMARY Cerebrorascular responses to a 20% toJume hemorrhage were studied In chloraloseanesthetized dogs with tbe Doppler cerebral venous outflow method. Arterial Pco,, Po t , and pH were held constant by servocontrol of ventilation. Tbe experimental results were divided into 2 groups as determined by the spontaneous responses of mean arterial pressure (MAP) to hemorrhage. In Group 1 (n ** 11), steady state MAP decreased 25%, cerebral blood flow (CBF) decreased 15%, and cerebrovascular resistance (CVR) decreased 13% (autoregulatory vasodilatation). In group 2 (n = 23), MAP changed less than 10 mm Hg, CBF decreased 13%, and CVR increased 15%. Tbe hemorrhage-Induced cerebral vasoconstriction In Group 2 was characterized by the following: pbenoxybenzamine (2 mg/kg i.r., n •» 3) reduced post-bemorrfaage CVR from 116% to 95% of prebemorrhage CVR (cCVR); phentolamine (2 mg/kg i.v., n = 5) reduced post-hemorrhage CVR from 114% to 91% of cCVR; and verified local anesthetization of both superior cervical ganglia (n = 5) reduced post-hemorrhage CVR from 116% to 94% of cCVR. Thus in Group 2, sympatbetic vasoconstriction contributed approximately 5% of cCVR; following normotensive hemorrhage, it accounted for up to 20% of post-hemorrhage CVR. In combination witb previous studies, these data suggest that cerebrovascular responses to hemorrhage balance between autoregulatory vasodilatatloa and sympatbetic vasoconstriction. Stroke, Vol 11, No 2, 1980DESPITE the widely accepted existence of a sympathetic cerebrovascular innervation, 1 the functional significance of this innervation remains unclear. Methodological controversy complicates interpretation of the results of electrical stimulation of this innervation. Reflex stimulation, however, as produced during studies of cerebral blood flow (CBF) autoregulation, has suggested a physiological role for these nerves. When arterial hypotension was produced by graded hemorrhage, the lower limit of CBF autoregulation was approximately 70 mm Hg.2 "* When arterial hypotension was produced by pharmacological ganglionic blockade, however, the lower limit of CBF autoregulation was approximately 40 mm Hg.3 ' *•" In other words, the maximal cerebral vasodilatation observed during hypotension resulting from ganglionic blockade was greater than that observed during hemorrhagic hypotension. Since sympathetic outflow is interrupted by ganglionic blockade and is augmented by hemorrhage, these results may be interpreted to suggest reflex sympathetic cerebral vasoconstriction during hemorrhage. Consistent with this interpretation are the findings that pretreatment with alpha-receptor blockade (ARB) or acute cervical sympathectomy (CSx) extends the lower limit of CBF autoregulation.7 ' $ A common problem complicating demonstrations of reflex sympathetic cerebral vasoconstriction has been the simultaneous vasoconstriction or vasodilatation attributable to metabolic or autoregulatory mechanisms. For example, the sympathetic cerebral vasoconstriction suggested to occur during hemorrhagic hypotension ha...

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Parasympathetic cholinergic control of cerebral blood flow in dogs.

Cited by 94 publications

References 32 publications

Cholinergic Cerebral Vasodilatation: Lack of Involvement of Cranial Parasympathetic Nerves

Cholinergic Cerebral Vasodilatation: Lack of Involvement of Cranial Parasympathetic Nerves

The Electroencephalogram, Blood Flow, and Oxygen Uptake in Rabbit Cerebrum

Hemorrhage-induced cerebral vasoconstriction in dogs.

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