Erythrocyte Extracts Enhance Neurogenic Vasoconstriction of Dog Cerebral Arteries <i>in vitro</i>

Lee, Tony J.‐F.; McIlhany, Michael; Sarwinski, S.

doi:10.1038/jcbfm.1984.68

Cited by 47 publications

(10 citation statements)

References 10 publications

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“…3) without affecting VIPor CGRP-induced relaxation in isolated cerebral arteries [36,46]. These findings further support the notion that these two peptides were not the primary transmitters in mediating cerebral neurogenic vasodilation.…”

supporting

confidence: 76%

Nitric Oxide and the Cerebral Vascular Function

Lee¹

2000

J Biomed Sci

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The presence of a cholinergic vasodilator innervation to cerebral circulation is well established. Despite its high endogenous concentration in cerebral blood vessels, acetylcholine (ACh) is not the transmitter for vasodilation. This finding has led to the discovery that nitric oxide (NO), which is coreleased with ACh and neural peptides such as vasoactive intestinal polypeptide (VIP) from the respective cholinergic-nitrergic (nitric oxidergic) nerves and the VIPergic-nitrergic nerves, is the primary transmitter in relaxing smooth muscle. ACh and VIP act presynaptically to inhibit and facilitate, respectively, the release of NO. Release of NO from cerebral vascular endothelial cells is also well established. A similar system for recycling L-citrulline to L-arginine for synthesizing more NO has been demonstrated in both cerebral perivascular nerves and endothelial cells. Neuronal and endothelial NO appears to play an important role in controlling cerebral vascular tone and circulation in health and disease.

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supporting

confidence: 76%

Nitric Oxide and the Cerebral Vascular Function

Lee¹

2000

J Biomed Sci

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“…It is known that, albeit limitations in studying a complex phenomenon such as SAH, the cerebral vascular ring-segment-mounted tissue bath method has supported most of the isolated in vitro work in cerebrovascular spasm (Lee et al, 1984;Cook, 1995). In our study, both PGE 2 -induced constriction and its potentiation by HbO 2 were blocked by neomycin, a phospholipase C inhibitor, and SC-19220, a selective EP 1 -receptor antagonist.…”

Section: Figmentioning

confidence: 52%

EP₁- and EP₃-Receptors Mediate Prostaglandin E₂–Induced Constriction of Porcine Large Cerebral Arteries

Jadhav

Jabre

Lin

et al. 2004

J Cereb Blood Flow Metab

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Summary:Prostaglandin E 2 (PGE 2 ) has been shown to dilate and constrict the systemic vascular beds, including cerebral vessels. The exact mechanism of PGE 2 -induced cerebral vasoconstriction, however, is less clarified. The authors' preliminary studies showed that PGE 2 exclusively constricted the adult porcine basilar arteries. The present study, therefore, was designed to examine the receptor mechanisms involved in PGE 2 -induced constriction of large cerebral arteries in the adult pig. Results from an in vitro tissue-bath study indicated that PGE 2 and its agonists 17-phenyl trinor PGE 2 (17-PGE 2 ), sulprostone (EP 1 /EP 3 receptor agonists), and 11-deoxy-16,16-dimethyl PGE 2 (11-PGE 2 , an EP 2 /EP 3 -receptor agonist) induced exclusive constriction, which was not affected by endothelium denudation or cold-storage denervation of perivascular nerves. The constriction induced by PGE 2 , 17-PGE 2 , and sulprostone, but not by potassium chloride, was blocked by SC-19220 (a selective EP 1 -receptor antagonist), AH-6809 (an EP 1 /EP 2 -receptor antagonist), and U-73122 and neomycin (phospholipase C inhibitors). AH-6809, however, did not affect 11-PGE 2 -induced contraction. These results suggest that the contraction was not mediated by the EP 2 -receptor, but was mediated by EP 1 -and EP 3 -receptors. Furthermore, EP 1 -receptor immunoreactivities were found across the entire medial smooth muscle layers, whereas EP 3 -receptor immunoreactivities were limited to the outer smooth muscle layer toward the adventitia. Western blotting also showed the presence of EP 1 -and EP 3 -receptor proteins in cultured primary cerebral vascular smooth muscle cells. In conclusion, PGE 2 exclusively constricts the adult porcine large cerebral arteries. This constriction is mediated by phosphatidyl-inositol pathway via activation of EP 1 -and EP 3 -receptors located on the smooth muscle cells. These two receptor subtypes may play important roles in physiologic and pathophysiologic control of cerebral vascular tone.

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“…1416 " 19 Moreover, hemolysates have been reported to inhibit neurogenic vasodilation and to potentiate neurogenic vasoconstriction. 8 In the present experiments, AChinduced relaxation of the arterial rings from animals killed 4 days after the first SAH was inhibited by pretreatment with 10 ~6 M hemoglobin and completely abolished by 10~3 M hemoglobin. The present result is consistent with that seen in normal rabbit basilar arteries 7 and suggests that hemoglobin has basically the same inhibitory action on the ACh-induced relaxation in normal arteries and those exposed to SAH.…”

Section: Discussionmentioning

confidence: 74%

“…4 " 6 Moreover, in normal cerebral arteries, hemoglobin selectively inhibits endothelium-dependent vasodilation 7 as well as neurogenic vasodilation. 8 It is well documented that endothelial damage occurs frequently after SAH. We have recently demonstrated that endothelium-dependent vasodilation induced by adenosine triphosphate (ATP) is impaired after SAH in a rabbit single hemorrhage model (T. Nakagomi, unpublished data).…”

mentioning

confidence: 99%

Impairment of endothelium-dependent vasodilation induced by acetylcholine and adenosine triphosphate following experimental subarachnoid hemorrhage.

Nakagomi¹,

Kassell²,

Sasaki³

et al. 1987

Stroke

116

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The effect of subarachnoid hemorrhage (SAH) on endotbelium-dependent vasodilation of isolated rabbit basilar artery was examined using an isometric tension recording method. Thirty-five rabbits that had 2 successive blood injections were divided into 3 groups: normal animals (control), 4 days, and 3 weeks after the first SAH. Acetylcholine (ACh) (10~6-10~4 M) and adenosine triphosphate (ATP) (10~6-10~4 M) were used to evoke dose-dependent vasodilation of isolated arterial rings previously contracted by 10~6 M serotonin. In the animals killed 4 days after the first SAH, both AChand ATP-induced relaxation were suppressed, and the degree of relaxation of this group was 38 ± 4.5% (mean ± SEM) and 22 ± 3.9% of the initial contractile tone in response to 10" 3 Despite extensive efforts to identify measures to dilate the narrowed arteries, no reliable measure exists for preventing vasospasm from developing or for reversing it. One of the major reasons for this inadequacy is a lack in understanding the pathogenesis of vasospasm. The cause of cerebral vasospasm following SAH is likely to be multifactorial.It has been recently suggested that impairment of the vasodilatory activity of cerebral arteries following SAH may play an important role in the pathogenesis of vasospasm. Arterial wall prostacyclin, a powerful vasodilator, decreases progressively following SAH. 8 It is well documented that endothelial damage occurs frequently after SAH. We have recently demonstrated that endothelium-dependent vasodilation induced by adenosine triphosphate (ATP) is impaired after SAH in a rabbit single hemorrhage model (T. Nakagomi, unpublished data). However, acetylcholine (ACh)-induced vasodilation was well preserved following SAH in that model. This may reflect a partial, less severe damage to the endothelium. The present experiments were conducted to investigate 1) the effect of SAH on endothelium-dependent vasodilation induced by ACh and ATP in a rabbit double hemorrhage model, which should result in more severe damage to the endothelium than a single injection model, and 2) to study the inhibitory effect of hemoglobin on endothelium-dependent vasodilation in basilar arteries exposed to SAH. Materials and Methods Animal PreparationsThirty-five male New Zealand white rabbits weighing 2.9-3.4 kg were anesthetized with an i.m. injection of ketamine (20 mg/kg), xylazine (5 mg/kg), and acepromazine (0.25 mg/kg) in a ratio of 8:1:1. The animals were intubated and received muscular paralysis with i.v. pancuronium bromide (0.08 mg/kg). Ventilation was maintained with a Harvard dual-phase control respirator. In each animal, the left ear artery was cannulated for monitoring blood pressure and withdrawing arterial blood.A 23-gauge butterfly needle was inserted into the cisterna magna percutaneously and connected to a pressure transducer via one outlet of a three-way stopcock. The other outlet was used for the injection of arterial blood. Intracranial pressure (ICP) was monitored immediately after the injection of arterial blood through the st...

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Erythrocyte Extracts Enhance Neurogenic Vasoconstriction of Dog Cerebral Arteries in vitro

Cited by 47 publications

References 10 publications

Nitric Oxide and the Cerebral Vascular Function

Nitric Oxide and the Cerebral Vascular Function

EP₁- and EP₃-Receptors Mediate Prostaglandin E₂–Induced Constriction of Porcine Large Cerebral Arteries

Impairment of endothelium-dependent vasodilation induced by acetylcholine and adenosine triphosphate following experimental subarachnoid hemorrhage.

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Erythrocyte Extracts Enhance Neurogenic Vasoconstriction of Dog Cerebral Arteries in vitro

Cited by 47 publications

References 10 publications

Nitric Oxide and the Cerebral Vascular Function

Nitric Oxide and the Cerebral Vascular Function

EP1- and EP3-Receptors Mediate Prostaglandin E2–Induced Constriction of Porcine Large Cerebral Arteries

Impairment of endothelium-dependent vasodilation induced by acetylcholine and adenosine triphosphate following experimental subarachnoid hemorrhage.

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EP₁- and EP₃-Receptors Mediate Prostaglandin E₂–Induced Constriction of Porcine Large Cerebral Arteries