scholarly journals Inhibition of Nitric Oxide Synthase Attenuates the Cerebral Blood Flow Response to Stimulation of Postganglionic Parasympathetic Nerves in the Rat

1993 ◽  
Vol 13 (6) ◽  
pp. 993-997 ◽  
Author(s):  
Yoko Morita-Tsuzuki ◽  
Jan Erik Hardebo ◽  
Eliete Bouskela
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Systemic Blood Pressure ◽  
High Dose ◽  
Parasympathetic Nerve ◽  
Doppler Flowmetry ◽  
Cortical Blood Flow ◽  
Parasympathetic Nerves ◽  
Flow Response ◽  
Stimulation Of

Stimulation of cerebrovascular parasympathetic nerves markedly increases cortical blood flow. Nitric oxide (NO) or a NO-containing compound is present in these nerves and may therefore, upon release, be partly responsible for the flow increase. In addition, transmitters released from the nerves may cause synthesis and release of this compound from the endothelium. The contribution of NO synthesis to the cortical blood flow (CoBF) increase during parasympathetic stimulation was elucidated in rat by laser–Doppler flowmetry. Thirty-minute exposure to circulating Nω-nitro-l-arginine methyl ester (l-NAME) 50 mg kg−1 eliminated most of the response (from 104 to 8% increase), whereas 10-min exposure to this dose or 30-min exposure to 5 mg kg−1 caused a less marked reduction. The reducing effect was particularly evident after elimination of the systemic blood pressure increase caused by l-NAME (only 3% increase after the high dose). Infusion of l-arginine restored the flow response. Resting CoBF was not substantially affected by blockade of NO formation. Thus, release of an NO-containing compound constitutes a major component of the increase in CoBF caused by parasympathetic nerve stimulation but does not seem to contribute to cortical flow regulation during resting conditions.

The Effect of Electrical Stimulation of the Pudendal Nerve on Sciatic Nerve Blood Flow in Animals

2008 ◽  
Vol 26 (3) ◽  
pp. 145-148 ◽  
Author(s):  
Motohiro Inoue ◽  
Tatsuya Hojo ◽  
Miwa Nakajima ◽  
Hiroshi Kitakoji ◽  
Megumi Itoi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Electrical Stimulation ◽  
Sciatic Nerve ◽  
Pudendal Nerve ◽  
Systemic Blood Pressure ◽  
Nerve Blood Flow ◽  
Doppler Flowmetry ◽  
Canal Stenosis ◽  
Stimulation Of

Objective To investigate the mechanism of the clinical effect of electroacupuncture of the pudendal nerve on the lumbar and lower limb symptoms caused by lumbar spinal canal stenosis, we studied changes in sciatic nerve blood flow during electrical stimulation of the pudendal nerve in the rat. Methods Using rats (n=5), efferent electrical stimulation to the pudendal nerve was performed and sciatic nerve blood flow was measured with laser Doppler flowmetry. Simultaneously, changes in the blood pressure and cardiac rate were measured. Furthermore, the effect of atropine on these responses to the stimulation was also studied. Results Electrical stimulation of the pudendal nerve significantly increased blood flow in the sciatic nerve transiently without increasing heart rate and systemic blood pressure. The significant increase in the sciatic nerve blood flow disappeared after administration of atropine. Conclusion Electrical stimulation of the pudendal nerve causes a transient and significant increase in sciatic nerve blood flow. This response is eliminated or attenuated by administration of atropine, indicating that it occurs mainly via cholinergic nerves.

Isoflurane-induced Cerebral Hyperemia Is Partially Mediated by Nitric Oxide and Epoxyeicosatrienoic Acids in Mice In Vivo 

2002 ◽  
Vol 97 (6) ◽  
pp. 1528-1533 ◽  
Author(s):  
Franz Kehl ◽  
Hui Shen ◽  
Carol Moreno ◽  
Neil E. Farber ◽  
Richard J. Roman ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Epoxyeicosatrienoic Acids ◽  
Acute Administration ◽  
Doppler Flowmetry ◽  
Cortical Blood Flow ◽  
Oxide Synthase ◽  
Cerebral Cortical Blood Flow

Background Despite intense investigation, the mechanism of isoflurane-induced cerebral hyperemia is unclear. The current study was designed to determine the contributions of neuronal nitric oxide synthase, prostaglandins, and epoxyeicosatrienoic acids to isoflurane-induced cerebral hyperemia. Methods Regional cerebral cortical blood flow was measured with laser Doppler flowmetry during stepwise increases of isoflurane from 0.0 to 1.2, 1.8, and 2.4 vol% end-tidal concentration in alpha-chloralose-urethane-anesthetized, C57BL/6 mice before and 45 min after administration of the neuronal nitric oxide synthase inhibitor 7-nitroindazole (7-NI, 40 mg/kg, intraperitoneal), the cyclooxygenase inhibitor indomethacin (INDO, 10 mg/kg, intravenous), and the cytochrome P450 epoxygenase inhibitor N-methylsulfonyl-6-(2-proparglyoxyphenyl)hexanoic acid (PPOH, 20 mg/kg, intravenous). Results Isoflurane increased regional cerebral cortical blood flow by 9 +/- 3, 46 +/- 21, and 101 +/- 26% (SD) at 1.2, 1.8, and 2.4 vol%, respectively. The increases in regional cerebral cortical blood flow were significantly (*P < 0.05) smaller after 7-NI (5 +/- 6, 29 +/- 19*, 68 +/- 15%*) or PPOH (4 +/- 8, 27 +/- 17*, 67 +/- 30%*), but not after administration of INDO (4 +/- 4, 33 +/- 18 [NS], 107 +/- 35% [NS]). The effect of combined treatment with 7-NI, PPOH, and INDO was not additive and was equal to that of either 7-NI or PPOH alone (5 +/- 5, 30 +/- 12*, 76 +/- 24%*). Chronic treatment of mice for 5 days with 7-NI (2 x 40 mg/kg, intraperitoneal) produced similar decreases in regional cerebral cortical blood flow as those seen with acute administration. Neither PPOH nor INDO conferred a significant additional block of the hyperemia in these animals. Conclusions Nitric oxide and epoxyeicosatrienoic acids contribute to isoflurane-induced hyperemia. However, only approximately one third of the cerebral hyperemic response to isoflurane is mediated by autacoids. The remaining part of this response appears to be mediated by a direct action of isoflurane on smooth muscle by some yet-unknown mechanism.

scholarly journals Selective Electrical Stimulation of Postganglionic Cerebrovascular Parasympathetic Nerve Fibers Originating from the Sphenopalatine Ganglion Enhances Cortical Blood Flow in the Rat

1990 ◽  
Vol 10 (3) ◽  
pp. 383-391 ◽  
Author(s):  
Norihiro Suzuki ◽  
Jan Erik Hardebo ◽  
Jan Kåhrström ◽  
Christer Owman
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Nerve Fibers ◽  
Microvascular Blood Flow ◽  
Sphenopalatine Ganglion ◽  
Flow Measurements ◽  
Parasympathetic Nerve ◽  
Cortical Blood Flow ◽  
Arterial Blood ◽  
Stimulation Of

Recently, the origins and pathways of cerebrovascular acetylcholine- and vasoactive intestinal polypeptide-containing nerves have been elucidated in detail in the rat: The sphenopalatine ganglion is the major source for postganglionic parasympathetic fibers to the vascular beds of the cerebral hemispheres. To clarify the functional role of the nerves on cerebral blood vessels in vivo, brain cortical microvascular blood flow was measured in rats during electrical stimulation of these particular postganglionic fibers. Animals were subjected to transection of the right nasociliary nerve 2 weeks before the flow measurements to eliminate activation of peptidergic sensory fibers. Relative change in microvascular blood flow was continuously recorded by a laser-Doppler flowmeter system under α-chloralose anesthesia. The postganglionic fibers were electrically stimulated just proximal to the ethmoidal foramen by a bipolar platinum electrode (5 V; 0.5 ms; 3, 10, 30, 60 Hz; as a continuous stimulation for 90 s). Stimulation at 10 Hz induced a marked increase of the cortical blood flow (CoBF) on the ipsilateral side, whereas no change was observed on the contralateral side. It reached a maximum mean value of 42.5% at 46 s, and then slightly declined during the remaining stimulation period. No significant changes were observed in the mean arterial blood pressure or blood gases during or after stimulation. Both atropine and scopolamine failed to alter this flow increase. Electrical stimulation of the postganglionic fibers at different frequencies revealed a maximal increase in the CoBF at 30 Hz in the control situation (47.2%), but at 10 Hz after scopolamine administration (51.6%). This provides the first report showing that selective postganglionic stimulation of the parasympathetic nerve fibers markedly enhances blood flow in the brain, and it supports the view that the neurogenic vasodilatation is primarily noncholinergic.

scholarly journals Nitric oxide is the predominant mediator of cerebellar hyperemia during somatosensory activation in rats

1999 ◽  
Vol 277 (6) ◽  
pp. R1760-R1770 ◽  
Author(s):  
Guang Yang ◽  
Gang Chen ◽  
Timothy J. Ebner ◽  
Costantino Iadecola
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Synaptic Function ◽  
Kainate Receptors ◽  
No Production ◽  
Field Potentials ◽  
Doppler Flowmetry ◽  
Somatosensory Stimuli ◽  
Synthase Inhibitor ◽  
Stimulation Of

Crus II is an area of the cerebellar cortex that receives trigeminal afferents from the perioral region. We investigated the mechanisms of functional hyperemia in cerebellum using activation of crus II by somatosensory stimuli as a model. In particular, we sought to determine whether stimulation of the perioral region increases cerebellar blood flow (BFcrb) in crus II and, if so, whether the response depends on activation of 2-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-kainate receptors and nitric oxide (NO) production. Crus II was exposed in anesthetized rats, and the site was superfused with Ringer. Field potentials were recorded, and BFcrb was measured by laser-Doppler flowmetry. Crus II was activated by electrical stimulation of the perioral region (upper lip). Perioral stimulation evoked the characteristic field potentials in crus II and increased BFcrb (34 ± 6%; 10 Hz-25 V; n = 6) without changing arterial pressure. The BFcrb increases were associated with a local increase in glucose utilization (74 ± 8%; P < 0.05; n = 5) and were attenuated by the AMPA-kainate receptor antagonist 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo-[f]quinoxaline (−71 ± 3%; 100 μM; P < 0.01; n = 5). The neuronal NO synthase inhibitor 7-nitroindazole (7-NI, 50 mg/kg; n = 5) virtually abolished the increases in BFcrb(−90 ± 2%; P < 0.01) but did not affect the amplitude of the field potentials. In contrast, 7-NI attenuated the increase in neocortical cerebral blood flow produced by perioral stimulation by 52 ± 6% ( P < 0.05; n = 5). We conclude that crus II activation by somatosensory stimuli produces localized increases in local neural activity and BFcrbthat are mediated by activation of glutamate receptors and NO. Unlike in neocortex, in cerebellum the vasodilation depends almost exclusively on NO. The findings underscore the unique role of NO in the mechanisms of synaptic function and blood flow regulation in cerebellum.

scholarly journals Nitric Oxide and Prostanoids Participate in Cerebral Vasodilation Elicited by Electrical Stimulation of the Rostral Ventrolateral Medulla

1994 ◽  
Vol 14 (3) ◽  
pp. 492-502 ◽  
Author(s):  
Eugene V. Golanov ◽  
Donald J. Reis
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Electrical Stimulation ◽  
Cerebral Arteries ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Doppler Flowmetry ◽  
Cerebral Vasodilation ◽  
The Brain ◽  
Stimulation Of

We investigated, using laser-Doppler flowmetry, whether nitric oxide (NO)- and/or indomethacin (IND)-sensitive mechanisms mediate the elevations of regional cerebral blood flow (rCBF) elicited by electrical stimulation of the rostral ventrolateral medulla (RVL) in the anesthetized spinalized rat. Stimulation of the RVL for 10 s caused increased rCBF in the frontal cortex by 31% ( n = 46), peaking at 22 s and persisting for up to 8 min. Intravenous l-nitro- NG-arginine (NNA) dose dependently and reversibly increased arterial pressure and reduced basal and evoked rCBF to 74 and 54% of the control, respectively ( p < 0.05; n = 7). Superfused over the cortex, NNA dose dependently reduced only the evoked elevations of rCBF, to 39% of the control ( p < 0.05; n = 6). Intravenous IND decreased the basal rCBF dose dependently and decreased the elevations evoked from the RVL by 38% ( p < 0.05), but IND was without effect when superfused. Combined, the effects of intravenous NNA and IND summated, reducing rCBF by 70%. However, when NNA and IND were superfused together, the inhibition of the evoked vasodilation was comparable to that elicited by NNA alone. We conclude that the elevation in rCBF elicited from the RVL is partially mediated by (a) NO synthesized locally in the cortex in response to an afferent neural signal and (b) an IND-sensitive mechanism, probably a product of cyclooxygenase, located in larger cerebral arteries, in response to a retrograde vascular signal resulting from increased blood flow within the brain.

Effects of capsaicin and nitric oxide synthase inhibitor on increase in cerebral blood flow induced by sensory and parasympathetic nerve stimulation in the rat

2005 ◽  
Vol 98 (5) ◽  
pp. 1792-1798 ◽  
Author(s):  
Kazuhide Ayajiki ◽  
Hideyuki Fujioka ◽  
Kazuya Shinozaki ◽  
Tomio Okamura
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Trigeminal Nerve ◽  
Nerve Stimulation ◽  
Nerve Fibers ◽  
Parasympathetic Nerve ◽  
Parasympathetic Nerves ◽  
Nerve Bundles

Effects of electrical stimulation of the nerve bundles including sensory and parasympathetic nerves innervating cerebral arteries on cerebral blood flow (CBF) and mean arterial blood pressure (MABP) were investigated with a laser-Doppler flowmeter and a blood pressure monitoring system in anesthetized rats pretreated with and without capsaicin. The electrode was hooked on the nerve bundles including the distal nasociliary nerve from trigeminal nerve and parasympathetic nerve fibers from sphenopalatine ganglion. In control rats, the nerve stimulation for 30 s increased CBF in the ipsilateral side and MABP. Hexamethonium attenuated the increase in CBF and abolished that in MABP. Under treatment with hexamethonium, NG-nitro-l-arginine (l-NNA, 1 mg/kg) significantly attenuated the stimulation-induced increase in CBF, which was restored by the addition of l-arginine. Although the dose of l-NNA was raised up to 10 mg/kg, the stimulation-induced increase in CBF was not further inhibited and was never abolished. In capsaicin-pretreated rats, magnitudes of the stimulation-induced increases in CBF and MABP were lower than those in control rats. Hexamethonium attenuated the increase in CBF and abolished that in MABP. Under treatment with hexamethonium, l-NNA abolished the stimulation-induced increase in CBF in capsaicin-pretreated rats. In conclusion, nitric oxide released from parasympathetic nerves and neuropeptide(s) released antidromically from sensory nerves may be responsible for the increase in CBF in the rat. The afferent impulses by nerve stimulation may stimulate the trigeminal nerve and lead to the rapid increase in MABP, which partly contributes to the increase in CBF.

scholarly journals Brief Hypercapnia Enhances Somatosensory Activation of Blood Flow in Rat

1996 ◽  
Vol 16 (6) ◽  
pp. 1307-1311 ◽  
Author(s):  
Bernd Schmitz ◽  
Bernd W. Böttiger ◽  
Konstantin-Alexander Hossmann
Keyword(s):  
Blood Flow ◽  
Cerebrovascular Reactivity ◽  
Somatosensory Stimulation ◽  
Doppler Flowmetry ◽  
Mechanically Ventilated ◽  
Coupling Process ◽  
Physiological Variables ◽  
Flow Response ◽  
Functional Stimulation ◽  
Stimulation Of

Activation of CBF by hypercapnia or functional stimulation has been attributed to multiple mediators, most of which are thought to interfere with cerebrovascular reactivity in a closely time-related manner. Here we describe that brief hypercapnia produces marked up-regulation of somatosensory activation of blood flow that outlasts carbon dioxide exposure for at least 60 min. In chloralose-anesthetized, mechanically ventilated rats, somatosensory activation was carried out by electrical stimulation of the forepaw. Blood flow was measured in the contralateral primary somatosensory cortex by laser-Doppler flowmetry (LDF). Under control conditions, somatosensory stimulation increased LDF by 38.8 ± 11.0%. Ventilation with 6% CO2 for 3 min caused a rise of LDF by 28.0 ± 8.7%. Baseline CBF and Paco2 returned to control values within 20 min. Repetition of somatosensory stimulation after hypercapnia revealed a long-lasting up-regulation of the flow response: 25 min after hypercapnia, functional stimulation increased LDF by 86.0 ± 18.1%, and 60 min after hypercapnia even by 96.0 ± 26.0%. This is the first demonstration of CO2-induced up-regulation of functional activation of blood flow and an example of the importance of general physiological variables for the modulation of the coupling process.

Effects of Stellate Ganglion Stimulation on Bilateral Cochlear Blood Flow

1993 ◽  
Vol 102 (5) ◽  
pp. 378-384 ◽  
Author(s):  
Tianying Ren ◽  
Esa Laurikainen ◽  
Wayne S. Quirk ◽  
Josef M. Miller ◽  
Alfred L. Nuttall
Keyword(s):  
Blood Flow ◽  
Superior Cervical Ganglion ◽  
Stellate Ganglion ◽  
Systemic Blood Pressure ◽  
Nerve Fibers ◽  
Cochlear Blood Flow ◽  
Doppler Flowmetry ◽  
Cervical Ganglion ◽  
Pass Through ◽  
Stimulation Of

The effect of intraneural electrical stimulation of the stellate ganglion (SG) on bilateral cochlear blood flow (CBF) was investigated with laser-Doppler flowmetry. The SG of 15 anesthetized guinea pigs was exposed by a novel surgical approach and stimulated with a specially designed intraneural bipolar platinum-iridium electrode. Bilateral CBF was continuously monitored. Stimulation of 0.25 mA caused a detectable increase of the systemic blood pressure (BP) and a bilateral decrease of the cochlear vascular conductance (R, defined as the ratio CBF/BP). A stimulus of 0.5 mA elicited a statistically significant ipsilateral CBF (CBFi) decrease of 3.6% ± 5.1% from the baseline and a contralateral CBF (CBFc) decrease of 3.1% ± 5.5%. That no statistical difference was found between CBFi and CBFc indicates that a unilateral sympathetic stimulation of the SG can cause equal bilateral responses. These responses were accompanied by a significantly increased BP (8.7% ± 5.2% of baseline) and consequently a greatly decreased R (12.2% ± 6.5%) of the ipsilateral cochlea. Bilateral sections of the cervical sympathetic trunk below the level of the superior cervical ganglion did not alter the evoked changes in CBF, BP, and R. It is concluded that SG stimulation can decrease the conductivity of the cochlear vessels or the supplying vessels of the cochlea. Additionally, the SG nerve fibers that cause these effects do not pass through the superior cervical ganglion.

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