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 The Trigeminal Nerve and Augmentation of Regional Cerebral Blood Flow during Experimental Bacterial Meningitis

1996 ◽  
Vol 16 (6) ◽  
pp. 1319-1324 ◽  
Author(s):  
Joerg R. Weber ◽  
Klemens Angstwurm ◽  
Geoffrey M. Bove ◽  
Wolf Bürger ◽  
Karl M. Einhäupl ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Bacterial Meningitis ◽  
Trigeminal Nerve ◽  
Regional Cerebral Blood Flow ◽  
Nerve Fibers ◽  
Regional Cerebral Blood ◽  
Doppler Flowmetry ◽  
Wall Components ◽  
Brain Water

We investigated whether trigeminal nerve fibers contribute to enhanced regional cerebral blood flow (rCBF) in a rat model of experimental bacterial meningitis. rCBF was measured continuously for 6 h by laser Doppler flowmetry through thinned bone over the frontal cortex. Meningitis was induced with pneumococcal cell wall components and confirmed by a significant increase of (a) leukocytes within the cerebrospinal fluid, (b) brain water content, (c) intracranial pressure and (d) rCBF. The increase of rCBF was significantly attenuated ( p < 0.05) at 3, 4, 5, and 6 h in animals after a chronic (200 ± 21% versus 138 ± 13% at 6 h on the intact and denervated sides, respectively) but not after an acute section of the nasociliary branch of the trigeminal nerve. We conclude that elevations in blood flow during the early phase of bacterial meningitis are mediated in part by the trigeminal nerve, probably by local perivascular release of neuropeptides from afferent axons innervating the meninges.

scholarly journals Local NADPH—Diaphorase Neurons Innervate Pial Arteries and Lie Close or Project to Intracerebral Blood Vessels: A Possible Role for Nitric Oxide in the Regulation of Cerebral Blood Flow

1993 ◽  
Vol 13 (6) ◽  
pp. 978-984 ◽  
Author(s):  
Carmen Estrada ◽  
Elisa Mengual ◽  
Carmen González
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Vessels ◽  
Neuronal Cell ◽  
Histochemical Staining ◽  
Nerve Fibers ◽  
No Synthase ◽  
Nadph Diaphorase ◽  
Pial Arteries

Electrical stimulation of perivascular nerves induced a relaxation of endothelium-denuded cat pial arteries that was significantly reduced by nitric oxide (NO) synthase inhibition, indicating that NO was involved in the neurogenic relaxation of these vessels. Histochemical staining of the pial arteries for NADPH-diaphorase (NADPH-d), used as a marker for NO synthase, showed positive nerve fibers in the adventitial layer. Interestingly, in some restricted areas stained neuronal cell bodies were also observed. These neurons were scattered or distributed in small groups in a ganglion-like manner, and they sent fibers to the vessel wall. No NADPH-d-positive nerve fibers or cell bodies were detected in forelimb, pulmonary, or coronary arteries. Within the brain parenchyma, blood vessels also showed positive fibers around their walls. These fibers were organized in a branching pattern and presented varicosities. NADPH-d-positive neurons were found in the proximity of the intracerebral vascular profiles, sending processes to the vessels and/or being directly apposed to their wall. The neurovascular contacts were preferentially located close to the interface between the cerebral cortex and white matter. The anatomical relationship between NADPH-d-positive neurons and fibers and the cerebral blood vessels, together with the participation of NO in the neurogenic relaxation of pial arteries, suggests that NO is involved in the regulation of cerebral blood flow.

Cortical NOS inhibition raises the lower limit of cerebral blood flow-arterial pressure autoregulation

1999 ◽  
Vol 276 (4) ◽  
pp. H1253-H1262 ◽  
Author(s):  
Stephen C. Jones ◽  
Carol R. Radinsky ◽  
Anthony J. Furlan ◽  
Douglas Chyatte ◽  
Alejandro D. Perez-Trepichio
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Lower Limit ◽  
Blood Withdrawal ◽  
Arterial Blood ◽  
Pressure Autoregulation

The maintenance of constant cerebral blood flow (CBF) as arterial blood pressure is reduced, commonly referred to as CBF-pressure autoregulation, is typically characterized by a plateau until the vasodilatory capacity is exhausted at the lower limit, after which flow falls linearly with pressure. We investigated the effect of cortical, as opposed to systemic, nitric oxide synthase (NOS) inhibition on the lower limit of CBF-pressure autoregulation. Forty-four Sprague-Dawley rats were anesthetized with halothane and N2O in O2. With a closed cranial window placed the previous day in a ventilated and physiologically stable preparation, we determined the CBF using laser-Doppler flowmetry. Animals with low reactivity to inhaled CO2 and suffused ADP or ACh were excluded. Five arterial pressures from 100 to 40 mmHg were obtained with controlled hemorrhagic hypotension under cortical suffusion with artificial cerebrospinal fluid (aCSF) and then again after suffusion for 35 ( n = 5) and 105 min ( n = 10) with aCSF, 10−3 M N ω-nitro-l-arginine (l-NNA; n = 12), or 10−3 M N ω-nitro-d-arginine (d-NNA; n = 5). An additional group ( n = 7) was studied after a 105-min suffusion of l-NNA followed by a single blood withdrawal procedure. The lower limit of autoregulation was identified visually by four blinded reviewers as a change in the slope of the five-point plot of CBF vs. mean arterial blood pressure. The lower limit of 90 ± 4.3 mmHg after 105 min of 1 mMl-NNA suffusion was increased compared with the value in the time-control group of 75 ± 5.3 mmHg ( P < 0.01; ANOVA) and the initial value of 67 ± 3.7 mmHg ( P < 0.001). The lower limit of 84 ± 5.9 mmHg in seven animals with 105 min of suffusion of 1 mM l-NNA without previous blood withdrawal was significantly increased ( P < 0.01) in comparison with 70 ± 1.9 mmHg from those with just aCSF suffusion ( n = 37). No changes in lower limit for the other agents or conditions, including 105 or 35 min of aCSF or 35 min of l-NNA suffusion, were detected. The lack of effect on the lower limit withd-NNA suffusion suggests an enzymatic mechanism, and the lengthyl-NNA exposure of 105 min, but not 35 min, suggests inhibition of a diffusionally distant NOS source that mediates autoregulation. Thus cortical suffusion ofl-NNA raises the lower limit of autoregulation, strongly suggesting that nitric oxide is at least one of the vasodilators active during hypotension as arterial pressure is reduced from normal.

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.

Patterns of Cerebral Blood Flow and Systemic Hemodynamics During Arithmetic Processing

2008 ◽  
Vol 22 (2) ◽  
pp. 81-90 ◽  
Author(s):  
Natalie Werner ◽  
Neval Kapan ◽  
Gustavo A. Reyes del Paso
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Time Course ◽  
Doppler Sonography ◽  
Transcranial Doppler Sonography ◽  
Systemic Hemodynamics ◽  
Heart Period ◽  
Blood Flow Velocities ◽  
Flow Velocities

The present study explored modulations in cerebral blood flow and systemic hemodynamics during the execution of a mental calculation task in 41 healthy subjects. Time course and lateralization of blood flow velocities in the medial cerebral arteries of both hemispheres were assessed using functional transcranial Doppler sonography. Indices of systemic hemodynamics were obtained using continuous blood pressure recordings. Doppler sonography revealed a biphasic left dominant rise in cerebral blood flow velocities during task execution. Systemic blood pressure increased, whereas heart period, heart period variability, and baroreflex sensitivity declined. Blood pressure and heart period proved predictive of the magnitude of the cerebral blood flow response, particularly of its initial component. Various physiological mechanisms may be assumed to be involved in cardiovascular adjustment to cognitive demands. While specific contributions of the sympathetic and parasympathetic systems may account for the observed pattern of systemic hemodynamics, flow metabolism coupling, fast neurogenic vasodilation, and cerebral autoregulation may be involved in mediating cerebral blood flow modulations. Furthermore, during conditions of high cardiovascular reactivity, systemic hemodynamic changes exert a marked influence on cerebral blood perfusion.

Cerebral Blood Flow and Blood Pressure

2019 ◽  
Vol 47 (7) ◽  
pp. 1007-1009
Author(s):  
Douglas S. DeWitt ◽  
Donald S. Prough
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow
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