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.

Nitric oxide, prostaglandins, and impaired cerebral blood flow autoregulation in group B streptococcal neonatal meningitis

2000 ◽  
Vol 78 (3) ◽  
pp. 217-227 ◽  
Author(s):  
Carmen Mertineit ◽  
Jacqueline Samlalsingh-Parker ◽  
Maria Glibetic ◽  
Ginette Ricard ◽  
Francisco JD Noya ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Early Onset ◽  
No Synthase ◽  
Neonatal Meningitis ◽  
Cerebrovascular Autoregulation ◽  
Upper Limit ◽  
Group B

Impaired autoregulation of cerebral blood flow (CBF) contributes to CNS damage during neonatal meningitis. We tested (i) the hypothesis that cerebrovascular autoregulation is impaired during early onset group B streptococcal (GBS) meningitis, (ii) whether this impairment is regulated by vasoactive mediators such as prostaglandins and (or) nitric oxide (NO), and (iii) whether this impairment is preventable by specific and (or) nonspecific inhibitors: dexamethasone, ibuprofen, and Nω-nitro-L-arginine, a NO inhibitor. Sterile saline or 109colony-forming units (cfu) of heat-killed GBS was injected into the cerebral ventricle of newborn piglets. CBF autoregulation was determined by altering cerebral perfusion pressure (CPP) with balloon-tipped catheters placed in the aorta. GBS produced a narrow range of CBF autoregulation due to an impairment at the upper limit of CPP. We report that in vivo in the early stages (first 2 h) of induced GBS inflammation (i) GBS impairs the upper limit of cerebrovascular autoregulation; (ii) ibuprofen, dexamethasone, and Nω-nitro-L-arginine not only prevent this GBS-induced autoregulatory impairment but improve the range of cerebrovascular autoregulation; (iii) these autoregulatory changes do not involve circulating cerebral prostanoids; and (iv) the observed changes correlate with the induction of NO synthase gene expression. Thus, acute early onset GBS-induced impairment of the upper limit of CBF autoregulation can be correlated with increases of NO synthase production, suggesting that NO is a vasoactive mediator of CBF.Key words: cerebrovascular autoregulation, group B Streptococcus, neonatal meningitis, anti-inflammatory agents, prostanoids, nitric oxide synthase, gene expression, nitric oxide.

scholarly journals PACAP, a VIP-like Peptide: Immunohistochemical Localization and Effect upon Cat Pial Arteries and Cerebral Blood Flow

1993 ◽  
Vol 13 (2) ◽  
pp. 291-297 ◽  
Author(s):  
R. Uddman ◽  
P. J. Goadsby ◽  
I. Jansen ◽  
L. Edvinsson
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Arteries ◽  
Immunohistochemical Localization ◽  
Nerve Fibers ◽  
Moderate Increase ◽  
Pial Arteries ◽  
Maximal Increase ◽  
Middle Cerebral Arteries ◽  
Prostaglandin F

Pituitary adenylate cyclase activating peptide (PACAP) is a vasoactive intestinal polypeptide (VIP)–like peptide recently isolated from ovine hypothalami. Nerve fibers containing PACAP immunoreactivity were present in the adventitia and the adventitia-media border of cat cerebral arteries. Double immunostaining revealed that PACAP-immunoreactive nerve fibers constituted a sub-population of the VIP-containing fibers. PACAP effected a concentration-dependent relaxation of feline middle cerebral arteries that had been precontracted with prostaglandin F2α. The maximum relaxation, 24 and 34% of precontraction, was achieved with PACAP-38 and PACAP-27, respectively, at a concentration of 10−6 M. In cats anesthetized with α-chloralose, intracerebral microinjection of PACAP effected a moderate increase in cerebral blood flow. The maximal increase (18.6 ± 6%) was observed following the injection of 5 μg PACAP.

scholarly journals Augmentation of Blood Flow through Cerebral Collaterals by Inhibition of Nitric Oxide Synthase

1994 ◽  
Vol 14 (5) ◽  
pp. 704-714 ◽  
Author(s):  
Michael G. Muhonen ◽  
Donald D. Heistad ◽  
Frank M. Faraci ◽  
Christopher M. Loftus
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Aortic Pressure ◽  
No Synthase ◽  
Artery Pressure ◽  
Pial Artery ◽  
Anesthetized Dogs ◽  
Oxide Synthase

We examined the influence of nitric oxide (NO) on normal and collateral cerebral blood flow after occlusion of the middle cerebral artery (MCA). Effects of NG-nitro-l-arginine (nitroarginine), an inhibitor of NO synthase, were examined during normotension and hypotension (arterial pressure, 50 mm Hg) in 49 anesthetized dogs. Following a craniotomy, a branch of the MCA was cannulated, and collateral-dependent tissue was identified using the shadow-flow technique. Regional cerebral blood flow was measured with microspheres, and pial artery pressure was measured with a micropipette. Intravenous nitroarginine reduced blood flow to normal cerebrum by approximately 40% (p < 0.05) during normotension and hypotension, with aortic pressure maintained constant after nitroarginine administration. Injection of nitroarginine during hypotension, without control of pressor effects, increased aortic and pial artery pressure approximately twofold. Concurrently, blood flow to normal cerebrum decreased (p < 0.05), while flow to collateral-dependent cerebrum increased (p < 0.05). Phenylephrine was infused during hypotension to increase arterial pressure to values similar to those achieved following nitroarginine. Blood flow to collateral-dependent cerebrum increased (p < 0.05), but flow to normal cerebrum was not altered during infusion of phenylephrine. Thus, inhibition of NO synthase during hypotension increases arterial pressure, decreases blood flow to normal cerebrum, and increases blood flow to collateral-dependent cerebrum. Phenylephrine also increases perfusion pressure and blood flow to collateral-dependent cerebrum, but in contrast to nitroarginine, it does not redistribute blood flow from normal cerebrum.

Hemodynamic effects of nitric oxide synthase inhibition before and after cardiac arrest in infant piglets

1998 ◽  
Vol 274 (4) ◽  
pp. H1378-H1385 ◽  
Author(s):  
Charles L. Schleien ◽  
John W. Kuluz ◽  
Barry Gelman
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cardiac Arrest ◽  
Cerebral Blood Flow ◽  
Cerebral Metabolism ◽  
Lactate Production ◽  
No Synthase ◽  
Metabolic Effects ◽  
Successful Resuscitation ◽  
Baseline Levels

Using infant piglets, we studied the effects of nonspecific inhibition of nitric oxide (NO) synthase by N G-nitro-l-arginine methyl ester (l-NAME; 3 mg/kg) on vascular pressures, regional blood flow, and cerebral metabolism before 8 min of cardiac arrest, during 6 min of cardiopulmonary resuscitation (CPR), and at 10 and 60 min of reperfusion. We tested the hypotheses that nonspecific NO synthase inhibition 1) will attenuate early postreperfusion hyperemia while still allowing for successful resuscitation after cardiac arrest, 2) will allow for normalization of blood flow to the kidneys and intestines after cardiac arrest, and 3) will maintain cerebral metabolism in the face of altered cerebral blood flow after reperfusion. Before cardiac arrest, l-NAME increased vascular pressures and cardiac output and decreased blood flow to brain (by 18%), heart (by 36%), kidney (by 46%), and intestine (by 52%) compared with placebo. During CPR, myocardial flow was maintained in all groups to successfully resuscitate 24 of 28 animals [ P value not significant (NS)]. Significantly,l-NAME attenuated postresuscitation hyperemia in cerebellum, diencephalon, anterior cerebral, and anterior-middle watershed cortical brain regions and to the heart. Likewise, cerebral metabolic rates of glucose (CMRGluc) and of lactate production (CMRLac) were not elevated at 10 min of reperfusion. These cerebral blood flow and metabolic effects were reversed byl-arginine. Flows returned to baseline levels by 60 min of reperfusion. Kidney and intestinal flow, however, remained depressed throughout reperfusion in all three groups. Thus nonspecific inhibition of NO synthase did not adversely affect the rate of resuscitation from cardiac arrest while attenuating cerebral and myocardial hyperemia. Even though CMRGluc and CMRLac early after resuscitation were decreased, they were maintained at baseline levels. This may be clinically advantageous in protecting the brain and heart from the damaging effects of hyperemia, such as blood-brain barrier disruption.

Coupling of cerebral blood flow to neuronal activation: role of adenosine and nitric oxide

1994 ◽  
Vol 267 (1) ◽  
pp. H296-H301 ◽  
Author(s):  
U. Dirnagl ◽  
K. Niwa ◽  
U. Lindauer ◽  
A. Villringer
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Receptor Antagonist ◽  
Barrel Cortex ◽  
No Synthase ◽  
Neuronal Activation ◽  
Whisker Stimulation ◽  
Relationship Of

We studied the role and relationship of the putative mediators of coupling of cerebral blood flow (CBF) and neuronal activation, adenosine (Ado) and nitric oxide (NO). Topical brain application over the whisker barrel cortex of anesthetized rats (n = 24) of the Ado receptor antagonist theophylline (Theo, 5 x 10(-5) M) for 30 min reduced the CBF response to deflection of the contralateral whiskers from 17.9 +/- 3.0% of baseline to 10.6 +/- 2.7% (P < 0.05). Coapplication of Theo (5 x 10(-5) M) and the NO synthase blocker N omega-nitro-L-arginine (L-NNA, 10(-3) M) for 30 min led to a further reduction in the CBF response to whisker stimulation to 7.5 +/- 1.3% (P < 0.05 compared with Theo alone). The CBF effect of sodium nitroprusside (10(-5) M) was not affected by Theo-L-NNA coapplication (122 +/- 25 vs. 140 +/- 25%, n = 5). Application of adenosine deaminase (1 U/ml, n = 5) reduced the CBF response to whisker stimulation from 18.2 +/- 0.7 to 10.7 +/- 1.9% (P < 0.05). Superfusion of L-NNA (10(-3) M, 30 min, n = 7) attenuated the CBF response to application of Ado (10(-4) M) from 39.4 +/- 10.4 to 22.9 +/- 10.5% (P < 0.05). N omega-nitro-D-arginine did not affect the CBF response to Ado (n = 5). We conclude that 1) Ado is involved in coupling of CBF to neuronal activation, 2) NO is involved in this response as well, and 3) there is an interaction between the vasodilator pathways of Ado and NO.

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.

l-Citrulline conversion tol-arginine in sphenopalatine ganglia and cerebral perivascular nerves in the pig

1997 ◽  
Vol 273 (5) ◽  
pp. H2192-H2199 ◽  
Author(s):  
J. G. Yu ◽  
T. Ishine ◽  
T. Kimura ◽  
W. E. O’Brien ◽  
T. J. F. Lee
Keyword(s):  
Nitric Oxide ◽  
Cerebral Arteries ◽  
Neuronal Cell ◽  
Histochemical Staining ◽  
Nerve Fibers ◽  
Neuronal Cell Bodies ◽  
Nos Inhibitors ◽  
Perivascular Nerves ◽  
Almost All

The presence of nitric oxide synthase (NOS), argininosuccinate synthetase (ASS), and argininosuccinate lyase (ASL) and their coexistence with NADPH-diaphorase (NADPHd), a marker for NOS, in the porcine sphenopalatine ganglia (SPG), pial veins, and the anterior cerebral arteries was examined using immunohistochemical and histochemical staining techniques. NOS-immunoreactive (I), ASS-I, and ASL-I fibers were found in pial veins and the anterior cerebral arteries. NOS, ASS, and ASL immunoreactivities were also found in neuronal cell bodies in the SPG. Almost all neuronal cell bodies in the SPG and nerve fibers in pial veins and the anterior cerebral arteries that were reactive to ASS, ASL, and NOS were also stained positively with NADPHd, suggesting that ASS, ASL, and NOS were colocalized in the same neurons in the SPG and perivascular nerves. With the use of in vitro tissue bath techniques,l-citrulline but notd-citrulline reversed inhibition of neurogenic vasodilation in isolated porcine pial veins produced by NOS inhibitors such as N G-nitro-l-arginine methyl ester. In the presence of l-aspartate,l-arginine was synthesized froml-citrulline in homogenates of SPG and endothelium-denuded cerebral arteries and pial veins. These results provide evidence indicating that perivascular nerves in pial veins like cerebral arteries can convertl-citrulline tol-arginine for synthesizing nitric oxide. The conversion is most likely via an argininosuccinate pathway.

Hypoxia, alpha 2-adrenergic, and nitric oxide-dependent interactions on canine cerebral blood flow

1994 ◽  
Vol 266 (2) ◽  
pp. H476-H482 ◽  
Author(s):  
R. W. McPherson ◽  
R. C. Koehler ◽  
R. J. Traystman
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Methyl Ester ◽  
No Synthase ◽  
Hypoxic Hypoxia ◽  
Control Group ◽  
O2 Transport ◽  
Anesthetized Dogs

We tested the hypothesis that NO synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) and alpha 2-adrenoreceptor stimulation with dexmedetomidine (Dex) decreases the cerebral blood flow (CBF) response to hypoxia. In isoflurane-anesthetized dogs, CBF was measured during two episodes of hypoxic hypoxia. In a control group (n = 6), CBF increased similarly from 83 +/- 4 to 210 +/- 30 ml.min-1 x 100 g-1 and from 88 +/- 7 to 205 +/- 27 (+/- SE) ml.min-1 x 100 g-1 during two hypoxic episodes. In a second group (n = 6), hypoxia increased CBF from 88 +/- 15 to 204 +/- 38 ml.min-1 x 100 g-1. Dex (10 micrograms/kg i.v.) reduced normoxic CBF to 54 +/- 8 ml.min-1 x 100 g-1, and subsequent hypoxia increased CBF to 97 +/- 14 ml.min-1 x 100 g-1. In a third group pretreated with L-NAME (40 mg/kg i.v.) 1 h before anesthesia (n = 6), normoxic CBF was less than in the control group (52 +/- 2 vs. 83 +/- 4 ml.min-1 x 100 g-1). Hypoxia increased CBF to 177 +/- 13 ml.min-1 x 100 g-1. Dex after L-NAME further decreased normoxic CBF to 37 +/- 3 ml.min-1 x 100 g-1, and subsequent hypoxia increased CBF to 106 +/- 18 ml.min-1 x 100 g-1. Dex, L-NAME, and Dex + L-NAME each reduced cerebral O2 transport (CBF x arterial O2 content) during normoxia, but the increase in CBF during hypoxia was sufficient to prevent further decreases in O2 transport. Thus the response to hypoxia remained proportional to normoxic levels of CBF.(ABSTRACT TRUNCATED AT 250 WORDS)

Innervation of endoneurial microvessels in human sural nerve

1992 ◽  
Vol 50 (1) ◽  
pp. 920-921
Author(s):  
John L. Beggs ◽  
Peter C. Johnson ◽  
Astrid G. Olafsen ◽  
C. Jane Watkins
Keyword(s):  
Blood Flow ◽  
Blood Vessels ◽  
Blood Supply ◽  
Peripheral Nerves ◽  
Sural Nerve ◽  
Nerve Fibers ◽  
Arterial Supply ◽  
Autonomic Nerve ◽  
Vasa Nervorum ◽  
Endoneurial Blood Flow

The blood supply (vasa nervorum) to peripheral nerves is composed of an interconnected dual circulation. The endoneurium of nerve fascicles is maintained by the intrinsic circulation which is composed of microvessels primarily of capillary caliber. Transperineurial arterioles link the intrinsic circulation with the extrinsic arterial supply located in the epineurium. Blood flow in the vasa nervorum is neurogenically influenced (1,2). Although a recent hypothesis proposes that endoneurial blood flow is controlled by the action of autonomic nerve fibers associated with epineurial arterioles (2), our recent studies (3) show that in addition to epineurial arterioles other segments of the vasa nervorum are also innervated. In this study, we examine blood vessels of the endoneurium for possible innervation.

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