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.

scholarly journals Stimulation of C1 Area Neurons Globally Increases Regional Cerebral Blood Flow but Not Metabolism

1992 ◽  
Vol 12 (5) ◽  
pp. 844-855 ◽  
Author(s):  
Mark D. Underwood ◽  
Costantino Iadecola ◽  
Alan Sved ◽  
D. J. Reis
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Electrical Stimulation ◽  
Regional Cerebral Blood Flow ◽  
Ventrolateral Medulla ◽  
Medial Longitudinal Fasciculus ◽  
Neural Pathways ◽  
Regional Cerebral Blood ◽  
The Brain ◽  
Stimulation Of

We examined the effects of electrical and chemical stimulation of the C1 area of the rostral ventrolateral medulla (RVL) on regional cerebral blood flow (rCBF) and regional cerebral glucose utilization (rCGU) in anesthetized (chloralose), paralyzed (curare) and ventilated rats. rCBF and rCGU were measured using 14C-iodoantipyrine (IAP) and 14C-deoxyglucose (2-DG), respectively, as indicators, with bilateral regional dissection of 11 brain regions. Electrical stimulation of the RVL elicited increases in arterial pressure (AP), heart rate (HR) and plasma concentration of epinephrine (EPI) and norepinephrine (NE). In addition, stimulation of the RVL, but not the adjacent medial longitudinal fasciculus, with AP maintained, increased rCBF ( p < 0.05, n = 6), but not rCGU, bilaterally and symmetrically (134–169% of control) throughout the brain. Bilateral adrenalectomy abolished the increase in plasma EPI elicited by stimulation of the RVL but did not affect resting rCBF ( n = 5) or the elevation in rCBF elicited by RVL stimulation ( n = 5). Increases in rCBF elicited by RVL stimulation were also unaffected by acute transection of the superior cervical ganglion ( p > 0.05). Kainic acid (KA) microinjected into the RVL unilaterally ( n = 6) at a dose producing sustained elevation in AP (5 nmol in 100 nl), elicited changes in rCBF similar to those elicited by electrical stimulation. We conclude that neurons within the RVL, possibly those of the adrenergic C1 group, can initiate a global cerebrovasodilation, but not an increase in rCGU, largely through neural pathways intrinsic to the brain. The responses may represent activation of networks in RVL mediating circulatory adjustments to hypoxia.

scholarly journals Reductions in Focal Ischemic Infarctions Elicited from Cerebellar Fastigial Nucleus Do Not Result from Elevations in Cerebral Blood Flow

1993 ◽  
Vol 13 (6) ◽  
pp. 1020-1024 ◽  
Author(s):  
Seiji Yamamoto ◽  
Eugene V. Golanov ◽  
Donald J. Reis
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Parietal Cortex ◽  
Occipital Cortex ◽  
Fastigial Nucleus ◽  
Ventrolateral Medulla ◽  
Ischemic Lesion ◽  
Doppler Flowmetry ◽  
Mca Occlusion ◽  
Stimulation Of

To determine whether the neuroprotection elicited from electrical stimulation of the cerebellar fastigial nucleus (FN) is attributable to the elevation in regional cerebral blood flow (rCBF), we compared the effects in spontaneously hypertensive rats of stimulation of the rostral ventrolateral medulla (RVL) or FN on (a) a focal ischemic lesion produced by middle cerebral artery (MCA) occlusion, and (b) the changes in rCBF, measured by laser-Doppler flowmetry for 1.5 h, over regions corresponding to the ischemic core (parietal cortex), penumbra (occipital cortex), and nonischemic area (contralateral parietal cortex). Stimulation of FN for 1 h following MCA occlusion reduced infarction 24 h later by 52%. Stimulation of RVL was ineffective. Changes in the lesion were confined to the penumbra. FN and RVL stimulation comparably and significantly increased rCBF up to 185% in unlesioned animals. Following MCA occlusion, stimulation of FN or RVL and hypercarbia failed to elevate rCBF in the ischemic area but did so in the nonischemic area, even though in the same animals only FN stimulation reduced infarction 24 h later. We conclude that (a) the neuroprotection elicited from FN is not the result of an increase in rCBF but results from another mechanism, possibly reduction of metabolism in penumbra, and (b) the pathways mediating central neurogenic vasodilation and neuroprotection are, in part, distinct.

Mechanism underlying the response to vasodilator nerve stimulation in isolated dog and monkey cerebral arteries

1990 ◽  
Vol 259 (5) ◽  
pp. H1511-H1517 ◽  
Author(s):  
N. Toda ◽  
T. Okamura
Keyword(s):  
Nitric Oxide ◽  
Electrical Stimulation ◽  
Coronary Artery ◽  
Substance P ◽  
Nerve Stimulation ◽  
Cerebral Arteries ◽  
Inhibitory Effect ◽  
Synthesis Inhibitor ◽  
Transmural Stimulation ◽  
Stimulation Of

Relaxant responses to transmural electrical stimulation and nicotine of cerebral artery strips obtained from dogs and Japanese monkeys were abolished by tetrodotoxin and hexamethonium, respectively, and suppressed by treatment with NG-monomethyl-L-arginine (L-NMMA), a nitric oxide (NO) synthesis inhibitor. The inhibitory effect was prevented and reversed by L-arginine but not by D-arginine. The relaxations suppressed by L-NMMA were not increased by exogenously applied NO. Endothelium denudation did not alter the response to transmural stimulation and nicotine or the inhibitory effect of L-NMMA. D-NMMA did not inhibit the response to vasodilator nerve stimulation. Dog coronary artery relaxations caused by transmural stimulation were not inhibited by L-NMMA but reversed to contractions by propranolol. Relaxations caused by substance P of dog cerebral arteries treated with indomethacin were dependent on endothelium and inhibited by L-NMMA, whereas those by NO and nitroglycerin, endothelium-independent relaxations, were unaffected. It is concluded that chemical and electrical stimulation of vasodilator nerves relaxes dog and monkey cerebral arteries, possibly by a mediation of NO rather than a stimulating action of NO on the release of vasodilator transmitter. Endothelium-dependent relaxations by substance P of dog cerebral arteries appear to be mediated by NO.

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.

scholarly journals Preganglionic and Postganglionic Neurons Responsible for Cerebral Vasodilation Mediated by Nitric Oxide in Anesthetized Dogs

2000 ◽  
Vol 20 (4) ◽  
pp. 700-708 ◽  
Author(s):  
Noboru Toda ◽  
Kazuhide Ayajiki ◽  
Toshiki Tanaka ◽  
Tomio Okamura
Keyword(s):  
Nitric Oxide ◽  
Cerebral Arteries ◽  
Nasal Secretion ◽  
Intravenous Injections ◽  
Pterygopalatine Ganglion ◽  
Anesthetized Dogs ◽  
Greater Superficial Petrosal Nerve ◽  
Cerebral Vasodilation ◽  
Stimulation Of

The authors performed investigations to functionally determine the route of efferent innervation in vivo responsible for cerebral vasodilation mediated by nitric oxide (NO). In anesthetized beagles, electrical stimulation of the pterygopalatine ganglion vasodilated ipsilateral cerebral arteries such as the middle cerebral and posterior communicating arteries. Intravenous injections of NG-nitro-L-arginine (L-NA) markedly inhibited the response to nerve stimulation, and the effect was reversed by L-arginine. Stimulation of the proximal portion of the greater superficial petrosal nerve, upstream of the pterygopalatine ganglion, also produced cerebral vasodilation, which was abolished by L-NA and restored by L-arginine. Treatment with hexamethonium abolished the response to stimulation of the petrosal nerve but did not affect the response to pterygopalatine ganglion stimulation. Destruction of the pterygopalatine ganglion by cauterization constricted the cerebral arteries. Postganglionic denervation abolished the vasodilation, lacrimation, and nasal secretion induced on the ipsilateral side by stimulation of the pterygopalatine ganglion and petrosal nerve. The vasodilator response was suppressed by L-NA but unaffected by atropine, whereas lacrimation and nasal secretion were abolished solely by atropine. It is concluded that postganglionic neurons from the pterygopalatine ganglion play crucial roles in cerebral vasodilation mediated by NO from the nerve, and preganglionic neurons, possibly from the superior salivatory nucleus through the greater superficial petrosal nerve, innervate the pterygopalatine ganglion. Tonic discharges from the vasomotor center participate significantly in the maintenance of cerebral vasodilation.

Sign in / Sign up

Export Citation Format

Share Document