Inhibition of spinal afferent nerve-mediated gastric hyperemia by nicotine: role of ganglionic blockade

1993 ◽  
Vol 264 (4) ◽  
pp. H1087-H1092
Author(s):  
F. W. Leung
Keyword(s):  
Blood Flow ◽  
Afferent Nerve ◽  
Gastric Blood Flow ◽  
Doppler Flowmetry ◽  
Afferent Nerves ◽  
Vasodilatory Effect ◽  
Blocking Property ◽  
Intravenous Nicotine ◽  
Ganglionic Blocking ◽  
Stimulation Of

The hypothesis that intravenous nicotine modulates gastric spinal afferent nerve function by its ganglionic-blocking property is tested. Stimulation of the gastric spinal afferent nerves in anesthetized rats is accomplished by intragastric capsaicin irrigation. Gastric blood flow is monitored by laser-Doppler flowmetry. The increase in gastric blood flow during intragastric capsaicin irrigation is significantly reduced by 4 and 40 micrograms.kg-1.min-1 of intravenous nicotine. The inhibition appears to be specific for the spinal afferent nerves as the increase in gastric blood flow induced by electrical stimulation of the vagal afferent nerves is unaltered by these doses of intravenous nicotine. A ganglionic-blocking dose (10 mg/kg) of intraperitoneal hexamethonium also significantly attenuates the gastric vasodilatory effect of intragastric capsaicin. Intravenous nicotine (40 micrograms.kg-1.min-1) combined with intraperitoneal hexamethonium (10 mg/kg) completely abolishes the gastric vasodilatory effect of intragastric capsaicin. These data suggest that intravenous nicotine offers a specific inhibition of the gastric spinal afferent nerve-mediated hyperemia, possibly as a consequence of its ganglionic-blocking property.

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.

scholarly journals Nervous rhythm arising from rivalry of antagonistic reflexes: Reflex stepping as outcome of double reciprocal innervation

1913 ◽  
Vol 86 (587) ◽  
pp. 233-261 ◽  
Keyword(s):  
Afferent Nerve ◽  
The Other ◽  
Present Communication ◽  
Simultaneous Stimulation ◽  
Afferent Nerves ◽  
Wide Range ◽  
Contralateral Muscle ◽  
Stimulation Of

The observations with which the present communication deals were met with in experiments continuing those on reciprocal innervation of symmetrical muscles. In my previous paper on that subject it had been reported that in regard to symmetrical extensors of the knee the ratio borne by intensity of the ipsilateral inhibition to the contralateral excitation is such that with equal stimuli to right and left symmetrical afferent nerves there is inhibitory suppression of contraction in both the muscles. In other words, under double reciprocal innervation the ipsilateral inhibition by each nerve completely overcomes the contralateral excitation of the other. It was shown that this mutual suppression holds over a wide range of the scale of intensities of stimulation. It was also shown that with quite weak stimuli a simultaneous stimulation of both nerves, stimuli being equal in intensity, often results in concurrent contraction of both muscles. Indeed, with quite weak stimuli, the effect of stimulation of each afferent nerve by itself is, in the decerebrate preparation, usually contraction of the ipsilateral as well as of the contralateral muscle. This being so, it is evident that at some point in the scale of intensities of stimulation there should be a place below which contralateral excitation is stronger than ipsilateral inhibition, whereas above it ipsilateral inhibition is stronger than contralateral excitation.

Interaction between primary afferent nerves in the elicitation of reflex swallowing

1980 ◽  
Vol 239 (5) ◽  
pp. R407-R414 ◽  
Author(s):  
A. Weerasuriya ◽  
D. Bieger ◽  
C. H. Hockman
Keyword(s):  
Contralateral Side ◽  
Afferent Nerve ◽  
Reflex Response ◽  
Solitary Tract ◽  
Primary Afferent ◽  
Afferent Nerves ◽  
Primary Afferent Nerves ◽  
Adult Cats ◽  
Primary Afferent Nerve ◽  
Stimulation Of

In adult cats anesthetized with urethan, a number of observations were made that support the concept that some control over the rate of reflexly induced swallowing occurs in the intermediate network at the level of the nucleus of the solitary tract. It was shown that different nerves, e.g., the two superior laryngeal and glossopharyngeal nerves, when activated in sequence interact in such a manner as to facilitate reflex swallowing. It was also shown that the decrement in the reflex response observed to continuous stimulation of a primary afferent nerve, e.g., one superior laryngeal, can be reversed by switching the stimulation to another nerve either on the same or contralateral side. And finally, following discrete medullary lesions, it was observed that that portion of the nucleus of the solitary tract located 2 mm or more rostral to the rostralmost point of the dorsal medial sulcus appears to contain an integral component of the intermediate network that governs reflexly induced swallowing, whereas lesions restricted to the ventrolateral portion of the nucleus of the solitary tract have no effect on the reflex response.

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.

Histamine is not involved in pentagastrin-induced gastric mucosal vasodilation in the rat

1994 ◽  
Vol 266 (1) ◽  
pp. G55-G61
Author(s):  
L. Holm ◽  
A. Jagare
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Receptor Antagonist ◽  
Vascular Resistance ◽  
Acid Output ◽  
Gastric Blood Flow ◽  
H2 Receptor Antagonist ◽  
Doppler Flowmetry ◽  
Blood Flow Reduction ◽  
H1 Receptor Antagonist

The effects of histamine and its role in the gastric mucosal vascular response to pentagastrin were studied in anesthetized rats. Blood flow was measured with laser-Doppler flowmetry (LDF) and with red blood cell velocity measurements in the superficial mucosal microcirculation. Acid secretion was determined by titration of the saline covering 0.8 cm2 of the fundic mucosa. Pentagastrin (40 micrograms.kg-1 x h-1 i.v. induced a blood flow increase (+40%), which was not significantly altered by ranitidine (H2-receptor antagonist, 2 mg/kg iv bolus), whereas the stimulated acid output was abolished. In experiments in which the H1-receptor antagonist pyrilamine (2.5 mg/kg i.v. bolus) was administered before pentagastrin stimulation, pentagastrin still increased blood flow by approximately 60%. Intravenous histamine (4 mg.kg-1 x h-1) induced a blood flow reduction in parallel with the reduction in blood pressure (vascular resistance unchanged). Even during intra-arterial (thoracic aorta) infusion of histamine (1 or 4 mg.kg-1 x h-1), gastric vascular resistance was unchanged. In animals pretreated with pyrilamine, histamine (4 mg.kg-1 x h-1 i.v.) left the gastric blood flow and blood pressure unchanged. These results indicate that the pentagastrin-induced increase in the rat gastric blood flow is not dependent on histamine.

Assessment of Gastric Blood Flow with Laser Doppler Flowmetry

1988 ◽  
Vol 23 (10) ◽  
pp. 1203-1210 ◽  
Author(s):  
H. Ahn ◽  
L. E. Ivarsson ◽  
K. Johansson ◽  
J. Lindhagen ◽  
O. Lundgren
Keyword(s):  
Blood Flow ◽  
Laser Doppler Flowmetry ◽  
Laser Doppler ◽  
Gastric Blood Flow ◽  
Doppler Flowmetry

Fos induction in rat brain neurons after stimulation of the hepatoportal Na-sensitive mechanism

1997 ◽  
Vol 272 (3) ◽  
pp. R913-R923 ◽  
Author(s):  
H. Morita ◽  
Y. Yamashita ◽  
Y. Nishida ◽  
M. Tokuda ◽  
O. Hatase ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Area Postrema ◽  
Vena Cava ◽  
Plasma Osmolality ◽  
Systemic Circulation ◽  
Afferent Nerve ◽  
Hypothalamic Nucleus ◽  
Nerve Activity ◽  
Afferent Nerves ◽  
Stimulation Of

Responses of hepatic afferent nerves to intraportal bolus injection of hypertonic solutions were examined in anesthetized rats. Hepatic afferent nerve activity increased in response to an intraportal injection of 0.75 M NaCl or NaHCO3 but did not respond to a similar injection of 1.5 M mannitol, 0.75 M LiCl, or 0.15 M NaCl, implying that nerves in the hepatoportal area are sensitive to increases in Na concentrations and that this leads to stimulation of hepatic afferent nerve activity. To study central activation in response to stimulation of the hepatic Na-sensitive mechanism, c-fos induction was monitored. After electrical stimulation of hepatic afferent nerves, neurons containing Fos-like immunoreactivity (Fos-li) were found in the area postrema, nucleus of the solitary tract, paraventricular hypothalamic nucleus, and supraoptic nucleus at 90 min after stimulation. Induction of Fos-li was also studied after simultaneous infusion of 0.45 M NaCl into the portal vein and distilled water into the inferior vena cava in conscious rats so as to keep the total amount of solution introduced into the systemic circulation isotonic, thus avoiding changes in mean arterial pressure, plasma osmolality, and plasma NaCl concentrations. Fos-li-containing neurons were found in the same regions in which they were found after electrical stimulation. However, few, if any, Fos-li-containing cells were found if the rats were hepatically denervated or if they received an intraportal infusion of hypertonic LiCl or mannitol. These data provide evidence for involvement of the brain stem and forebrain structures in NaCl regulatory functions induced by stimulation of the hepatoportal Na-sensitive mechanism. However, stimulation of the hepatoportal osmosensitive mechanism does not activate these central structures.

Thyroidal vascular responsiveness to parasympathetic stimulation is increased in hyperthyroidism

1993 ◽  
Vol 264 (3) ◽  
pp. E398-E402 ◽  
Author(s):  
M. Dey ◽  
M. Michalkiewicz ◽  
L. J. Huffman ◽  
G. A. Hedge
Keyword(s):  
Blood Flow ◽  
Sympathetic Nerves ◽  
Treated Group ◽  
Receptor Activation ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Pretreated Group ◽  
Vascular Responsiveness ◽  
Stimulation Of

It has been suggested that thyroid blood flow (TBF) is regulated by both parasympathetic and sympathetic nerves. Because thyroxine (T4) pretreatment increases the sensitivity of the thyroid to the effects of thyrotropin, the present study was conducted to determine whether T4 pretreatment can also sensitize the thyroid to the effect of parasympathetic stimulation on TBF. Untreated or T4-pretreated rats were anesthetized, and both superior laryngeal nerves (SLN) were transected. TBF was continuously monitored by laser Doppler flowmetry (LDF), and thyroid vascular conductance (TVC) was also determined by the microsphere technique. Stimulation of the SLN had no effect on TBF or TVC in untreated rats when measured by LDF or microspheres. In contrast, stimulation of the SLN after T4 pretreatment increased TBF by 65 +/- 21% over prestimulus levels as measured by LDF. TVC was also increased significantly (P < 0.05) in these rats compared with TVC in a nonstimulated T4-pretreated group. To examine the role of muscarinic receptor activation in the mediation of these increases in TVC, T4 pretreated rats were given saline or atropine prior to SLN transection. Stimulation of the SLN in T4-pretreated rats given saline increased TVC significantly (P < 0.05) compared with TVC in the nonstimulated saline-treated or atropine-treated group. In contrast, TVC in the stimulated group given saline was not significantly different from the group that was stimulated after atropine injection. Our results suggest that the thyroidal vascular responsiveness to parasympathetic stimulation is increased in the hyperthyroid condition.

Noxious Chemical Stimulation of Rat Facial Mucosa Increases Intracranial Blood Flow Through a Trigemino-Parasympathetic Reflex — An Experimental Model for Vascular Dysfunctions in Cluster Headache

Cephalalgia ◽  
2004 ◽  
Vol 24 (3) ◽  
pp. 206-214 ◽  
Author(s):  
R Gottselig ◽  
K Messlinger
Keyword(s):  
Blood Flow ◽  
Cluster Headache ◽  
Experimental Model ◽  
Dura Mater ◽  
Chemical Stimulation ◽  
Noxious Stimulation ◽  
Doppler Flowmetry ◽  
Release Of Acetylcholine ◽  
Flow Through ◽  
Stimulation Of

Cluster headache is characterized by typical autonomic dysfunctions including facial and intracranial vascular disturbances. Both the trigeminal and the cranial parasympathetic systems may be involved in mediating these dysfunctions. An experimental model was developed in the rat to measure changes in lacrimation and intracranial blood flow following noxious chemical stimulation of facial mucosa. Blood flow was monitored in arteries of the exposed cranial dura mater and the parietal cortex using laser Doppler flowmetry. Capsaicin (0.01-1 mM) applied to oral or nasal mucosa induced increases in dural and cortical blood flow and provoked lacrimation. These responses were blocked by systemic pre-administration of hexamethonium chloride (20 mg/kg). The evoked increases in dural blood flow were also abolished by topical pre-administration of atropine (1 mM) and [Lys1, Pro2,5, Arg3,4, Tyr6]-VIP (0.1 mM), a vasoactive intestinal polypeptide (VIP) antagonist, onto the exposed dura mater. We conclude that noxious stimulation of facial mucosa increases intracranial blood flow and lacrimation via a trigemino-parasympathetic reflex. The blood flow responses seem to be mediated by the release of acetylcholine and VIP within the meninges. Similar mechanisms may be involved in the pathogenesis of cluster headache.

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