Fade of the responses of the isolated, blood-perfused dog atrium to cholinergic interventions

1984 ◽  
Vol 62 (5) ◽  
pp. 524-530 ◽  
Author(s):  
Yasuyuki Furukawa ◽  
Paul Martin ◽  
Matthew N. Levy
Keyword(s):  
Nerve Stimulation ◽  
Time Course ◽  
Acetylcholine Release ◽  
Neural Stimulation ◽  
Inotropic Response ◽  
Progressive Reduction ◽  
Parasympathetic Nerve ◽  
Cardiac Responses ◽  
Inotropic Responses ◽  
Stimulation Voltage

In the isolated, blood-perfused, canine right atrium, intramural parasympathetic nerve stimulation and intra-arterial infusions of acetylcholine induced substantial negative chronotropic and inotropic responses. The responses to parasympathetic stimulation reached their maximum values quickly, and then usually faded back toward control levels over the next 1 or 2 min of stimulation. The fade of the responses at high stimulation frequencies (≥30 Hz) was significantly greater than that at lower frequencies. The inotropic responses to acetylcholine infusion (1 μg/min) faded slightly but significantly, whereas the chronotropic responses did not fade at all. These results suggest that the fade of the cardiac responses to parasympathetic stimulation is mainly ascribable to a progressive reduction in the rate of acetylcholine release from the nerve endings, especially at higher stimulation frequencies. The fade of the inotropic responses was more pronounced and had a longer time course than that of the chronotropic responses. Furthermore, the fade of the inotropic responses diminished significantly as the response magnitude was augmented by an increase in stimulation voltage. Conversely, the fade of chronotropic responses was not significantly affected by this intervention. These differences in the inotropic and chronotropic responses to neural stimulation, and the occurrence of a slight fade of the inotropic response to acetylcholine infusion, suggest that in addition to the predominant prejunctional mechanism, a postjunctional phenomenon may also be partly responsible for the fade of the inotropic response to cholinergic interventions.

Attenuation of the responses to repeated cholinergic interventions in the isolated dog atrium

1986 ◽  
Vol 64 (2) ◽  
pp. 206-212 ◽  
Author(s):  
Yasuyuki Furukawa ◽  
Paul Martin
Keyword(s):  
Nerve Stimulation ◽  
Rest Period ◽  
Nerve Fibers ◽  
Maximal Amplitude ◽  
Parasympathetic Nerve ◽  
Chronotropic Response ◽  
Cardiac Responses ◽  
Frequency Stimulation ◽  
Inotropic Responses ◽  
Stimulation Of

In the isolated, blood-perfused canine right atrium, which was pretreated with propranolol, negative chronotropic and inotropic responses were evoked by stimulation of the intramural parasympathetic nerve fibers or by intra-arterial infusion of acetylcholine (ACh). Successive cholinergic interventions were applied; first, a conditioning intervention for 2 min was given, then this was followed by a test intervention for 4 min. The two interventions were separated by a rest period that varied from 15 to 240 s. The cardiac responses to the conditioning parasympathetic nerve stimulation quickly reached maximum levels, and then they "faded" or progressively diminished back toward the control level. The inotropic responses to the conditioning infusion of ACh (1 μg/min) faded slightly but the chronotropic response did not. After the rest period, the test nerve stimulation evoked responses that also gradually faded with time. The maximal amplitude of the responses to the test simuli were less than those to the conditioning stimuli. This reduction in the maximal amplitude of the cardiac responses to the test stimuli was more pronounced with high frequency stimulation (30 Hz) than with low frequency stimulation (5 Hz). The decrement was also more pronounced the shorter the rest period, and it was greater at earlier times after beginning the stimulation. Conversely, the maximal cardiac responses to test infusions of ACh were not appreciably less than the responses to the conditioning infusions. We conclude, therefore, that the diminution of the cardiac responses to the second test stimulation of the parasympathetic nerve fibers was mainly ascribable to a prejunctional rather than to a postjunctional mechanism.

Effects of Ca2+ channel antagonists on nerve stimulation-induced and ischemia-induced myocardial interstitial acetylcholine release in cats

2006 ◽  
Vol 291 (5) ◽  
pp. H2187-H2191 ◽  
Author(s):  
Toru Kawada ◽  
Toji Yamazaki ◽  
Tsuyoshi Akiyama ◽  
Kazunori Uemura ◽  
Atsunori Kamiya ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Acetylcholine Release ◽  
Local Administration ◽  
Ach Release ◽  
Parasympathetic Nerve ◽  
Nonselective Cation Channels ◽  
Voltage Dependent ◽  
Stretch Activated Channels ◽  
Postganglionic Nerve

Although an axoplasmic Ca2+ increase is associated with an exocytotic acetylcholine (ACh) release from the parasympathetic postganglionic nerve endings, the role of voltage-dependent Ca2+ channels in ACh release in the mammalian cardiac parasympathetic nerve is not clearly understood. Using a cardiac microdialysis technique, we examined the effects of Ca2+ channel antagonists on vagal nerve stimulation- and ischemia-induced myocardial interstitial ACh releases in anesthetized cats. The vagal stimulation-induced ACh release [22.4 nM (SD 10.6), n = 7] was significantly attenuated by local administration of an N-type Ca2+ channel antagonist ω-conotoxin GVIA [11.7 nM (SD 5.8), n = 7, P = 0.0054], or a P/Q-type Ca2+ channel antagonist ω-conotoxin MVIIC [3.8 nM (SD 2.3), n = 6, P = 0.0002] but not by local administration of an L-type Ca2+ channel antagonist verapamil [23.5 nM (SD 6.0), n = 5, P = 0.758]. The ischemia-induced myocardial interstitial ACh release [15.0 nM (SD 8.3), n = 8] was not attenuated by local administration of the L-, N-, or P/Q-type Ca2+ channel antagonists, by inhibition of Na+/Ca2+ exchange, or by blockade of inositol 1,4,5-trisphosphate [Ins( 1 , 4 , 5 )P3] receptor but was significantly suppressed by local administration of gadolinium [2.8 nM (SD 2.6), n = 6, P = 0.0283]. In conclusion, stimulation-induced ACh release from the cardiac postganglionic nerves depends on the N- and P/Q-type Ca2+ channels (with a dominance of P/Q-type) but probably not on the L-type Ca2+ channels in cats. In contrast, ischemia-induced ACh release depends on nonselective cation channels or cation-selective stretch activated channels but not on L-, N-, or P/Q type Ca2+ channels, Na+/Ca2+ exchange, or Ins( 1 , 4 , 5 )P3 receptor-mediated pathway.

Presynaptic modulation of acetylcholine release from cardiac parasympathetic neurons

1985 ◽  
Vol 248 (1) ◽  
pp. H33-H39 ◽  
Author(s):  
G. T. Wetzel ◽  
J. H. Brown
Keyword(s):  
Receptor Antagonist ◽  
Adrenergic Receptor ◽  
Acetylcholine Release ◽  
Electrical Field Stimulation ◽  
Inhibitory Effect ◽  
Muscarinic Agonist ◽  
Parasympathetic Nerve ◽  
Presynaptic Modulation ◽  
Rat Atria ◽  
Alpha Adrenergic Receptors

Acetylcholine can be released from parasympathetic nerve endings in rat atria by 57 mM K+ depolarization or by electrical field stimulation. We have studied the presynaptic modulation of [3H]acetylcholine release from superfused rat atria prelabeled with [3H]choline. Exogenous acetylcholine and the specific muscarinic agonist oxotremorine inhibit the stimulation-induced overflow of [3H]acetylcholine into the superfusion medium. The half-maximal inhibitory concentration (IC50) of oxotremorine is 0.3 microM. The cholinesterase inhibitor neostigmine also decreases K+-stimulated [3H]acetylcholine overflow, whereas the muscarinic antagonist atropine enhances the overflow of [3H]acetylcholine. These data suggest that acetylcholine release in atria is modulated through negative feedback by the endogenous transmitter. The sympathetic adrenergic neurotransmitter norepinephrine and the neurohormone epinephrine also inhibit the overflow of [3H]acetylcholine by approximately 60%. The IC50 values for the inhibitory effects of these catecholamines are 6.3 and 2.2 microM, respectively. The inhibitory effect of norepinephrine is blocked by the alpha-adrenergic receptor antagonist yohimbine but not by the beta-adrenergic receptor antagonist propranolol. We suggest that presynaptic muscarinic and alpha-adrenergic receptors participate in the physiological and pharmacological control of cardiac parasympathetic activity.

Electrical properties and innervation of fibers in the orbital layer of rat extraocular muscles

1989 ◽  
Vol 61 (1) ◽  
pp. 116-125 ◽  
Author(s):  
J. Jacoby ◽  
D. J. Chiarandini ◽  
E. Stefani
Keyword(s):  
Electrical Properties ◽  
Nerve Stimulation ◽  
Action Potentials ◽  
Time Course ◽  
Lucifer Yellow ◽  
Extraocular Muscles ◽  
Resting Potential ◽  
Inferior Rectus ◽  
End Plate ◽  
Orbital Layer

1. The inferior rectus muscle of rat, one of the extraocular muscles, contains two populations of multiply innervated fibers (MIFs): orbital MIFs, located in the orbital layer of the muscle and global MIFs, found in the global layer. The electrical properties and the responses to nerve stimulation of orbital MIFs were studied with single intracellular electrodes and compared with those of twitch fibers of the orbital layer, MIFs of the global layer, and tonic fibers of the frog. 2. About 90% of the orbital MIFs did not produce overshooting action potentials. In these fibers the characteristics and time course of the responses to nerve stimulation varied along the length of the fibers. Within 2 mm of the end-plate band of the muscle, the responses consisted of several small end-plate potentials (EPPs) and a nonovershooting spike. Distal to 2 mm, the responses in most fibers consisted of large and small EPPs with no spiking response. Some fibers produced very small spikes surmounted on large EPPs. 3. Overshooting action potentials were observed in approximately 10% of the orbital MIFs recorded between the end-plate band and 2 mm distal. The presence or absence of action potentials was not related to the magnitude of the resting potential of the fibers. 4. The threshold of nerve stimulated responses in orbital MIFs was the same as that in orbital twitch fibers. A large number of orbital MIFs had latencies equal to those for the orbital twitch fibers recorded at the same distance from the end-plate band, but the average latency was greater in the MIFs. The latency of orbital MIFs was about one-half of that for the MIFs of the global layer. The values for the effective resistance and membrane time constant of orbital MIFs fell between those for orbital twitch fibers on the one hand, and global MIFs and frog tonic fibers on the other. 5. In order to compare electrical properties with innervation patterns, fibers identified electrophysiologically as orbital MIFs were injected with the fluorescent dye Lucifer yellow and then traced in Epon-embedded, serial transverse sections. In addition to numerous superficial endings distributed along the fibers, a single "en plaque" ending was also found in the end-plate band that resembled the end plates of the adjacent orbital twitch fibers. 6. From these results we conclude that the electrical activity of orbital MIFs varies along the length of the fibers.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Rehabilitation of a Completely Edentulous Patient using TENS to record Functional Borders and Cheek Plumpers for Esthetics

2013 ◽  
Vol 3 (2) ◽  
pp. 78-82
Author(s):  
Shilpa Kulkarni ◽  
Nilesh Shrikant Bulbule ◽  
Jay Shah ◽  
Dilip Kakade
Keyword(s):  
Nerve Stimulation ◽  
Cranial Nerves ◽  
Neural Stimulation ◽  
Psychological Effect ◽  
Complete Denture ◽  
Edentulous Patient ◽  
Transcutaneous Electric Nerve Stimulation ◽  
Facial Disfigurement ◽  
Electric Nerve Stimulation ◽  
Actual Loss

ABSTRACT The facial disfigurement associated with the loss of teeth has greater psychological effect on the patient than the actual loss of teeth. Presented herein, is a novel, precise and accurate technique of performing border molding using transcutaneous electric nerve stimulation (TENS). The electronic stimulator is programed to deliver precisely controlled, uniform stimuli transmitted by transcutaneous electrical neural stimulation through fifth and seventh cranial nerves.   Plumping the cheeks by using cheek plumpers attached to the conventional complete denture using magnets was also done. The greatest advantage lies in the fact that they are completely detachable. How to cite this article Bulbule NS, Shah J, Kulkarni S, Kakade D. Rehabilitation of a Completely Edentulous Patient using TENS to record Functional Borders and Cheek Plumpers for Esthetics. Int J Prosthodont Restor Dent 2013;3(2):78-82.

scholarly journals Stretch Reflex Latencies in Spastic Hemiparetic Subjects are Prolonged After Transcutaneous Electrical Nerve Stimulation

1993 ◽  
Vol 20 (2) ◽  
pp. 97-106 ◽  
Author(s):  
Christina W.Y. Hui-Chan ◽  
Mindy F. Levin
Keyword(s):  
Nerve Stimulation ◽  
Transcutaneous Electrical Nerve Stimulation ◽  
Stretch Reflex ◽  
Time Course ◽  
Dorsal Column ◽  
Electrical Nerve Stimulation ◽  
Reflex Excitability ◽  
Reflex Threshold ◽  
Repetitive Electrical Stimulation

ABSTRACT:Low-intensity repetitive electrical stimulation such as dorsal column and transcutaneous electrical nerve stimulation (TENS) reportedly decreases spasticity and improves voluntary motor control. However, the mechanisms mediating these effects are unclear. Recent findings suggest that spasticity may be characterized more appropriately by a decrease in the stretch reflex threshold than by an increase in gain. Our objectives were: (1) to examine possible changes in stretch reflex excitability following 45 min of TENS, (2) to map out the time course of possible post-stimulation effects via both latency and magnitude (amplitude or area) measurements, and (3) to determine the role of segmental versus non-segmental mechanisms involved in mediating these changes. The effects of 45 min of segmentally and heterosegmentally applied TENS on lower limb reflexes in ten spastic hemiparetic subjects were contrasted with those resulting from placebo stimulation. We found that both segmentally and heterosegmentally applied TENS caused an immediate increase in soleus H reflex latencies that was evident for up to 60 minutes post-stimulation in over 75% of the subjects. Similar increases for up to 60 and 40 minutes post-stimulation was noted for the stretch reflex latencies in 50% and 67% of the subjects respectively for segmental and heterosegmental stimulation. These results suggested that manipulation of segmental and heterosegmental afférents for 45 min may lead to a decrease of the otherwise augmented stretch reflex excitability accompanying hemiparetic spasticity.

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