Effect of anesthetic on sympathetic responses evoked from cerebellar uvula in decerebrate cats

1992 ◽  
Vol 263 (4) ◽  
pp. H1285-H1291 ◽  
Author(s):  
J. F. Paton ◽  
M. P. Gilbey
Keyword(s):  
Time Course ◽  
Pressor Response ◽  
Conditioning Stimulus ◽  
Sympathetic Nerves ◽  
Decerebrate Cat ◽  
Test Response ◽  
Recovery From Anesthesia ◽  
Decerebrate Cats ◽  
Train Stimulation ◽  
Stimulation Of

The sympathetic mechanisms involved in the conversion of the tachycardia-pressor response evoked by electrical stimulation of the uvula (lobule IX of the posterior cerebellar cortex) in the unanesthetized decerebrate cat to a bradycardia-depressor response in the same, but anesthetized preparation, were investigated. Sympathoexcitation was produced in the inferior cardiac and renal sympathetic nerves in response to short train stimulation (2-5 pulses, 100-500 Hz) of the uvula in the unanesthetized decerebrate cat, and when paired stimuli (conditioning and test) were applied, the test-evoked potential in both nerves was similar to the response elicited by the conditioning stimulus. Anesthetic administered to these same animals caused the test response in both sympathetic nerves to be greatly decreased, yet the conditioning response was unchanged. The attenuation of the test response by the conditioning stimulus diminished during recovery from anesthesia. The recovery of the test response paralleled the time course of the return of the tachycardia-pressor effect evoked by long train stimulation of the uvula. It appears that anesthesia does not block the sympathoexcitatory response but acts to augment sympathoinhibitory processes associated with uvula stimulation; some possible mechanisms are discussed.

Reflex responses to stimulation of baroreceptors in the right subclavian artery

1964 ◽  
Vol 206 (4) ◽  
pp. 918-922 ◽  
Author(s):  
Hiromasa Okada
Keyword(s):  
Subclavian Artery ◽  
Impulse Activity ◽  
Sympathetic Nerves ◽  
Appreciable Change ◽  
Anesthetized Dogs ◽  
The Right ◽  
Carotid Arterial ◽  
Decerebrate Cats ◽  
Common Carotid Arteries ◽  
Stimulation Of

The effect of stimulation of the baroreceptors of the right subclavian artery upon the efferent impulse activity of the cardioregulatory and abdominal sympathetic nerves was investigated in decerebrate cats and anesthetized dogs. Increase in the pressure in the isolated and perfused right subclavian-carotid arterial segment diminished or abolished the impulse activity in the cardiac and abdominal sympathetic nerves. Simultaneously there was an increase of impulse activity in the cardiac vagus. No appreciable change of impulse activity in the long ciliary nerve was noticed. Impulse activity in the cardiac vagus nerve was found to be predominant during expiration both in decerebrated and anesthetized dogs with bilateral occlusion of the common carotid arteries.

Fastigial stimulation in rats releases adrenomedullary catecholamines

1983 ◽  
Vol 244 (6) ◽  
pp. R801-R809 ◽  
Author(s):  
A. Del Bo ◽  
C. A. Ross ◽  
J. F. Pardal ◽  
J. M. Saavedra ◽  
D. J. Reis
Keyword(s):  
Pressor Response ◽  
Plasma Catecholamines ◽  
Sympathetic Nerves ◽  
Relative Increase ◽  
Elevated Plasma ◽  
Response Curves ◽  
Stimulus Train ◽  
Basal Plasma ◽  
6 Hydroxydopamine ◽  
Stimulation Of

Electrical stimulation of the rostral fastigial nucleus (FN) in anesthetized, paralyzed, and artificially ventilated rats with a 10-s stimulus train elicited a stimulus-locked elevation of arterial pressure (AP) and heart rate (HR) (the fastigial pressor response, FPR) and elevated plasma catecholamines (CA) within 20 s from the onset of stimulus. Norepinephrine (NE) increased from 139 +/- 24 to 280 +/- 43 pg/ml (P less than 0.05, n = 8) and epinephrine (E) from 70 +/- 26 to 360 +/- 107 pg/ml (P less than 0.02, n = 8). Acute adrenalectomy increased basal plasma NE (362 +/- 108 pg/ml, P less than 0.05, n = 6) and reduced E (9 +/- 4 pg/ml, P less than 0.02, n = 6). The magnitude and duration of the FPR and the relative increase of NE were unchanged; however, the elevation of E was abolished. Chemosympathectomy, produced by 6-hydroxydopamine hydrobromide (100 mg/kg iv, 24 h before the experiment), lowered resting AP (from 122 +/- 2 to 77 +/- 1 mmHg, P less than 0.001) and NE (16 +/- 5 pg/ml, P less than 0.01), but not E. After chemosympathectomy, FN stimulation induced a pressor response of greater magnitude and longer latency and duration than in controls, increased NE 3.5-fold (from 16 +/- 5 to 56 +/- 14 pg/ml, P less than 0.05, n = 5) and E 9-fold (from 38 +/- 11 to 336 +/- 88, P less than 0.05, n = 5). The increases in CA were abolished by adrenalectomy. Chemosympathectomy shifted the pressor-dose-response curves of NE and E to the left; thus, the enhanced pressor response to FN stimulation after chemosympathectomy was possibly a consequence of supersensitivity to circulatory CA. Stimulation of cerebellar FN increased plasma CA, as a consequence of coexcitation of both neural and adrenomedullary components of the autonomic nervous system. However, in rats with intact sympathetic nerves the release of adrenomedullary CA did not contribute to the elevation in AP.

Cerebral blood flow during fastigial pressor response in cats

1990 ◽  
Vol 258 (3) ◽  
pp. H729-H733
Author(s):  
J. L. Williams ◽  
M. A. Murray ◽  
K. A. Schalk ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Severe Hypertension ◽  
Pressor Response ◽  
Sympathetic Nerves ◽  
Fastigial Nucleus ◽  
Acute Hypertension ◽  
Cervical Sympathetic ◽  
Stimulation Of

We tested the hypotheses that electrical stimulation of the fastigial nucleus increases cerebral blood flow by a dilator mechanism, impairs autoregulation during increases in arterial pressure, and attenuates increases in cerebral blood flow during acute hypertension by activation of sympathetic nerves. Cerebral blood flow was measured with microspheres in anesthetized cats during control and moderate or severe hypertension produced by stimulation of the rostral fastigial nucleus. Cervical sympathetic nerves to one cerebral hemisphere were cut to compare responses in the innervated and denervated hemispheres. Fastigial stimulation at a level that raised arterial pressure from 94 +/- 10 (mean +/- SE) to 133 +/- 6 mmHg had no significant effect on cerebral blood flow. Autoregulation was preserved because cerebral vascular resistance increased approximately 40% during the fastigial pressure response. When mean arterial pressure was raised to 189 +/- 9 mmHg by stimulation of the fastigial nucleus, cerebral blood flow increased similarly in the denervated hemisphere and the hemisphere with intact sympathetic nerves. We conclude that stimulation of the fastigial nucleus in cats does not have a direct dilator effect on cerebral vessels, does not impair autoregulation during moderate hypertension, and does not attenuate increases in cerebral blood flow during severe hypertension by activation of sympathetic pathways.

Midbrain central gray: influence on medullary sympathoexcitatory neurons and the baroreflex in rats

1992 ◽  
Vol 263 (1) ◽  
pp. R24-R33 ◽  
Author(s):  
A. J. Verberne ◽  
P. G. Guyenet
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Nerves ◽  
Ventrolateral Medulla ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Central Gray ◽  
Train Stimulation ◽  
Pulse Stimulation ◽  
Site Of Stimulation ◽  
Stimulation Of

The influence of the central gray (CG) of the midbrain on the activity of 19 barosensitive sympathoexcitatory neurons of the rostral ventrolateral medulla (RVLM) and on the sympathetic vasomotor baroreflex was studied in halothane-anesthetized rats. Eighteen RVLM barosensitive units were readily activated by train stimulation of the CG, although twin-pulse stimulation was less effective (10 of 19 neurons responded). Inhibition of neurons within the RVLM by bilateral microinjection of the GABA-mimetic drug muscimol abolished the pressor responses to CG stimulation, while the accompanying lumbar nerve sympathoexcitation was converted to sympathoinhibition. In baroreceptor-denervated vagotomized animals, unilateral microinjection of muscimol into the RVLM ipsilateral or contralateral to the site of CG stimulation resulted in approximately equal attenuation of the CG sympathoexcitatory and pressor responses. In contrast, the sympathoexcitatory response to electrical stimulation of the sciatic nerve was reduced more effectively by inhibition of the RVLM contralateral to the site of stimulation. Electrical stimulation of the CG lateral and ventrolateral to the aqueduct produced sympathoexcitation [increased discharge of the greater splanchnic and lumbar sympathetic nerves (SSN and LSN)] with an increase in mean arterial blood pressure. Activation of the SSN by CG stimulation was greater than that observed for the LSN (n = 5 rats). This differential influence of the CG on the sympathetic outflow was not a result of a differential influence of the baroreflex. Electrical stimulation of the CG produced elevations of the gain and the cut-off pressure of the baroreflex for both the SSN and LSN.(ABSTRACT TRUNCATED AT 250 WORDS)

Cholinergic stimulation of the pons depresses respiration in decerebrate cats

1990 ◽  
Vol 69 (6) ◽  
pp. 2280-2289 ◽  
Author(s):  
H. Kimura ◽  
L. Kubin ◽  
R. O. Davies ◽  
A. I. Pack
Keyword(s):  
Respiratory Rate ◽  
Rem Sleep ◽  
Neural Pathways ◽  
Related Activity ◽  
Motor Branch ◽  
Decerebrate Cat ◽  
Complete Reversal ◽  
Motor Nerves ◽  
Decerebrate Cats ◽  
Stimulation Of

The injection of carbachol into the pontine tegmentum of decerebrate cats evokes a postural motor atonia that has many of the characteristics of the atonia of natural rapid-eye-movement (REM) sleep (Morales et al. J. Neurophysiol. 57: 1118-1129, 1987). We have used the carbachol-injected decerebrate cat to study the changes in respiratory neuronal activity that accompany the atonia. The activities of representative respiratory motor nerves--phrenic, intercostal, and hypoglossal--and that of a motor branch of C4 were recorded in decerebrate, vagotomized, paralyzed, and artificially ventilated cats. After the microinjection of carbachol, there was a profound suppression of activity in all the nerves and a decrease in respiratory rate. This was a consistent stereotyped response in which the magnitude of the suppression of respiratory-related activity was phrenic (to approximately 65% of control) less than inspiratory intercostal (approximately 50%) less than hypoglossal (approximately 10%) less than expiratory intercostal (approximately 5%). The decrease in respiratory rate (to approximately 70% of control) was caused by a prolongation of both inspiratory and expiratory durations. Complete reversal of the carbachol effect was elicited by the microinjection of atropine into the same site as the carbachol injection. This allowed us to produce a second episode of atonia by the injection of carbachol into the contralateral pons. Thus we have demonstrated the existence of neural pathways originating in the cholinoceptive cells of the pons that have the potential to powerfully and differentially depress various respiratory motoneuronal pools and to reduce the respiratory rate. These pathways are likely to be activated along with the atonia of REM sleep.

Nonlinear properties of stretch reflex studied in the decerebrate cat

1982 ◽  
Vol 47 (2) ◽  
pp. 179-192 ◽  
Author(s):  
J. W. Aldridge ◽  
R. B. Stein
Keyword(s):  
Electrical Stimulation ◽  
Neural Activity ◽  
Stretch Reflex ◽  
Time Course ◽  
Nonlinear Interactions ◽  
Motor Axons ◽  
Plantaris Muscle ◽  
Decerebrate Cat ◽  
Reflex Responses ◽  
Stimulation Of

1. Pairs of brief stretches or a series of stretches at random intervals (Poisson process) were applied to a slow (soleus) and a fast (plantaris) muscle in decerebrate cats to analyze the nonlinear effects of one stretch on the reflex responses to subsequent stretches. Neural activity, electromyogram (EMG), and force were recorded. The reflex responses due to stretch were compared with reflexes as a result of electrical stimulation of nerves. Nonlinearities of muscle were also examined in the absence of reflexes. Short-latency neural activity produced by the stimuli at all intervals studied was quite constant, so changes in sensory activity cannot account for the nonlinearities. Three phases of nonlinear interactions were observed, and mechanisms for these nonlinearities are suggested. 2. For short intervals (less than 100 ms) following a stretch the force and EMG produced by a second stretch is depressed. This early depression could be due to the after hyperpolarization of the motoneuron cel body or to synaptic mechanisms, since the depression of EMG is seen with electrical stimulation of Ia sensory, but not alpha-motor axons. In addition, a second stretch can disrupt the reflex contraction produced by the first stretch if it occurs at a time when new actomyosin bonds are not readily formed. Because of this force suppression, the total reflex force produced in response to two stretches may be less than the response to a single stretch. 3. For intervals between 100 and 300 ms the force and EMG produced by a second stretch is enhanced. This potentiation is also seen with electrical stimulation of large sensory but not motor axons and could result from a synchronization of motoneuronal excitability cycles. It is more prominent in the homogeneous (soleus) muscle than the mixed (plantaris) muscle, probably because the motoneuron cell bodies will reach a period of high excitability at more nearly the same time in the homogeneous muscle. 4. For longer intervals the force produced by a second stretch is reduced even when the EMG is close to control values. This late depression is also observed with electrical stimulation of cut motor axons and therefore arises from the contractile properties of muscles. 5. With a random series of stretches, the same time course of nonlinear interactions is observed. However, as the mean rate of the random stretches is increased, the average response of the reflex decreases. Thus, the stretch reflex will be most effective in correcting for occasional perturbations to a movement, rather than for continuously varying disturbances.

Adrenergic Stimulation of Regional Plasminogen Activator Release in Rabbits

1992 ◽  
Vol 68 (05) ◽  
pp. 545-549 ◽  
Author(s):  
W L Chandler ◽  
S C Loo ◽  
D Mornin
Keyword(s):  
Lower Extremity ◽  
Plasminogen Activator ◽  
Beta Blocker ◽  
Time Course ◽  
Vascular System ◽  
Adrenergic Stimulation ◽  
Epinephrine Administration ◽  
Adrenergic Antagonist ◽  
Vascular Beds ◽  
Stimulation Of

SummaryThe purpose of this study was to determine whether different regions of the rabbit vascular system show variations in the rate of plasminogen activator (PA) secretion. To start, we evaluated the time course, dose response and adrenergic specificity of PA release. Infusion of 1 µg/kg of epinephrine stimulated a 116 ± 60% (SD) increase in PA activity that peaked 30 to 60 s after epinephrine administration. Infusion of 1 µg/kg of norepinephrine, isoproterenol and phenylephrine had no effect on PA activity. Pretreatment with phentolamine, an alpha adrenergic antagonist, blocked the release of PA by epinephrine while pretreatment with the beta blocker propranolol had no effect. This suggests that PA release in the rabbit was mediated by some form of alpha receptor.Significant arterio-venous differences in basal PA activity were found across the pulmonary and splanchnic vascular beds but not the lower extremity/pelvic bed. After stimulation with epinephrine, PA activity increased 46% across the splanchnic bed while no change was seen across the lower extremity/pelvic bed. We conclude that several vascular beds contribute to circulating PA activity in the rabbit, and that these beds secrete PA at different rates under both basal and stimulated conditions.

Peripheral muscarinic control of norepinephrine release in the cardiovascular system

1980 ◽  
Vol 239 (6) ◽  
pp. H713-H720 ◽  
Author(s):  
E. Muscholl
Keyword(s):  
Physiological Role ◽  
Sympathetic Nerves ◽  
Adrenergic Nerve ◽  
Sequence Of Events ◽  
Adrenergic Response ◽  
Adrenergic Nerve Terminals ◽  
Muscarinic Cholinergic ◽  
Related Compounds ◽  
Stimulation Of

Activation of muscarinic cholinergic receptors located at the terminal adrenergic nerve fiber inhibits the process of exocytotic norepinephrine (NE) release. This neuromodulatory effect of acetylcholine and related compounds has been discovered as a pharmacological phenomenon. Subsequently, evidence for a physiological role of the presynaptic muscarinic inhibition was obtained on organs known to be innervated by the autonomic ground plexus (Hillarp, Acta. Physiol. Scand. 46, Suppl. 157: 1-68, 1959) in which terminal adrenergic and cholinergic axons run side by side. Thus, in the heart electrical vagal stimulation inhibits the release of NE evoked by stimulation of sympathetic nerves, and this is reflected by a corresponding decrease in the postsynaptic adrenergic response. On the other hand, muscarinic antagonists such as atropine enhance the NE release evoked by field stimulation of tissues innervated by the autonomic ground plexus. The presynaptic muscarine receptor of adrenergic nerve terminals probably restricts the influx of calcium ions that triggers the release of NE. However, the sequence of events between recognition of the muscarinic compound by the receptor and the process of exocytosis still remains to be clarified.

Effects of low-frequency stimulation of the superior colliculus on spontaneous and visually guided saccades

1993 ◽  
Vol 69 (3) ◽  
pp. 953-964 ◽  
Author(s):  
P. W. Glimcher ◽  
D. L. Sparks
Keyword(s):  
Superior Colliculus ◽  
Time Course ◽  
Low Frequency ◽  
Arbitrary Point ◽  
Visually Guided ◽  
Spontaneous Movements ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation ◽  
Stimulation Current ◽  
Stimulation Of

1. The first experiment of this study determined the effects of low-frequency stimulation of the monkey superior colliculus on spontaneous saccades in the dark. Stimulation trains, subthreshold for eliciting short-latency fixed-vector saccades, were highly effective at biasing the metrics (direction and amplitude) of spontaneous movements. During low-frequency stimulation, the distribution of saccade metrics was biased toward the direction and amplitude of movements induced by suprathreshold stimulation of the same collicular location. 2. Low-frequency stimulation biased the distribution of saccade metrics but did not initiate movements. The distribution of intervals between stimulation onset and the onset of the next saccade did not differ significantly from the distribution of intervals between an arbitrary point in time and the onset of the next saccade under unstimulated conditions. 3. Results of our second experiment indicate that low-frequency stimulation also influenced the metrics of visually guided saccades. The magnitude of the stimulation-induced bias increased as stimulation current or frequency was increased. 4. The time course of these effects was analyzed by terminating stimulation immediately before, during, or after visually guided saccades. Stimulation trains terminated at the onset of a movement were as effective as stimulation trains that continued throughout the movement. No effects were observed if stimulation ended 40–60 ms before the movement began. 5. These results show that low-frequency collicular stimulation can influence the direction and amplitude of spontaneous or visually guided saccades without initiating a movement. These data are compatible with the hypothesis that the collicular activity responsible for specifying the horizontal and vertical amplitude of a saccade differs from the type of collicular activity that initiates a saccade.

scholarly journals Renal sensory and sympathetic nerves reinnervate the kidney in a similar time-dependent fashion after renal denervation in rats

2013 ◽  
Vol 304 (8) ◽  
pp. R675-R682 ◽  
Author(s):  
Jan Mulder ◽  
Tomas Hökfelt ◽  
Mark M. Knuepfer ◽  
Ulla C. Kopp
Keyword(s):  
Substance P ◽  
Optical Density ◽  
Renal Denervation ◽  
Time Course ◽  
Sympathetic Nerves ◽  
Sensory Nerves ◽  
Sensory Innervation ◽  
Multiple Time ◽  
Sensory Reinnervation ◽  
Renal Sympathetic

Efferent renal sympathetic nerves reinnervate the kidney after renal denervation in animals and humans. Therefore, the long-term reduction in arterial pressure following renal denervation in drug-resistant hypertensive patients has been attributed to lack of afferent renal sensory reinnervation. However, afferent sensory reinnervation of any organ, including the kidney, is an understudied question. Therefore, we analyzed the time course of sympathetic and sensory reinnervation at multiple time points (1, 4, and 5 days and 1, 2, 3, 4, 6, 9, and 12 wk) after renal denervation in normal Sprague-Dawley rats. Sympathetic and sensory innervation in the innervated and contralateral denervated kidney was determined as optical density (ImageJ) of the sympathetic and sensory nerves identified by immunohistochemistry using antibodies against markers for sympathetic nerves [neuropeptide Y (NPY) and tyrosine hydroxylase (TH)] and sensory nerves [substance P and calcitonin gene-related peptide (CGRP)]. In denervated kidneys, the optical density of NPY-immunoreactive (ir) fibers in the renal cortex and substance P-ir fibers in the pelvic wall was 6, 39, and 100% and 8, 47, and 100%, respectively, of that in the contralateral innervated kidney at 4 days, 4 wk, and 12 wk after denervation. Linear regression analysis of the optical density of the ratio of the denervated/innervated kidney versus time yielded similar intercept and slope values for NPY-ir, TH-ir, substance P-ir, and CGRP-ir fibers (all R2 > 0.76). In conclusion, in normotensive rats, reinnervation of the renal sensory nerves occurs over the same time course as reinnervation of the renal sympathetic nerves, both being complete at 9 to 12 wk following renal denervation.

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