Attenuation of reactive and active hyperemia by sympathetic stimulation in dog gracilis muscle

1986 ◽  
Vol 251 (6) ◽  
pp. H1183-H1187 ◽  
Author(s):  
R. E. Klabunde
Keyword(s):  
Reactive Hyperemia ◽  
Low Frequency ◽  
Arterial Occlusion ◽  
Sympathetic Nerves ◽  
Sympathetic Stimulation ◽  
Tetanic Contraction ◽  
Contraction Duration ◽  
Muscle Ischemia ◽  
Frequency Of Stimulation ◽  
Stimulation Of

The effects of sympathetic stimulation (SS) on reactive hyperemia (RH) and active hyperemia (AH) were evaluated in dog gracilis muscles. Sympathetic nerves to the muscle vasculature were activated by electrical stimulation of the obturator nerve during neuromuscular blockade. The frequency of stimulation was adjusted to decrease control conductance by 50%. RH responses to 1 and 5 min of arterial occlusion and AH after 1, 4, 7, and 10 s of tetanic contraction (direct muscle stimulation) at 30% maximal tensions were recorded in the absence and presence of SS. RH peak conductance (Cp), recovery half-time (T0.5), and excess flow (EQ) were significantly attenuated by SS at both occlusion durations. The change in conductance (delta C) during RH was not altered by SS, since the absolute reductions in control and peak conductances were not different. The Cp of AH was reduced at each contraction duration while the delta C was reduced only with 1-s contractions. The T0.5 and EQ of AH were not affected by SS. The data demonstrate that low frequency SS limits the degree of vasodilation associated with both muscle ischemia and tetanic contraction. Furthermore, the more pronounced effects of SS on RH suggest that there is greater inhibition of sympathetic vasoconstrictor influences associated with muscle contraction than muscle ischemia possibly due to the production of a substance during contraction, but not ischemia, that antagonizes sympathetic vasoconstrictor mechanisms.

Effect of sympathetic stimulation on gastric secretion of pepsinogen

1960 ◽  
Vol 199 (1) ◽  
pp. 131-135 ◽  
Author(s):  
M. Altamirano ◽  
L. Chiang ◽  
I. Bravo
Keyword(s):  
Low Frequency ◽  
Sympathetic Stimulation ◽  
Basal Secretion ◽  
Long Period ◽  
Pepsinogen Secretion ◽  
Transitory Effect ◽  
Frequency Of Stimulation ◽  
High Output ◽  
Stimulation Of

In dogs the stimulation of the sympathetic fibers innervating a segment of resting gastric mucosa of the corpus did not augment the basal secretion of pepsinogen when the frequency of stimulation varied between 1 and 10/sec. At rates of 15/sec. or higher the pepsinogen output was markedly increased. Secretion of hydrochloric acid was not elicited by sympathetic stimulation alone. The output of pepsinogen was increased transiently by histamine; however, the concomitant use of histamine and sympathetic stimulation even at low frequency (less than 10/sec.) resulted in a high output of pepsinogen for a long period of time. These findings are considered to be evidence that the pepsinogen-secreting glands are stimulated by histamine. Intravenous Dibenzyline antagonized the effect of the sympathetic stimulation. The transitory effect of histamine on pepsinogen secretion and the role of the sympathetic thereon are discussed.

Differential pattern of spinal sympathetic outflow in response to stimulation of the caudal medullary raphe

2000 ◽  
Vol 279 (1) ◽  
pp. R210-R221 ◽  
Author(s):  
Peter D. Larsen ◽  
Sheng Zhong ◽  
Gerard L. Gebber ◽  
Susan M. Barman
Keyword(s):  
Stimulus Intensity ◽  
Low Frequency ◽  
Sympathetic Nerves ◽  
Frequency Domain Analysis ◽  
Band Power ◽  
Medullary Raphe ◽  
High Stimulus ◽  
Differential Pattern ◽  
Low Frequency Power ◽  
Stimulation Of

In urethan-anesthetized cats, frequency domain analysis was used to explore the mechanisms of differential responses of inferior cardiac (CN), vertebral (VN), and renal (RN) sympathetic nerves to electrical stimulation of a discrete region of the medullary raphe (0–2 mm caudal to the obex). Raphe stimulation in baroreceptor-denervated cats at frequencies (7–12 Hz) that entrained the 10-Hz rhythm in nerve activity decreased CN and RN activities but increased VN activity. The reductions in CN and RN discharges were associated with decreased low-frequency (≤6 Hz) power and either increased (low stimulus intensity) or decreased (high stimulus intensity) 10-Hz band power. In contrast, VN 10-Hz band power was increased at all stimulus intensities, without changes in low-frequency power. High-frequency (25 Hz) stimulation decreased low-frequency activity of CN and RN discharges in both baroreceptor-denervated and baroreceptor-intact cats, without decreasing VN low-frequency activity. We propose that the differential pattern produced by raphe stimulation involves resonance at the level of the 10-Hz oscillators and differential inhibition of follower circuits that transmit both 10-Hz and low-frequency activity to sympathetic nerves.

Increased activity of carotid sinus baroreceptors by sympathetic stimulation and norepinephrine

1981 ◽  
Vol 240 (4) ◽  
pp. H650-H658 ◽  
Author(s):  
E. Tomomatsu ◽  
K. Nishi
Keyword(s):  
Carotid Sinus ◽  
Sympathetic Innervation ◽  
Sympathetic Nerves ◽  
Nerve Endings ◽  
Discharge Frequency ◽  
Sympathetic Stimulation ◽  
High Concentration ◽  
Excitatory Effect ◽  
Pressure Step ◽  
Stimulation Of

Effects of electrical stimulation of sympathetic nerves to the carotid sinus on the discharge of single active baroreceptor fibers of the rabbit were examined in situ and in functionally isolated carotid sinus preparations with an intact sympathetic innervation under controlled conditions of pressure and temperature. Among 30 single units, 18 units responded to sympathetic stimulation of increasing discharge frequency. The excitatory effect of sympathetic stimulation on baroreceptor activity was not abolished by phentolamine (1 mg/kg iv or 10(-6) g/ml in perfusate). In isolated carotid sinus preparations perfused with Krebs-Henseleit solution, various pressure steps were applied to the sinus, and effects of norepinephrine (NE; 10(-9) and 10(-6) g/ml) on activity of nine single baroreceptor units were examined. In the presence of 10(-9) g/ml NE, discharge frequency of all units significantly increased at a given pressure step when compared with the control, whereas NE at a high concentration (10(-6) g/ml) did not produce significant changes in the discharge frequency. It is concluded that NE released by sympathetic nerve endings most likely acts directly on the baroreceptor nerve endings and sensitizes them.

Intestinal O2 uptake during sympathetic stimulation and partial arterial occlusion

1979 ◽  
Vol 236 (5) ◽  
pp. H731-H735
Author(s):  
A. P. Shepherd
Keyword(s):  
Blood Flow ◽  
Arterial Occlusion ◽  
Sympathetic Nerves ◽  
Capillary Density ◽  
Sympathetic Stimulation ◽  
O2 Uptake ◽  
Diffusion Limitations ◽  
O2 Extraction ◽  
Series Of Experiments ◽  
Through Diffusion

In isolated loops of canine small bowel perfused at constant blood flow, stimulating perivascular sympathetic nerves (8--10 Hz) depressed O2 extraction and O2 uptake. Because sympathetic stimulation also decreased 86Rb extraction, the results confirmed earlier studies indicating that sympathetic stimulation closes "precapillary sphincters" and through diffusion limitations reduces the capillary-to-cell flux of oxygen. To determine if sympathetic stimulation could lower O2 uptake under more physiologic circumstances, a second series of experiments was performed during constant arterial pressure perfusion. Sympathetic stimulation reduced blood flow by about 30% in the steady phase. Oxygen extraction did not increase appreciably, so O2 uptake was also reduced. When partial arterial occlusion was used to lower the blood flow to the level that it reached during sympathetic stimulation, large increases (37%) in O2 extraction occurred so that O2 uptake remained near control levels. The results indicate that after arterial occlusion local mechanisms maintain O2 uptake by increasing O2 extraction through capillary density increases, but that this mechanism is impaired by sympathetic stimulation.

Autonomic Balance in Cardiac Control

1958 ◽  
Vol 192 (3) ◽  
pp. 631-634 ◽  
Author(s):  
Robert F. Rushmer
Keyword(s):  
Heart Rate ◽  
Mechanical Performance ◽  
Stimulus Frequency ◽  
Sympathetic Nerves ◽  
Left Ventricular ◽  
Sympathetic Stimulation ◽  
Vagus Nerves ◽  
Ventricular Performance ◽  
Anesthetized Dogs ◽  
Stimulation Of

Stimulation of the sympathetic nerves to the heart in anesthetized dogs produced tachycardia and changes in left ventricular performance, including alterations in both pressures and dimensions. Stimulation of the vagus nerves in dogs predominately induced a bradycardia. When the heart rate was controlled by an artificial pacemaker, sympathetic stimulation produced changes in ventricular performance. By adjustments in stimulus frequency, the effects of vagal and sympathetic stimulation on heart rate could be balanced, but complete cancellation of effects was impossible because the vagus had a more powerful effect on heart rate and the sympathetic nerves had a greater influence on mechanical performance.

Sympathetic outflow to resting muscles during static handgrip and postcontraction muscle ischemia

1989 ◽  
Vol 256 (1) ◽  
pp. H105-H110 ◽  
Author(s):  
B. G. Wallin ◽  
R. G. Victor ◽  
A. L. Mark
Keyword(s):  
Sympathetic Activity ◽  
Healthy Subjects ◽  
Arterial Occlusion ◽  
Voluntary Contraction ◽  
Similar Degree ◽  
Sympathetic Outflow ◽  
Burst Frequency ◽  
Leg Muscles ◽  
Muscle Ischemia ◽  
Stimulation Of

Simultaneous microneurographic recordings were made of muscle sympathetic activity (MSA) in the radial and the peroneal nerves of seven healthy subjects during 2-min static handgrip (30% of maximal voluntary contraction) followed by 2 min of forearm ischemia induced by arterial occlusion. At rest sympathetic burst frequency was similar in both nerves, but relative burst strengths differed between the two neurograms, suggesting that sympathetic outflows to arm and leg were not identical. Both radial and peroneal MSA were unchanged during the first minute of handgrip and increased to a similar degree during the second minute. Thus previously reported differences in vascular resistance between forearm and calf during static handgrip cannot be explained by differences in MSA to arm and leg muscles. During forearm ischemia after handgrip, peroneal MSA remained at the same level as during the second minute of handgrip but there was a further increase of radial MSA. This shows that stimulation of chemosensitive endings in forearm muscles induces differentiation of sympathetic neural outflow to muscles in the leg and the contralateral arm.

Uptake and re-use of sympathetic transmitter in the cat’s spleen

1969 ◽  
Vol 174 (1034) ◽  
pp. 51-68 ◽  
Keyword(s):  
Sympathetic Nerve ◽  
Present Method ◽  
Sympathetic Nerves ◽  
Homologous Blood ◽  
Progressive Decline ◽  
The Relationship ◽  
Frequency Of Stimulation ◽  
Sympathetic Transmitter ◽  
Stimulation Of

The output of transmitter resulting from stimulation of the sympathetic nerves of the cat’s spleen, perfused with homologous blood, is described and compared with similar results obtained from the spleen in situ . Transmitter overflows are somewhat lower in the spleen perfused by the present method, but the relationship between overflow and frequency of stimulation is the same as in the spleen in situ . Noradrenaline added to the perfusate at rates as high as 6 μ g/min is taken up by the spleen which shows no sign of saturation even at these high levels of presentation. Loss of transmitter from the spleen causes a progressive decline in the overflow of transmitter produced by successive trains of stimuli. Evidence is presented to support the hypothesis that the continued effectiveness of a sympathetic nerve depends upon the uptake and re-use of the transmitter that it liberates.

Adrenergic modulation of reactive hyperemia in rat gut

1991 ◽  
Vol 261 (3) ◽  
pp. G392-G400 ◽  
Author(s):  
W. W. Pawlik ◽  
O. D. Hottenstein ◽  
E. D. Jacobson
Keyword(s):  
Adrenergic Receptors ◽  
Reactive Hyperemia ◽  
Arterial Occlusion ◽  
Sympathetic Nerves ◽  
Arterial Blood Flow ◽  
Dependent Manner ◽  
Alpha Adrenergic Receptors ◽  
Arterial Blood ◽  
Adrenergic Modulation ◽  
Rat Gut

The hypothesis was tested that peripheral, adrenergic nerves modulate reactive hyperemia (RH) in the intestinal circulation. In anesthetized rats, anterior mesenteric arterial occlusion for 30-120 s elicited subsequent RH responses, including 63-118% increases in the velocity of arterial blood flow, even greater increases in conductance, and durations of 64-139 s. The longer the period of arterial occlusion, the greater the magnitude of RH. Electrical stimulation of postganglionic, sympathetic nerves reduced RH responses in a frequency-dependent manner. RH responses were enhanced by pretreatment with hexamethonium and phenoxybenzamine and were diminished by pretreatment with propranolol. Propranolol also prevented the enhanced RH responses caused by hexamethonium and phenoxybenzamine. Reserpine prevented the enhanced RH responses to hexamethonium, but bilateral adrenalectomy did not. These findings support the hypothesis that peripheral sympathetic nerves modulate RH in rat gut, with alpha-adrenergic receptors restricting and beta-adrenergic receptors enhancing the hyperemia.

scholarly journals Deep Brain Stimulation of the Posterior Insula in Chronic Pain: A Theoretical Framework

2021 ◽  
Vol 11 (5) ◽  
pp. 639
Author(s):  
David Bergeron ◽  
Sami Obaid ◽  
Marie-Pierre Fournier-Gosselin ◽  
Alain Bouthillier ◽  
Dang Khoa Nguyen
Keyword(s):  
Chronic Pain ◽  
Electrical Stimulation ◽  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
High Frequency ◽  
Brain Lesion ◽  
Low Frequency ◽  
Posterior Insula ◽  
Deep Brain ◽  
Stimulation Of

Introduction: To date, clinical trials of deep brain stimulation (DBS) for refractory chronic pain have yielded unsatisfying results. Recent evidence suggests that the posterior insula may represent a promising DBS target for this indication. Methods: We present a narrative review highlighting the theoretical basis of posterior insula DBS in patients with chronic pain. Results: Neuroanatomical studies identified the posterior insula as an important cortical relay center for pain and interoception. Intracranial neuronal recordings showed that the earliest response to painful laser stimulation occurs in the posterior insula. The posterior insula is one of the only regions in the brain whose low-frequency electrical stimulation can elicit painful sensations. Most chronic pain syndromes, such as fibromyalgia, had abnormal functional connectivity of the posterior insula on functional imaging. Finally, preliminary results indicated that high-frequency electrical stimulation of the posterior insula can acutely increase pain thresholds. Conclusion: In light of the converging evidence from neuroanatomical, brain lesion, neuroimaging, and intracranial recording and stimulation as well as non-invasive stimulation studies, it appears that the insula is a critical hub for central integration and processing of painful stimuli, whose high-frequency electrical stimulation has the potential to relieve patients from the sensory and affective burden of chronic pain.

scholarly journals MONOSYNAPTIC REFLEX RESPONSE OF INDIVIDUAL MOTONEURONS AS A FUNCTION OF FREQUENCY

1957 ◽  
Vol 40 (3) ◽  
pp. 435-450 ◽  
Author(s):  
David P. C. Lloyd
Keyword(s):  
High Frequency ◽  
Temporal Summation ◽  
Low Frequency ◽  
Stimulation Frequency ◽  
Monosynaptic Reflex ◽  
Reflex Response ◽  
High Frequency Stimulation ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation ◽  
Frequency Of Stimulation

An assemblage of individual motoneurons constituting a synthetic motoneuron pool has been studied from the standpoint of relating monosynaptic reflex responses to frequency of afferent stimulation. Intensity of low frequency depression is not a simple function of transmitter potentiality. As frequency of stimulation increases from 3 per minute to 10 per second, low frequency depression increases in magnitude. Between 10 and approximately 60 per second low frequency depression apparently diminishes and subnormality becomes a factor in causing depression. At frequencies above 60 per second temporal summation occurs, but subnormality limits the degree of response attainable by summation. At low stimulation frequencies rhythm is determined by stimulation frequency. Interruptions of rhythmic firing depend solely upon temporal fluctuation of excitability. At high frequency of stimulation rhythm is determined by subnormality rather than inherent rhythmicity, and excitability fluctuation leads to instability of response rhythm. In short, whatever the stimulation frequency, random excitability fluctuation is the factor disrupting rhythmic response. Monosynaptic reflex response latency is stable during high frequency stimulation as it is in low frequency stimulation provided a significant extrinsic source of random bombardment is not present. In the presence of powerful random bombardment discharge may become random with respect to monosynaptic afferent excitation provided the latter is feeble. When this occurs it does so equally at low frequency and high frequency. Thus temporal summation is not a necessary factor. There is, then, no remaining evidence to suggest that the agency for temporal summation in the monosynaptic system becomes a transmitting agency in its own right.

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