Intravenous injection of hypertonic NaCl solution stimulates pulmonary C-fibers in dogs

1991 ◽  
Vol 260 (5) ◽  
pp. H1522-H1530 ◽  
Author(s):  
T. E. Pisarri ◽  
A. Jonzon ◽  
H. M. Coleridge ◽  
J. C. Coleridge
Keyword(s):  
Intravenous Injection ◽  
Pulmonary Circulation ◽  
Bronchial Artery ◽  
Dependent Manner ◽  
Nacl Solution ◽  
Impulse Frequency ◽  
Minimum Effective Concentration ◽  
C Fibers ◽  
Hypertonic Solutions ◽  
Stimulation Of

Intravenous injection of hypertonic NaCl solution evokes reflex bradycardia and hypotension, effects thought to result from stimulation of afferent vagal endings in the lungs. To identify the afferents responsible for these effects, we recorded vagal impulses arising from endings in the lungs and lower airways of anesthetized dogs and examined the response to injection of hypertonic solutions into the pulmonary circulation. Injection of 4,800 mmol/l NaCl solution (1 ml/kg) stimulated 39 of 49 pulmonary C-fibers, their impulse frequency increasing 35-fold. Stimulation was concentration dependent, the minimum effective concentration being between 1,200 and 4,800 mmol/l. Rapidly adapting receptors were also stimulated in a concentration-dependent manner, 35 of 41 receptors being stimulated by 4,800 mmol/l NaCl solution, firing increasing fivefold. Bronchial C-fibers were not stimulated by injection into the pulmonary circulation but were by injection into the bronchial artery. Hypertonic urea solutions had qualitatively similar but smaller effects on pulmonary C-fibers and rapidly adapting receptors. The results suggest that the reflex effects of intravenous injection of hypertonic solutions result principally from stimulation of pulmonary C-fibers.

Stimulation of vagal afferents inhibits locomotion in mesencephalic cats

1993 ◽  
Vol 74 (1) ◽  
pp. 103-110 ◽  
Author(s):  
J. G. Pickar ◽  
J. M. Hill ◽  
M. P. Kaufman
Keyword(s):  
Intravenous Injection ◽  
Left Atrial ◽  
Onset Time ◽  
Vagal Afferents ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
C Fibers ◽  
Cervical Vagotomy ◽  
Reflex Arc ◽  
Stimulation Of

Using electrical stimulation of the mesencephalic locomotor region, we made decerebrate unanesthetized cats walk on a treadmill. The locomotion induced by stimulation of this midbrain area was assessed before and during activation of vagal afferents by either intravenous injection of phenylbiguanide or inflation of a balloon placed in the left atrium. Inflation of a balloon, which increased left atrial pressure by 7–25 mmHg, abolished locomotion in 9 of 10 cats tested. Bilateral cervical vagotomy prevented the abolition of locomotion by balloon inflation in each of two cats tested. Intravenous phenylbiguanide (50 or 100 micrograms/kg) or serotonin (40 micrograms/kg) injections abolished or attenuated walking induced by midbrain stimulation in 11 of 13 cats tested. In addition, intravenous phenylbiguanide injections abolished or attenuated locomotion with a shorter onset time than did systemic injections of this substance in five of six cats tested. Bilateral cervical vagotomy prevented the abolition of locomotion by phenylbiguanide injection in each of five cats tested. We conclude that locomotion can be prevented by a viscerosomatic reflex arising from the lungs and heart. The afferent arm of this reflex arc is the vagus nerve. Afferents such as slowly and rapidly adapting pulmonary stretch receptors, atrial receptors, and lung C-fibers may have had a role in preventing locomotion during the increase in left atrial pressure in our experiments. On the other hand, pulmonary C-fibers had a crucial role in preventing locomotion during intravenous injection of phenyl-biguanide. We speculate that this viscerosomatic reflex may help to explain in part the intolerance for exercise displayed by patients with congestive heart failure.

Rapid shallow breathing evoked by capsaicin from isolated pulmonary circulation

1986 ◽  
Vol 61 (3) ◽  
pp. 1237-1240 ◽  
Author(s):  
E. R. Schertel ◽  
L. Adams ◽  
D. A. Schneider ◽  
K. S. Smith ◽  
J. F. Green
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Circulation ◽  
Nerve Activity ◽  
C Fibers ◽  
Shallow Breathing ◽  
Pulmonary Arterial ◽  
Alpha Chloralose ◽  
Spontaneously Breathing ◽  
Rapid Shallow Breathing ◽  
Stimulation Of

Recently Green et al. (J. Appl. Physiol. 57:562–567, 1984) reported that pulmonary C-fibers initiate the prompt apnea evoked by pulmonary arterial injections of capsaicin; however, their role in the subsequent rapid shallow breathing of the pulmonary chemoreflex is still in dispute. To determine whether this reflex tachypnea is triggered by pulmonary C-fibers rather than by afferents further downstream, we separately perfused the pulmonary and systemic circulations in dogs anesthetized with either halothane or alpha-chloralose as the lungs were ventilated with a servo-controlled ventilator driven by phrenic nerve activity. Injection of capsaicin (10 micrograms/kg) into the pulmonary artery of the isolated pulmonary circulation evoked an immediate apnea followed by rapid shallow breathing. Injection of the same dose of capsaicin into the left atrium of the isolated pulmonary circulation had no effect. By contrast, when capsaicin was administered at a slower rate into the pulmonary artery (10–20 micrograms X kg-1 X min-1) rapid shallow breathing occurred but without apnea. Our results are consistent with the hypothesis that in spontaneously breathing animals, stimulation of pulmonary C-fibers can evoke rapid shallow breathing.

Reflex tracheal contraction induced by stimulation of bronchial C-fibers in dogs

1981 ◽  
Vol 51 (2) ◽  
pp. 485-493 ◽  
Author(s):  
A. M. Roberts ◽  
M. P. Kaufman ◽  
D. G. Baker ◽  
J. K. Brown ◽  
H. M. Coleridge ◽  
...  
Keyword(s):  
Bronchial Artery ◽  
Muscle Tension ◽  
Posterior Wall ◽  
Vagal Afferents ◽  
Laryngeal Nerves ◽  
C Fibers ◽  
Upper Cervical ◽  
Cardiac Slowing ◽  
Anesthetized Dogs ◽  
Stimulation Of

Bradykinin stimulates the afferent vagal endings of bronchial C-fibers but has little effect on other pulmonary vagal afferents. In anesthetized dogs with open chest, we recorded transverse tension in the posterior wall (trachealis muscle) of an upper cervical tracheal segment and stimulated bronchial C-fibers selectively by injecting bradykinin (19 ng-3 microgram) into a bronchial artery. The recurrent and pararecurrent laryngeal nerves were cut so that the superior laryngeal nerves provided the motor supply to the segment. Bradykinin caused a dose-dependent increase in tracheal muscle tension and often a conspicuous decrease in heart rate, which were abolished by vagotomy or administration of atropine. Injection of bradykinin still evoked tracheal contraction when myelinated lung afferents were blocked by cooling the midcervical vagi to 7 degrees C, but contraction was abolished when unmyelinated lung afferents were blocked by cooling to 0-1 degrees C, the effects of cooling being reversible. Our results indicate that stimulation of bronchial C-fibers, like that of pulmonary C-fibers, evokes reflux contraction of airway smooth muscle and reflex cardiac slowing.

scholarly journals Incerto-thalamic modulation of fear via GABA and dopamine

2021 ◽  
Author(s):  
Archana Venkataraman ◽  
Sarah C. Hunter ◽  
Maria Dhinojwala ◽  
Diana Ghebrezadik ◽  
JiDong Guo ◽  
...  
Keyword(s):  
Brain Regions ◽  
Zona Incerta ◽  
Dependent Manner ◽  
Post Traumatic Stress ◽  
Functional Roles ◽  
Functional Connections ◽  
Optogenetic Stimulation ◽  
Fear Generalization ◽  
Stimulation Of

AbstractFear generalization and deficits in extinction learning are debilitating dimensions of Post-Traumatic Stress Disorder (PTSD). Most understanding of the neurobiology underlying these dimensions comes from studies of cortical and limbic brain regions. While thalamic and subthalamic regions have been implicated in modulating fear, the potential for incerto-thalamic pathways to suppress fear generalization and rescue deficits in extinction recall remains unexplored. We first used patch-clamp electrophysiology to examine functional connections between the subthalamic zona incerta and thalamic reuniens (RE). Optogenetic stimulation of GABAergic ZI → RE cell terminals in vitro induced inhibitory post-synaptic currents (IPSCs) in the RE. We then combined high-intensity discriminative auditory fear conditioning with cell-type-specific and projection-specific optogenetics in mice to assess functional roles of GABAergic ZI → RE cell projections in modulating fear generalization and extinction recall. In addition, we used a similar approach to test the possibility of fear generalization and extinction recall being modulated by a smaller subset of GABAergic ZI → RE cells, the A13 dopaminergic cell population. Optogenetic stimulation of GABAergic ZI → RE cell terminals attenuated fear generalization and enhanced extinction recall. In contrast, optogenetic stimulation of dopaminergic ZI → RE cell terminals had no effect on fear generalization but enhanced extinction recall in a dopamine receptor D1-dependent manner. Our findings shed new light on the neuroanatomy and neurochemistry of ZI-located cells that contribute to adaptive fear by increasing the precision and extinction of learned associations. In so doing, these data reveal novel neuroanatomical substrates that could be therapeutically targeted for treatment of PTSD.

scholarly journals Stimulation of production of prostaglandin E in gingival cells exposed to products of human blood mononuclear cells

1981 ◽  
Vol 198 (2) ◽  
pp. 391-396 ◽  
Author(s):  
S M D'Souza ◽  
D J Englis ◽  
A Clark ◽  
R G Russell
Keyword(s):  
Mononuclear Cell ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Gingival Tissue ◽  
Prostaglandin E ◽  
Dependent Manner ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells ◽  
Gingival Cells ◽  
Stimulation Of

1. Supernatant media from cultures of unstimulated human peripheral blood mononuclear cells contained one or more factors that increased by several hundred-fold the production of prostaglandin E by fibroblast-like cells derived from both inflamed and normal human gingival tissue. 2. This stimulation occurred in a dose-dependent manner and was completely inhibited by 14 microM-indomethacin. 3. Responsiveness to the factor declined as the age of the cell culture increased. 4. An increase in prostaglandin E production was first observed after a 2h exposure to the mononuclear cell factor(s) and could be prevented by cycloheximide. 5. Brief exposure (0.5 and 1.0 h) to mononuclear cell factor did not increase prostaglandin E production by the cells in a subsequent 72 h incubation in the absence of mononuclear cell factor. 6. Addition of arachidonate (10 microM and 15 microM) further enhanced stimulation of prostaglandin E production in response to mononuclear cell factor. 7. The stimulatory activity was resistant to digestion by trypsin, but was heat-labile, so that only 17% remained after treatment at 56 degrees C for 30 min.

scholarly journals Establishment of a New Device for Electrical Stimulation of Non-Degenerative Cartilage Cells In Vitro

2021 ◽  
Vol 22 (1) ◽  
pp. 394
Author(s):  
Simone Krueger ◽  
Alexander Riess ◽  
Anika Jonitz-Heincke ◽  
Alina Weizel ◽  
Anika Seyfarth ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Electric Fields ◽  
Cartilage Tissue ◽  
Type I ◽  
Dependent Manner ◽  
New Device ◽  
Alternating Electric Fields ◽  
Cartilage Cells ◽  
Stimulation Of

In cell-based therapies for cartilage lesions, the main problem is still the formation of fibrous cartilage, caused by underlying de-differentiation processes ex vivo. Biophysical stimulation is a promising approach to optimize cell-based procedures and to adapt them more closely to physiological conditions. The occurrence of mechano-electrical transduction phenomena within cartilage tissue is physiological and based on streaming and diffusion potentials. The application of exogenous electric fields can be used to mimic endogenous fields and, thus, support the differentiation of chondrocytes in vitro. For this purpose, we have developed a new device for electrical stimulation of chondrocytes, which operates on the basis of capacitive coupling of alternating electric fields. The reusable and sterilizable stimulation device allows the simultaneous use of 12 cavities with independently applicable fields using only one main supply. The first parameter settings for the stimulation of human non-degenerative chondrocytes, seeded on collagen type I elastin-based scaffolds, were derived from numerical electric field simulations. Our first results suggest that applied alternating electric fields induce chondrogenic re-differentiation at the gene and especially at the protein level of human de-differentiated chondrocytes in a frequency-dependent manner. In future studies, further parameter optimizations will be performed to improve the differentiation capacity of human cartilage cells.

scholarly journals A new function for ATP: activating cardiac sympathetic afferents during myocardial ischemia

2010 ◽  
Vol 299 (6) ◽  
pp. H1762-H1771 ◽  
Author(s):  
Liang-Wu Fu ◽  
John C. Longhurst
Keyword(s):  
Myocardial Ischemia ◽  
Cardiovascular Responses ◽  
P2 Receptors ◽  
Nerve Fibers ◽  
Disulfonic Acid ◽  
Dependent Manner ◽  
P2 Receptor ◽  
C Fibers ◽  
Spinal Afferents ◽  
Cardiac Afferents

Myocardial ischemia activates cardiac sympathetic afferents leading to chest pain and reflex cardiovascular responses. Brief myocardial ischemia leads to ATP release in the interstitial space. Furthermore, exogenous ATP and α,β-methylene ATP (α,β-meATP), a P2X receptor agonist, stimulate cutaneous group III and IV sensory nerve fibers. The present study tested the hypothesis that endogenous ATP excites cardiac afferents during ischemia through activation of P2 receptors. Nerve activity of single unit cardiac sympathetic afferents was recorded from the left sympathetic chain or rami communicates (T2-T5) in anesthetized cats. Single fields of 45 afferents (conduction velocities = 0.25–4.92 m/s) were identified in the left ventricle with a stimulating electrode. Five minutes of myocardial ischemia stimulated 39 of 45 cardiac afferents (8 Aδ, 37 C fibers). Epicardial application of ATP (1–4 μmol) stimulated six ischemically sensitive cardiac afferents in a dose-dependent manner. Additionally, epicardial ATP (2 μmol), ADP (2 μmol), a P2Y agonist, and α,β-meATP (0.5 μmol) significantly activated eight other ischemically sensitive afferents. Third, pyridoxal phosphate-6-azophenyl-2′,4′-disulfonic acid, a P2 receptor antagonist, abolished the responses of six afferents to epicardial ATP (2 μmol) and attenuated the ischemia-related increase in activity of seven other afferents by 37%. In the absence of P2 receptor blockade, cardiac afferents responded consistently to repeated application of ATP ( n = 6) and to recurrent myocardial ischemia ( n = 6). Finally, six ischemia-insensitive cardiac spinal afferents did not respond to epicardial ATP (2–4 μmol), although these afferents did respond to epicardial bradykinin. Taken together, these data indicate that, during ischemia, endogenously released ATP activates ischemia-sensitive, but not ischemia-insensitive, cardiac spinal afferents through stimulation of P2 receptors likely located on the cardiac sensory neurites.

scholarly journals STUDIES ON THE EFFECT OF CERTAIN TOXIC SUBSTANCES IN BACTERIAL CULTURES ON THE MOVEMENT OF THE INTESTINES

1926 ◽  
Vol 43 (6) ◽  
pp. 785-795 ◽  
Author(s):  
E. E. Ecker ◽  
A. Rademaekers
Keyword(s):  
Intravenous Injection ◽  
Toxic Substances ◽  
Propulsive Efficiency ◽  
Spasmodic Contraction ◽  
Strong Stimulation ◽  
Small Intestines ◽  
Slight Rise ◽  
Longitudinal Muscles ◽  
Stimulation Of

Following intravenous injection, filtrates of young cultures of B. paratyphosus B often produce marked diarrhea in rabbits. A study was made of the effect of these toxic filtrates on the motility of the small intestines of the rabbit. The observations were made on a segment of the small intestines in situ, and in the living animal. It was found that an immediate slight rise of tone of the longitudinal muscles occurred following intravenous injection of sterile broth. The same rise was noted after the injection of the toxic filtrate; but with these it was followed later (10 minutes elapsing at least) by a very strong but gradual rise of the diastolic and systolic tone, i.e., by spasmodic contraction of the intestinal muscle, which persisted at times for as long as 2 hours. In order to record simultaneously the effect on the longitudinal and circular muscles, and the propulsive efficiency of the segment the Sollmann and Rademaekers modification of Baur's technique was employed. This arrangement showed that the stimulation of the longitudinal muscles is accompanied by a similarly strong stimulation of the circular muscles, by peristalsis, and therefore by a greatly increased propulsion of intestinal contents which was sufficient to overcome the inhibition that usually occurs after preparation of the animal. With this arrangement an instance of peristaltic spasm was also noted. Broth alone failed to produce the phenomenon. Isotonic magnesium chloride or sulfate added to the bath relaxed the muscles again. Animals under deep urethane anesthesia did not show the diarrhea occurring in the intact controls, but sometimes exhibited it after the effect of the anesthetic had disappeared. So far no effects have been observed on the isolated strip (Magnus method), and further studies are being made to localize the effect, to neutralize it with a specific antiserum, and to observe the effect of filtrates of other members of the bacterial group including the dysentery bacilli.

Endothelium and mechanical responses of isolated monkey pulmonary veins to histamine

1990 ◽  
Vol 259 (4) ◽  
pp. H1032-H1037 ◽  
Author(s):  
T. Matsuki ◽  
T. Ohhashi
Keyword(s):  
Pulmonary Veins ◽  
Dependent Manner ◽  
High Concentration ◽  
Concentration Dependent Manner ◽  
Mechanical Responses ◽  
Relaxing Factor ◽  
Prostaglandin F2 Alpha ◽  
H2 Receptors ◽  
Endothelium Derived Relaxing Factor ◽  
Stimulation Of

Ring strips of monkey pulmonary veins precontracted with a high concentration of prostaglandin F2 alpha (PGF2 alpha) relaxed in a concentration-dependent manner in response to histamine. Treatment with mepyramine and/or famotidine attenuated the relaxation. 2-Pyridylethylamine (2PEA) and dimaprit caused relaxations in the precontracted preparations, which were inhibited by pretreatment with mepyramine and famotidine, respectively. Removal of endothelium reversed the histamine- and 2PEA-induced relaxations to dose-related contractions. On the other hand, the removal had no effect on the dimaprit-induced relaxations, which were significantly reduced by pretreatment with famotidine. Histamine-induced relaxations in the precontracted strips with endothelium in the presence and absence of famotidine were suppressed or abolished by treatment with methylene blue or hemoglobin but were unaffected by aspirin. It may be concluded that histamine-induced relaxation in monkey pulmonary veins precontracted with PGF2 alpha is mediated by H2-receptors in smooth muscle and H1-receptors in endothelium. Also, stimulation of the endothelial H1-receptors liberates an endothelium-derived relaxing factor.

Direct effect of parathyroid hormone on insulin secretion from pancreatic islets

1990 ◽  
Vol 258 (6) ◽  
pp. E975-E984 ◽  
Author(s):  
G. Z. Fadda ◽  
M. Akmal ◽  
L. G. Lipson ◽  
S. G. Massry
Keyword(s):  
Insulin Secretion ◽  
Parathyroid Hormone ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Direct Effect ◽  
Indirect Evidence ◽  
Cytosolic Calcium ◽  
Dependent Manner ◽  
Stimulation Of

Indirect evidence indicates that parathyroid hormone (PTH) interacts with pancreatic islets and modulates their insulin secretion. This property of PTH has been implicated in the genesis of impaired insulin release in chronic renal failure. We examined the direct effect of PTH-(1-84) and PTH-(1-34) on insulin release using in vitro static incubation and dynamic perifusion of pancreatic islets from normal rats. Both moieties of the hormone stimulated in a dose-dependent manner glucose-induced insulin release but higher doses inhibited glucose-induced insulin release. This action of PTH was modulated by the calcium concentration in the media. The stimulatory effect of PTH was abolished by its inactivation and blocked by its antagonist [Tyr-34]bPTH-(7-34)NH2. PTH also augmented phorbol ester (TPA)-induced insulin release, stimulated adenosine 3',5'-cyclic monophosphate (cAMP) generation by pancreatic islets, and significantly increased (+50 +/- 2.7%, P less than 0.01) their cytosolic calcium. Verapamil inhibited the stimulatory effect of PTH on insulin release. The data show that 1) pancreatic islets are a PTH target and may have PTH receptors, 2) stimulation of glucose-induced insulin release by PTH is mediated by a rise in cytosolic calcium, 3) stimulation of cAMP production by PTH and a potential indirect activation of protein kinase C by PTH may also contribute to the stimulatory effect on glucose-induced insulin release, and 4) this action of PTH requires calcium in incubation or perifusion media.

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