The involvement of hydroxyl radical and cyclooxygenase metabolites in the activation of lung vagal sensory receptors by circulatory endotoxin in rats

2005 ◽  
Vol 98 (2) ◽  
pp. 620-628 ◽  
Author(s):  
Ching Jung Lai ◽  
Ting Ruan ◽  
Yu Ru Kou
Keyword(s):  
Hydroxyl Radical ◽  
Hydroxyl Radicals ◽  
Lung Compliance ◽  
Radical Scavenger ◽  
C Fibers ◽  
C Fiber ◽  
Underlying Mechanisms ◽  
Dynamic Lung Compliance ◽  
Fiber Stimulation ◽  
Stimulation Of

Circulatory endotoxin can stimulate vagal pulmonary C fibers and rapidly adapting receptors (RARs) in rats, but the underlying mechanisms are not clear. We investigated the involvement of hydroxyl radicals and cyclooxygenase metabolites in the stimulation of C fibers and RARs by circulatory endotoxin (50 mg/kg) in 112 anesthetized, paralyzed, and artificially ventilated rats. In rats pretreated with the vehicle, endotoxin stimulated C fibers and RARs and caused a slight increase in total lung resistance (Rl) and a decrease in dynamic lung compliance. In rats pretreated with dimethylthiourea (a hydroxyl radical scavenger) alone, indomethacin (a cyclooxygenase inhibitor) alone, or a combination of the two, C-fiber and RAR responses [C fiber: change (Δ) = −62, −79, and −85%; RAR: Δ = −80, −84, and −84%, respectively] were reduced, and the Rl response was prevented. The suppressive effects of a combination of dimethylthiourea and indomethacin on the C-fiber and RAR responses were not superior to indomethacin alone. In rats pretreated with isoproterenol (a bronchodilator), the C-fiber response was not significantly affected (Δ = −26%), the RAR response was reduced (Δ = −88%), and the Rl response was prevented. None of these pretreatments affected the dynamic lung compliance response. These results suggest that 1) both hydroxyl radicals and cyclooxygenase metabolites are involved in the endotoxin-induced stimulation of C fibers and RARs, and 2) the involvement of these two metabolites in the C-fiber stimulation may be due to their chemical effects, whereas that in the RAR stimulation may be due to their bronchoconstrictive effects.

scholarly journals Stimulation of vagal pulmonary C fibers by inhaled wood smoke in rats

1998 ◽  
Vol 84 (1) ◽  
pp. 30-36 ◽  
Author(s):  
C. J. Lai ◽  
Y. R. Kou
Keyword(s):  
Hydroxyl Radical ◽  
Combined Treatment ◽  
Wood Smoke ◽  
Radical Scavenger ◽  
C Fibers ◽  
Hydroxyl Radical Scavenger ◽  
C Fiber ◽  
Delayed Phase ◽  
Stimulation Of ◽  
Sustained Increase

Lai, C. J., and Y. R. Kou. Stimulation of vagal pulmonary C fibers by inhaled wood smoke in rats. J. Appl. Physiol. 84(1): 30–36, 1998.—This study investigated the stimulation of vagal pulmonary C fibers (PCs) by wood smoke. We recorded impulses from PCs in 58 anesthetized, open-chest, and artificially ventilated rats and delivered 6 ml of wood smoke into the lungs. Within 1 or 2 s after the smoke delivery, an intense and nonphasic burst of discharge [Δ = +7.4 ± 0.7 (SE) impulses/s, n = 68] was evoked in 60 of the 68 PCs studied and lasted for 4–8 s. This immediate stimulation was usually followed by a delayed and more sustained increase in C-fiber activity (Δ = +2.0 ± 0.4 impulses/s). The overall stimulation was not influenced by removal of smoke particulates ( n = 15) or by pretreatment with vehicle ( n = 8) for dimethylthiourea (DMTU; a hydroxyl radical scavenger) or indomethacin (Indo; a cyclooxygenase inhibitor). The immediate-phase stimulation was not affected by pretreatment with Indo ( n= 8) but was largely attenuated by pretreatment with DMTU ( n = 12) or by a combined treatment with DMTU and Indo (DMTU+Indo; n = 8). Conversely, the delayed-phase stimulation was partially suppressed either by DMTU or by Indo but was totally abolished by DMTU+Indo. These results suggest that 1) the stimulation of PCs is linked to the gas phase of wood smoke and 2) hydroxyl radical, but not cyclooxygenase products, is involved in the immediate-phase stimulation, whereas both metabolites are responsible for evoking the delayed-phase stimulation.

Diaphragmatic responses to graded stimulation of pulmonary C-fibers with capsaicin

1985 ◽  
Vol 59 (5) ◽  
pp. 1487-1494 ◽  
Author(s):  
J. R. Coast ◽  
S. S. Cassidy
Keyword(s):  
Dose Response ◽  
Strain Gauge ◽  
Contraction Rate ◽  
C Fibers ◽  
C Fiber ◽  
Shallow Breathing ◽  
Fiber Stimulation ◽  
Rapid Shallow Breathing ◽  
Stimulation Of

It has been suggested that pulmonary C-fiber stimulation is responsible for the rapid shallow breathing that accompanies pulmonary edema. However, pulmonary C-fiber stimulation also causes apnea. To determine whether it was possible for both responses to occur from one stimulus, we infused varying concentrations of capsaicin (a compound that selectively stimulates C-fiber receptors in the dog) into an in situ vascularly isolated dog lung and measured rates and strengths of diaphragmatic contractions with a strain gauge sutured to the diaphragm and electromyogram electrodes implanted in the diaphragm. There was a dose response to capsaicin in that increased doses were related directly with the duration of cessation of diaphragmatic contractions (2–100 s) and inversely with the latency from the start of stimulation to the beginning of the cessation of diaphragmatic contractions (100–5 s). There was no evidence, however, of rapid shallow breathing in this set of experiments. Either a gradual return to normal rate from prolonged contraction intervals or no change in contraction rate was seen, depending on capsaicin concentration. We conclude that the primary diaphragmatic response to pulmonary C-fiber stimulation is a cessation of diaphragmatic contractions rather than rapid shallow contractions.

Pattern of Cardiorespiratory Afferent Convergence to Solitary Tract Neurons Driven by Pulmonary Vagal C-Fiber Stimulation in the Mouse

1998 ◽  
Vol 79 (5) ◽  
pp. 2365-2373 ◽  
Author(s):  
Julian F. R. Paton
Keyword(s):  
Respiratory Activity ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Solitary Tract ◽  
C Fibers ◽  
C Fiber ◽  
Central Respiratory Activity ◽  
Fiber Stimulation ◽  
Cardiac Receptors ◽  
Stimulation Of

Paton, Julian F. R. Pattern of cardiorespiratory afferent convergence to solitary tract neurons driven by pulmonary vagal C-fiber stimulation in the mouse. J. Neurophysiol. 79: 2365–2373, 1998. The central integration of signals from pulmonary vagal C-fibers (or type-J receptors) with those arising from cardiac, peripheral chemoreceptor, and baroreceptor afferents to neurons within the nucleus of the solitary tract (NTS) was studied in an arterially perfused working heart–brain stem preparation of adult mouse. Pulmonary vagal C-fibers were excited by right atrial injection of phenylbiguanide (PBG) while cardiac receptors were stimulated by left ventricular injection of veratridine (1–3 μg/kg) or mechanically by distension of the left ventricle (20–50 μl perfusate) using an indwelling cannula. Carotid body chemoreceptors were activated by aortic injection of Na cyanide, whereas baroreceptors were stimulated by increasing arterial perfusion pressure. Stimulation of pulmonary C-fibers and cardiac, chemo-, and baroreceptors all produced a reflex bradycardia (23–133 bpm). Central respiratory activity, as recorded from the phrenic nerve, was depressed by stimulating pulmonary C-fibers and cardiac and baroreceptors but enhanced in amplitude and frequency during chemoreceptor stimulation. Twenty-seven NTS neurons were excited and three were inhibited after pulmonary C-fiber stimulation displaying decrementing discharges with a peak firing frequency of up to 42 Hz (15 ± 2.2 Hz, mean ± SE) that lasted for 8.8 ± 0.9 s. These responses occurred <1 s from the end of the PBG injection that was within the pulmonary circulation time. None of these cells responded to increases in right atrial pressure. All cells excited by PBG were also driven synaptically after electrical stimulation of the ipsilateral cervical vagus nerve at a latency of 32.9 ± 3.2 ms (range 20–62 ms). None of these neurons had ongoing activity related to central respiratory activity. Convergence from cardiorespiratory afferents to 21 neurons driven by pulmonary C-fibers was tested. Twenty-five percent of cells were selectively excited by chemical stimulation of cardiac receptors alone, 19% were driven by peripheral chemoreceptors, and 38% responded to both cardiac and chemoreceptor activation. In contrast, only 13% of the cells activated by PBG injection responded to stimulation of baroreceptors and only 6% to cardiac mechanoreceptor stimulation. None of these neurons were activated by increasing right atrial pressure. The data indicate a high proportion of afferent convergence from pulmonary C-fibers, cardiac receptors, and peripheral chemoreceptors in the NTS. However, these neurons appear not to integrate inputs from cardiovascular mechanoreceptors. The significance of the data is discussed in relation to pathological disease states such as pulmonary congestion and cardiac failure.

Pulmonary rapidly adapting receptors reflexly increase airway secretion in dogs

1989 ◽  
Vol 67 (2) ◽  
pp. 682-687 ◽  
Author(s):  
J. Yu ◽  
H. D. Schultz ◽  
J. Goodman ◽  
J. C. Coleridge ◽  
H. M. Coleridge ◽  
...  
Keyword(s):  
Lung Compliance ◽  
Base Line ◽  
Lung Collapse ◽  
C Fibers ◽  
Airway Secretion ◽  
Stretch Receptors ◽  
Dynamic Lung Compliance ◽  
Vagal Cooling ◽  
Tracheal Secretion ◽  
Stimulation Of

We attempted to determine whether stimulation of pulmonary rapidly adapting receptors (RARs) increase tracheal submucosal gland secretion in anesthetized open-chest dogs. Electroneurographic studies of pulmonary afferents established that RARs but not lung C-fibers were stimulated by intermittent lung collapse during deflation, collapse being produced by removing positive end-expiratory pressure (PEEP, 4 cmH2O) or by applying negative end-expiratory pressure (NEEP, -4 cmH2O). We measured tracheal secretion by the “hillocks” method. Removing PEEP or applying NEEP for 1 min increased secretion from a base line of 6.0 +/- 1.1 to 11.8 +/- 1.7 and 22.0 +/- 2.8 hillocks.cm-2.min-1, respectively (P less than 0.005). After PEEP was restored, dynamic lung compliance (Cdyn) was 37% below control, and secretion remained elevated (P less than 0.05). A decrease in Cdyn stimulates RARs but not other pulmonary afferents. Hyperinflation, which restored Cdyn and RAR activity to control, returned secretion rate to base line. Secretory responses to lung collapse were abolished by vagal cooling (6 degrees C), by pulmonary vagal section, or by atropine. We conclude that RAR stimulation reflexly increases airway secretion. We cannot exclude the possibility that reduced input from slowly adapting stretch receptors contributed to the secretory response.

Vagal and mediator mechanisms underlying the tachypnea caused by pulmonary air embolism in dogs

2000 ◽  
Vol 88 (4) ◽  
pp. 1247-1253 ◽  
Author(s):  
H. F. Chen ◽  
Y. R. Kou
Keyword(s):  
Hydroxyl Radical ◽  
Air Embolism ◽  
Radical Scavenger ◽  
C Fibers ◽  
Hydroxyl Radical Scavenger ◽  
C Fiber ◽  
Cervical Vagotomy ◽  
The Right ◽  
Spontaneously Breathing ◽  
Saline Vehicle

We investigated the vagal and mediator mechanisms underlying the tachypnea caused by pulmonary air embolism (PAE) in anesthetized and spontaneously breathing dogs. PAE was induced by infusion of air into the right atrium (0.2 ml ⋅ kg−1 ⋅ min−1for 10 min). The first PAE induction caused an increase in respiratory frequency accompanied by a decrease in tidal volume in each of the 30 animals studied. Subsequently, animals were evenly divided into five groups, and a second PAE induction was repeated after various experimental interventions. The tachypneic response to PAE was not significantly altered by pretreatment with a saline vehicle but was largely attenuated by either perivagal capsaicin treatment (a technique that selectively blocks the conduction of unmyelinated C fibers), pretreatment with ibuprofen (a cyclooxygenase inhibitor), or pretreatment with dimethylthiourea (a hydroxyl radical scavenger). Ultimately, the tachypneic response was nearly abolished by a bilateral cervical vagotomy. These results suggest that 1) lung vagal unmyelinated C-fiber afferents play a predominant role in evoking the reflex tachypneic response to PAE and 2) both cyclooxygenase products and hydroxyl radical are important in eliciting this vagally mediated response.

Neurophysiological basis for neurogenic-mediated articular cartilage anabolism alteration

2001 ◽  
Vol 280 (1) ◽  
pp. R115-R122 ◽  
Author(s):  
Elvire Gouze-Decaris ◽  
Lionel Philippe ◽  
Alain Minn ◽  
Philippe Haouzi ◽  
Pierre Gillet ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Ex Vivo ◽  
Cartilage Damage ◽  
Intrathecal Injection ◽  
Chronic Administration ◽  
C Fibers ◽  
Glutamatergic Synaptic Transmission ◽  
C Fiber ◽  
Fiber Stimulation ◽  
Neurophysiological Basis

This study was designed to investigate the pathways involved in neurogenic-mediated articular cartilage damage triggered by a nonsystemic distant subcutaneous or intra-articular inflammation. The cartilage damage was assessed 24 h after subcutaneous or intra-articular complete Freund's adjuvant (CFA) injection measuring patellar proteoglycan (PG) synthesis (ex vivo [Na2 35SO4] incorporation) in 96 Wistar rats. Unilateral subcutaneous or intra-articular injection of CFA induced significant decrease (25–29%) in PG synthesis in both patellae. Chronic administration of capsaicin (50 mg · kg−1 · day−1 during 4 days), which blunted the normal response of C fiber stimulation, prevented the bilateral significant decrease in cartilage synthesis. Similarly, intrathecal injection of MK-801 (10 nmol/day during 5 days), which blocked the glutamatergic synaptic transmission at the dorsal horn of signal originating in primary afferent C fibers, eliminated the CFA-induced PG synthesis decrease in both patellae. Chemical sympathectomy, induced by guanethidine (12.5 mg · kg−1 · day−1 during 6 wk), also prevented PG synthesis alteration. Finally, compression of the spinal cord at the T3-T5 level had a similar protective effect on the reduction of [Na2 35SO4] incorporation. It is concluded that the signal that triggers articular cartilage synthesis damage induced by a distant local inflammation 1) is transmitted through the afferent C fibers, 2) makes glutamatergic synaptic connections with the preganglionic neurons of the sympathetic system, and 3) involves spinal and supraspinal pathways.

scholarly journals Involvement of a local Fenton reaction in the reciprocal modulation by O2 of the glucagon-dependent activation of the phosphoenolpyruvate carboxykinase gene and the insulin-dependent activation of the glucokinase gene in rat hepatocytes

1998 ◽  
Vol 335 (2) ◽  
pp. 425-432 ◽  
Author(s):  
Thomas KIETZMANN ◽  
Torsten PORWOL ◽  
Karl ZIEROLD ◽  
Kurt JUNGERMANN ◽  
Helmut ACKER
Keyword(s):  
Hydroxyl Radical ◽  
Hydroxyl Radicals ◽  
Fenton Reaction ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Gene Activation ◽  
Three Dimensional ◽  
Rat Hepatocytes ◽  
Confocal Laser ◽  
Radical Scavenger ◽  
Insulin Dependent

H2O2 mimicked the action of periportal pO2 in the modulation by O2 of the glucagon-dependent activation of the phosphoenolpyruvate carboxykinase (PCK) gene and the insulin-dependent activation of the glucokinase (GK) gene. H2O2 can be converted in the presence of Fe2+ in a Fenton reaction into hydroxyl anions and hydroxyl radicals (•OH). The hydroxyl radicals are highly reactive and might interfere locally with transcription factors. It was the aim of the present study to investigate the role of and to localize such a Fenton reaction. Hepatocytes cultured for 24 h were treated under conditions mimicking periportal or perivenous pO2 with glucagon or insulin plus the iron chelator desferrioxamine (DSF) or the hydroxyl radical scavenger dimethylthiourea (DMTU) to inhibit the Fenton reaction. PCK mRNA was induced by glucagon maximally under conditions of periportal pO2 and half-maximally under venous pO2. GK mRNA was induced by insulin with reciprocal modulation by O2. DSF and DMTU reduced the induction of PCK mRNA to about half-maximal and increased the induction of GK mRNA to maximal under both O2 tensions. Hydroxyl radical formation was maximal under arterial pO2. Perivenous pO2, DSF and DMTU each decreased the formation of •OH to about 70% of control. The Fenton reaction could be localized in a perinuclear space by confocal laser microscopy and three-dimensional reconstruction techniques. In the same compartment, iron could be detected by electron-probe X-ray microanalysis. Thus a local Fenton reaction is involved in the O2 signalling, which modulated the glucagon- and insulin-dependent PCK gene and GK gene activation.

Endogenous BK stimulates ischemically sensitive abdominal visceral C fiber afferents through kinin B2 receptors

1994 ◽  
Vol 267 (6) ◽  
pp. H2398-H2406 ◽  
Author(s):  
H. L. Pan ◽  
G. L. Stahl ◽  
S. V. Rendig ◽  
O. A. Carretero ◽  
J. C. Longhurst
Keyword(s):  
Receptor Antagonist ◽  
Impulse Activity ◽  
Discharge Rate ◽  
Visceral Afferents ◽  
C Fibers ◽  
C Fiber ◽  
Hoe 140 ◽  
B2 Receptors ◽  
The Right ◽  
Stimulation Of

Abdominal ischemia and reperfusion reflexly activate the cardiovascular system. In the present study, we evaluated the role of endogenously produced bradykinin (BK) in the stimulation of ischemically sensitive visceral afferents. Single-unit activity of abdominal visceral C fiber afferents was recorded from the right thoracic sympathetic chain of anesthetized cats during 5 min of abdominal ischemia. Abdominal ischemia increased the portal venous plasma BK level from 49 +/- 10 to 188 +/- 66 pg/ml (P < 0.05). Injection of BK (1 microgram/kg ia) into the descending aorta significantly increased impulse activity (0.88 +/- 0.16 impulses/s) of 10 C fibers, whereas a kinin B1-receptor agonist, des-Arg9-BK (1 microgram/kg), did not alter the discharge rate. Inhibition of kininase II activity with captopril (4 mg/kg i.v.) potentiated impulse activity of 14 ischemically sensitive C fibers (0.44 +/- 0.09 vs. precaptopril, 0.33 +/- 0.08 impulses/s; P < 0.05). In addition, a kinin B2-receptor antagonist (NPC-17731; 40 micrograms/kg i.v.) attenuated activity of afferents during ischemia (0.39 +/- 0.08 vs. pre-NPC-17731, 0.72 +/- 0.13 impulses/s; P < 0.05) and eliminated the response of 10 C fibers to BK. Another kinin B2-receptor antagonist, Hoe-140 (30 micrograms/kg iv), had similar inhibitory effects on six other ischemically sensitive C fibers. In 15 separate cats treated with aspirin (50 mg/kg i.v.), Hoe-140 (30 micrograms/kg i.v.) attenuated impulse activity of only 3 of 16 ischemically sensitive C fibers. These data suggest that BK produced during abdominal ischemia contributes to the stimulation of ischemically sensitive visceral C fiber afferents through kinin B2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals On the Nature of Hydrodynamic Cavitation Process and Its Application for the Removal of Water Pollutants

2019 ◽  
Vol 12 ◽  
pp. 117862211988048 ◽  
Author(s):  
Erick R Bandala ◽  
Oscar M Rodriguez-Narvaez
Keyword(s):  
Hydroxyl Radical ◽  
Hydroxyl Radicals ◽  
High Energy ◽  
Optimal Operation ◽  
Hydrodynamic Cavitation ◽  
Radical Scavenger ◽  
Process Conditions ◽  
Cavitation Process ◽  
Operation Conditions ◽  
Hydroxyl Radical Scavenger

Cavitation is considered a high energy demanding process for water treatment. For this study, we used a simple experimental setup to generate cavitation at a low pressure (low energy) and test it for hydroxyl radical production using a well-known chemical probe as a hydroxyl radical scavenger. The conditions for generating the cavitation process (eg, pressure, flow velocity, temperature, and other significant variables) were used to degrade model contaminants, an azo dye and an antibiotic. The amount of hydroxyl radicals generated by the system was estimated using N,N-dimethyl-p-nitrosoaniline (pNDA) as hydroxyl radical scavenger. The capability of hydrodynamic cavitation (HC) to degrade contaminants was assessed using Congo red (CR) and sulfamethoxazole (SMX) as model contaminants. Different chemical models were analyzed using UV-visible spectrophotometry (for pNDA and CR) and high-performance liquid chromatography (HPLC) (for SMX) after HC treatment under different process conditions (ie, pressure of 13.7 and 10.3 kPa, and flow rates of 0.14 to 3.6 × 10−4 m3/s). No pNDA bleaching was observed for any of the reaction conditions tested after 60 minutes of treatment, which suggests that there was no hydroxyl radical generation during the process. However, 50% degradation of CR and 25% degradation of SMX were observed under the same process conditions, comparable with previously reported results. These results suggest that the process is most likely thermally based rather than radically based, and therefore, it can degrade organic pollutants even if no hydroxyl radicals are produced. Hydrodynamic cavitation, either alone or coupled with other advanced water technologies, has been identified as a promising technology for removing organic contaminants entering the water cycle; however, more research is still needed to determine the specific mechanisms involved in the process and the optimal operation conditions for the system.

Pulmonary C-fibers reflexly increase secretion by tracheal submucosal glands in dogs

1985 ◽  
Vol 58 (3) ◽  
pp. 907-910 ◽  
Author(s):  
H. D. Schultz ◽  
A. M. Roberts ◽  
C. Bratcher ◽  
H. M. Coleridge ◽  
J. C. Coleridge ◽  
...  
Keyword(s):  
Gland Secretion ◽  
Right Atrial ◽  
Vagus Nerves ◽  
C Fibers ◽  
Airway Secretion ◽  
Submucosal Glands ◽  
C Fiber ◽  
Anesthetized Dogs ◽  
The Right ◽  
Stimulation Of

Stimulation of bronchial C-fibers evokes a reflex increase in secretion by tracheal submucosal glands, but the influence of pulmonary C-fibers on tracheal gland secretion is uncertain. In anesthetized dogs with open chests, we sprayed powdered tantalum on the exposed mucosa of a segment of the upper trachea to measure the rate of secretion by submucosal glands. Secretions from the gland ducts caused elevations (hillocks) in the tantalum layer. We counted hillocks at 10-s intervals for 60 s before and 60 s after we injected capsaicin (10–20 micrograms/kg) into the right atrium to stimulate pulmonary C-fiber endings. Right atrial injection of capsaicin increased the rate of hillock formation fourfold, but left atrial injection had no significant effect. The response was abolished by cutting the vagus nerves or cooling them to 0 degree C. We conclude that the reflex increase in tracheal submucosal gland secretion evoked by right atrial injection of capsaicin was initiated as capsaicin passed through the pulmonary vascular bed, and hence that pulmonary C-fibers, like bronchial C-fibers, reflexly increase airway secretion.

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