Effect of vagal tone on airway diameters and on lung volume in anesthetized dogs

1976 ◽  
Vol 41 (4) ◽  
pp. 581-589 ◽  
Author(s):  
H. L. Hahn ◽  
P. D. Graf ◽  
J. A. Nadel
Keyword(s):  
Physical Properties ◽  
Lung Volume ◽  
Vagal Stimulation ◽  
Vagal Tone ◽  
Transpulmonary Pressure ◽  
Lung Parenchyma ◽  
Open Chest ◽  
Anesthetized Dogs

In 18 open-chest dogs we obtained pressure-diameter (P-D) curves from tantalum bronchograms and pressure-volume (P-V) curves by plethysmography. After vagotomy most of the decrease in diameter with decreasing transpulmonary pressure (Ptp) occured below 10 cmH2O and there was no P-D hysteresis. Smaller airways narrowed more with decreasing Ptp than larger ones. Bronchodilators did not increase diameters after vagotomy (P less than 0.2). With vagi intact, diameters were smaller at all Ptp (P less than 0.01) and exhibited hysteresis, but the lung P-V curve was unchanged. Vagal stimulation narrowed airways further at all Ptp and hysteresis was marked. Smaller airways narrowed more with vagal stimulation than larger ones. Vagal stimulation did not change the deflation limb of the P-V curve but decreased inflation volumes slightly at all Ptp (P less than 0.01). We conclude that in vivo toneis vagal and that it affects the physical properties of airways, but not oflungs, making the airways remarkably independent from lung parenchyma.

In vivo estimation of tracheal distensibility and hysteresis in normal adults

1987 ◽  
Vol 63 (6) ◽  
pp. 2482-2489 ◽  
Author(s):  
V. Hoffstein ◽  
R. G. Castile ◽  
C. R. O'Donnell ◽  
G. M. Glass ◽  
D. J. Strieder ◽  
...  
Keyword(s):  
Lung Volume ◽  
Transpulmonary Pressure ◽  
Lung Parenchyma ◽  
Esophageal Pressure ◽  
Transmural Pressure ◽  
Variable Degree ◽  
Cross Sectional ◽  
Acoustic Reflection ◽  
Direct Measurements

We used the acoustic reflection technique to measure the cross-sectional area of tracheal and bronchial airway segments of eight healthy adults. We measured airway area during a slow continuous expiration from total lung capacity (TLC) to residual volume (RV) and during inspiration back to TLC. Lung volume and esophageal pressure were monitored continuously during this quasi-static, double vital capacity maneuver. We found that 1) the area of tracheal and bronchial segments increases with increasing lung volume and transpulmonary pressure, 2) the trachea and bronchi exhibit a variable degree of hysteresis, which may be greater or less than that of the lung parenchyma, 3) extrathoracic and intrathoracic tracheal segments behaved as if they were subjected to similar transmural pressure and had similar elastic properties, and 4) specific compliance (means +/- SE) for the intrathoracic and bronchial segments, calculated with the assumption that transmural pressure is equal to the transpulmonary pressure, was significantly (P less than 0.05) smaller for the intrathoracic segment than for the bronchial segment: (2.1 +/- 2.0) X 10(-3) cmH2O-–1 vs. (9.1 +/- 2.1) X 10(-3) cmH2O–1. Direct measurements of airway area using acoustic reflections are in good agreement with previous estimates of airway distensibility in vivo, obtained by radiography or endoscopy.

Long-term effects of hyperpolarization-activated inward current blockade on cardiac parasympathetic activity

EP Europace ◽  
2021 ◽  
Vol 23 (Supplement_3) ◽  
Author(s):  
A Scridon ◽  
VB Halatiu ◽  
AI Balan ◽  
DA Cozac ◽  
GV Moldovan ◽  
...  
Keyword(s):  
Heart Rate ◽  
Vagus Nerve ◽  
Vagal Stimulation ◽  
Sinus Node ◽  
Vagal Tone ◽  
Right Atrial ◽  
The Right

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): This work was supported by a grant of the Romanian Ministry of Education and Research, CNCS - UEFISCDI Background The autonomic control of the pacemaker current, If, and the molecular mechanisms underlying parasympathetic If modulation are well understood. Conversely, the effects of chronic If blockade on the parasympathetic nervous system and on the heart rate (HR) response to acute parasympathetic changes are still largely unknown. Such interactions could significantly influence the course of patients undergoing chronic therapy with the If blocker ivabradine. Purpose We aimed to assess the effects of long-term If blockade using ivabradine on cardiac autonomic modulation and on the cardiovascular response to acute in vivo and in vitro parasympathetic stimulation. Methods Radiotelemetry ECG transmitters were implanted in 6 Control and 10 ivabradine-treated male Wistar rats (IVA; 3 weeks, 10 mg/kg/day); sympathetic and parasympathetic heart rate variability parameters were assessed. At the end of the study, the right atrium was removed and right atrial HCN(1-4) RNA expression levels were analyzed. The HR and systolic blood pressure (SBP) responses to in vivo electrical stimulation of the right vagus nerve (2–20 Hz) and the spontaneous sinus node discharge rate (SNDR) response to in vitro cholinergic receptors stimulation using carbamylcholine (10-9–10-6 mol/L) were assessed in 6 additional Control and 10 IVA rats. Results At the end of the study, mean 24-h HR was significantly lower in the IVA compared with the Control rats (301.3 ± 7.5 bpm vs. 341.5 ± 8.3 bpm; p< 0.01). Ivabradine administration led to a significant increase in vagal tone and shifted the sympatho-vagal balance towards vagal dominance (awake, asleep, and over 24-h; all p< 0.05). In the Control rats, in vivo vagus nerve stimulation induced a progressive decrease in both the SBP (p = 0.0001) and the HR (p< 0.0001). Meanwhile, in the IVA rats, vagal stimulation had no effect on the HR (p = 0.16) and induced a significantly lower drop in SBP (p< 0.05). Ivabradine-treated rats also presented a significantly lower SNDR drop in response to carbamylcholine (p< 0.01) and significantly higher HCN4 expression (p = 0.02). Conclusion Long-term If blockade using ivabradine caused a significant increase in vagal tone and shifted the autonomic balance towards vagal dominance in rats. Given the highly proarrhythmic effects of vagal activation at the atrial level, these findings could provide an explanation for the increased risk of atrial fibrillation associated with ivabradine use in clinical trials. In addition, ivabradine reduced the HR response to direct muscarinic receptors stimulation, canceled the cardioinhibitory response and blunted the hemodynamic response to in vivo vagal stimulation, and led to significant sinus node HCN4 up-regulation. These data suggest that ivabradine-induced HCN4 and the consequent If up-regulation could render the sinus node less sensitive to acute vagal inputs and could thus protect against excessive bradycardia induced by acute vagal activation.

Distribution oand pharmacological release of histamine in canine lung in vivo

1978 ◽  
Vol 44 (3) ◽  
pp. 455-463 ◽  
Author(s):  
M. R. Nisam ◽  
A. Zbinden ◽  
S. Chesrown ◽  
D. Barnett ◽  
W. M. Gold
Keyword(s):  
Lung Parenchyma ◽  
Smooth Muscle Contraction ◽  
Lung Compliance ◽  
Internal Diameter ◽  
Cellular Interactions ◽  
Arterial Blood ◽  
Beta Adrenergic Agonists ◽  
Anesthetized Dogs ◽  
Tissue Histamine

We have examined the physiological effects of stored mediators released from airways by compound 48/80 aerosols in anesthetized dogs. In 13 dogs, both mast cell numbers and tissue histamine were related inversely to bronchial internal diameter (P less than 0.0001). Compound 48/80 aerosols degranulated mast cells and decreased histamine content (-29.0 +/- 10.0%; mean +/- SE) in 5–10 mm bronchi, but not in 3–4 mm bronchi or lung parenchyma. This was associated with increased plasma histamine (31.8 +/- 18.4 ng/ml), increased airflow resistance (Rrs: + 452 +/- 257%), decreased lung compliance (-28 +/- 10%), and decreased arterial blood pressure (-41 +/- 6.5%) at 2 min. The increased Rrs was reversed by beta-adrenergic agonists, indicating it was caused by bronchial smooth muscle contraction; prevented by chlorpheniramine, indicating it was caused by histamine action on H1-receptors; and augmented and prolonged by propranolol, suggesting that histamine triggered sympathetic mechanisms which modulated the effect of 48/80. This experimental approach permits the study of mechanisms in vivo which may be involved in the sequence of reactions initiated by antigen-IgE interaction. However, the latter involve not only stored mediators, but also unstored mediators, neural reflexes, and complex cellular interactions.

Vasopressin-induced changes in cardiac vagal tone and oxygen consumption in dogs

1994 ◽  
Vol 266 (3) ◽  
pp. R838-R849
Author(s):  
J. F. Liard
Keyword(s):  
Heart Rate ◽  
Left Atrial ◽  
Vagal Stimulation ◽  
Vagal Tone ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Beta Blockade ◽  
Cardiac Denervation ◽  
Anesthetized Dogs ◽  
Atropine Treatment

Experiments were conducted in 63 dogs to determine whether stimulation of vagal tone contributes to the decrease in O2 consumption (VO2) that results from arginine vasopressin (AVP) administration. Vagal stimulation with pilocarpine did not reduce VO2 in conscious dogs. In anesthetized dogs, bilateral electrical cervical efferent vagal stimulation lowered both cardiac output (CO; by 46%) and VO2 (by 22%) over the first 5 min. Between 7 and 11 min of stimulation, CO remained decreased, but VO2 returned to control. Significant increases in left atrial pressure, bradycardia, and a fall in mean arterial pressure accompanied vagal stimulation. All these effects of cervical vagal stimulation were abolished by cardiac denervation and also by pacing. Administration of a selective AVP V1 agonist led to significant reductions of CO and VO2. Cardiac denervation prevented the decrease in VO2 induced by AVP infusion, but not the decrease in CO. During AVP infusions, pacing at a rate slightly higher than control heart rate did not prevent the fall in CO or in VO2, whereas pacing at 150 beats/min prevented part of the fall in VO2. Sinoaortic denervation or atropine treatment prevented the decrease in VO2 resulting from AVP infusion. The combination of alpha- and beta-blockade did not affect the CO or the VO2 response to AVP infusion, nor did naloxone treatment. The administration of atrial or ventricular extracts, but not that of alpha-human atrial natriuretic peptide, led to a significant reduction in VO2. These results are compatible with the hypothesis that AVP infusion increases vagal tone to the heart, which, possibly as a result of increased left atrial pressure and reduced heart rate, may release a factor reducing VO2.

Comparison of postnatal lung growth and development between C3H/HeJ and C57BL/6J mice

2006 ◽  
Vol 100 (5) ◽  
pp. 1577-1583 ◽  
Author(s):  
Shawn E. Soutiere ◽  
Wayne Mitzner
Keyword(s):  
Lung Volume ◽  
Lung Development ◽  
Inbred Mice ◽  
Left Lung ◽  
Transpulmonary Pressure ◽  
Mean Linear Intercept ◽  
Old Mice

Previous work by our group has demonstrated substantial differences in lung volume and morphometric parameters between inbred mice. Specifically, adult C3H/HeJ (C3) have a 50% larger lung volume and 30% greater mean linear intercept than C57BL/6J (B6) mice. Although much of lung development occurs postnatally in rodents, it is uncertain at what age the differences between these strains become manifest. In this study, we performed quasi-static pressure-volume curves and morphometric analysis on neonatal mice. Lungs from anesthetized mice were degassed in vivo using absorption of 100% O2. Pressure-volume curves were then recorded in situ. The lungs were then fixed by instillation of Zenker’s solution at a constant transpulmonary pressure. The left lung from each animal was used for morphometric determination of mean air space chord length ( Lma). We found that the lung volume of C3 mice was substantially greater than that of B6 mice at all ages. In contrast, there was no difference in Lma (62.7 μm in C3 and 58.5 μm in B6) of 3-day-old mice. With increasing age (8 days), there was a progressive decrease in the Lma of both strains, with the magnitude of the decrease in B6 Lma mice exceeding that of C3. C3 lung volume remained 50% larger. The combination of parenchymal architectural similarity with lung air volume differences and different rates of alveolar septation support the hypothesis that lung volume and alveolar dimensions are independently regulated.

Nitric oxide as a putative nonadrenergic noncholinergic inhibitory transmitter in the canine pylorus in vivo

1992 ◽  
Vol 262 (4) ◽  
pp. G695-G702 ◽  
Author(s):  
H. D. Allescher ◽  
G. Tougas ◽  
P. Vergara ◽  
S. Lu ◽  
E. E. Daniel
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Vagal Stimulation ◽  
Inhibitory Effect ◽  
Field Stimulation ◽  
Neural Inhibition ◽  
Anesthetized Dogs ◽  
Inhibitory Transmitter

Antropyloroduodenal motility was recorded in seven anesthetized dogs to assess the role of nitric oxide and L-arginine metabolites in nonadrenergic noncholinergic (NANC) mediation of pyloric relaxation. Pyloric activity induced by duodenal field stimulation was inhibited by antral field stimulation and electrical vagal stimulation. Intra-arterial NG-L-arginine-methyl-ester (L-NAME) reduced the inhibition from antral or vagal stimulation (P less than 0.05). Intravenous infusion of L-NAME also blocked the inhibitory effect of vagal and antral stimulation but left the tetrodotoxin-insensitive action of intra-arterial vasoactive intestinal peptide (VIP) and sodium nitroprusside unchanged. L-Arginine reversed the effect of L-NAME whereas D-arginine did not. L-NAME enhanced pyloric contractions to intra-arterial acetylcholine. The NANC inhibition of the substance P-stimulated pyloric response in vitro was blocked by L-NAME and reversed by addition of L-arginine. Sodium nitroprusside was effective as a relaxant in vitro but VIP was not. These data suggest that metabolites of L-arginine mediate neural inhibition of canine pyloric motor activity.

Alveolar surface area-to-lung volume ratio in oleic acid-induced pulmonary edema

1996 ◽  
Vol 80 (3) ◽  
pp. 742-746 ◽  
Author(s):  
S. Suzuki ◽  
T. Akahori ◽  
N. Miyazawa ◽  
M. Numata ◽  
T. Okubo ◽  
...  
Keyword(s):  
Surface Tension ◽  
Oleic Acid ◽  
Pulmonary Edema ◽  
Lung Volume ◽  
Volume Ratio ◽  
Transpulmonary Pressure ◽  
Mean Free Path ◽  
Alveolar Surface Area ◽  
Alveolar Surface

It is unknown how the in vivo alveolar surface area-to-volume ratio (S/V) changes in low-pressure pulmonary edema. Here, the S/V is the area of the air-tissue interface per unit total volume (air plus tissue). We hypothesized that in oleic acid (OA)-induced edema inactivation of the pulmonary surfactant may increase surface tension and decrease the S/V at any given lung volume. OA (0.04 mg/kg) was intravenously injected into dogs. We measured the in vivo S/V (equivalent to the inverse of optical mean free path by light-scattering stereology and the pressure-volume (PV) curve 60-90 min after OA administration. OA administration decreased the lung volume at each transpulmonary pressure and increased the wet-to-dry weight ratio. The S/V decreased after OA administration (optical mean free path increased). The air-filled PV curves shifted downward after OA, but the saline-filled PV curves after OA administration did not differ significantly from control saline-filled curves. The difference in transpulmonary pressure between air- and saline-filled PV curves (an index of the magnitude of surface tension) was increased in OA-induced pulmonary edema. This study suggests that in OA-induced pulmonary edema the alveolar surface tension increases and the S/V decreases, presumably due to inactivation of surfactant by serum leakage to alveoli.

Effects of tidal volume stretch on airway constriction in vivo

2001 ◽  
Vol 91 (5) ◽  
pp. 1995-1998 ◽  
Author(s):  
Robert Brown ◽  
Wayne Mitzner
Keyword(s):  
Lung Ventilation ◽  
Lung Parenchyma ◽  
One Lung Ventilation ◽  
High Resolution Computed Tomography ◽  
Airway Patency ◽  
Airway Constriction ◽  
Tidal Stress ◽  
Anesthetized Dogs ◽  
Airway Tone

Tidal stresses are thought to be involved in maintaining airway patency in vivo. The present study examined the effects of normal stresses exerted by the lung parenchyma during tidal ventilation on recovery from agonist-induced airway constriction. In seven anesthetized dogs, one lung was selectively ventilated with a Univent endotracheal tube (Vitaid, Lewiston, NY). Airway tone was increased either transiently (intravenous bolus) or continuously (intravenous infusion) with methacholine (MCh). During one-lung ventilation, changes in the airway size of both lungs were measured for up to 40 min during recovery from constriction by using high-resolution computed tomography. After recovery to baseline, the alternate lung was ventilated, and the protocol was repeated. The absence of tidal stresses led to an attenuated recovery from either transient or steady-state airway constriction. The effectiveness or lack thereof of normal tidal stress in stabilizing airway size may be one factor that contributes to the lack of reversal with tidal breathing and deep inspiration seen in asthmatic subjects.

Diaphragmatic contractility enhanced by aminophylline: role of extracellular calcium

1983 ◽  
Vol 54 (2) ◽  
pp. 460-464 ◽  
Author(s):  
M. Aubier ◽  
D. Murciano ◽  
N. Viires ◽  
Y. Lecocguic ◽  
R. Pariente
Keyword(s):  
Transpulmonary Pressure ◽  
Extracellular Calcium ◽  
Phrenic Nerve Stimulation ◽  
Transdiaphragmatic Pressure ◽  
Balloon Catheters ◽  
Residual Capacity ◽  
Anesthetized Dogs ◽  
Phrenic Nerves

We have studied the effects of aminophylline on diaphragmatic contractility in 12 anesthetized dogs. The phrenic nerves were stimulated supramaximally (20 Hz, 0.1 ms) with electrodes placed around the fifth roots, and the transdiaphragmatic pressure (Pdi) generated at functional residual capacity (FRC) was measured with balloon catheters. Constancy of FRC was monitored by measuring the end-expiratory transpulmonary pressure, the dogs being occluded at FRC before the stimulations. The electrical activity of the diaphragm (Edi) during the stimulations was recorded with electrodes inserted in both hemidiaphragms. Phrenic stimulations during an infusion of aminophylline (10 mg/kg in 5 min) increased Pdi by 25 +/- 8% of control values, whereas the Edi remained unchanged. This potentiating effect of aminophylline was abolished when an identical dose was injected during a continuous infusion of a calcium blocker (verapamil, 0.1 mg X kg-1 X min-1). Infusion of another methylxanthine compound, caffeine (10 mg/kg), also increased Pdi for an identical electrical phrenic nerve stimulation by 21 +/- 6% compared with control values. However, the potentiating effect of caffeine was not abolished by verapamil. We conclude that aminophylline in vivo increases diaphragmatic contractility and that extracellular calcium is necessary for this action, a mechanism not shared by another methylxanthine compound, caffeine.

Static lung mechanics of intact and excised rhesus monkey lungs and lobes

1978 ◽  
Vol 44 (4) ◽  
pp. 547-552 ◽  
Author(s):  
P. D. Pare ◽  
R. Boucher ◽  
M. C. Michoud ◽  
J. C. Hogg
Keyword(s):  
Lung Volume ◽  
Transpulmonary Pressure ◽  
Lung Mechanics ◽  
Unit Weight ◽  
Water Displacement ◽  
Lung Capacity ◽  
Residual Capacity ◽  
Boyle’S Law

Subdivisions of lung volume and pressure-volume (PV) curves of the lung and chest wall (CW) were measured in 12 rhesus monkeys (Macacca mulatta) under pentobarbital anesthesia. In addition, volumes and PV curves were obtained on the excised lungs and lobes of 12 cynomolgus monkeys (M. fasicularis). Boyle's law was used to determine functional residual capacity (FRC) in the intact animals and water displacement to determine minimal volume (MV) in the excised lungs. Total lung capacity (TLC = lung volume at a transpulmonary pressure of 30 cmH2O) was similar in vivo and in vitro (90 + 83 ml/kg) but residual volume (RV = volume at airway pressure of -50 cmH2O) and MV differed markedly (16.5 + 5.9 ml/kg). In the intact animals a very stiff CW appeared to determine RV, whereas airway closure determined MV in excised lungs. PV curves of upper and lower lobes were not different when expressed as %TLC but when expressed as milliliters of gas per gram of lung, the upper lobes contained significantly more gas per unit weight.

Sign in / Sign up

Export Citation Format

Share Document