Tracheal smooth muscle mechanics in vivo

1990 ◽  
Vol 68 (1) ◽  
pp. 209-219 ◽  
Author(s):  
M. Okazawa ◽  
P. Pare ◽  
J. Road

We applied the technique of sonomicrometry to directly measure length changes of the trachealis muscle in vivo. Pairs of small 1-mm piezoelectric transducers were placed in parallel with the muscle fibers in the posterior tracheal wall in seven anesthetized dogs. Length changes were recorded during mechanical ventilation and during complete pressure-volume curves of the lung. The trachealis muscle showed spontaneous fluctuations in base-line length that disappeared after vagotomy. Before vagotomy passive pressure-length curves showed marked hysteresis and length changed by 18.5 +/- 13.2% (SD) resting length at functional residual capacity (LFRC) from FRC to total lung capacity (TLC) and by 28.2 +/- 16.2% LFRC from FRC to residual volume (RV). After vagotomy hysteresis decreased considerably and length now changed by 10.4 +/- 3.7% LFRC from FRC to TLC and by 32.5 +/- 14.6% LFRC from FRC to RV. Bilateral supramaximal vagal stimulation produced a mean maximal active shortening of 28.8 +/- 14.2% resting length at any lung volume (LR) and shortening decreased at lengths above FRC. The mean maximal velocity of shortening was 4.2 +/- 3.9% LR.S-1. We conclude that sonomicrometry may be used to record smooth muscle length in vivo. Vagal tone strongly influences passive length change. In vivo active shortening and velocity of shortening are less than in vitro, implying that there are significant loads impeding shortening in vivo.

1992 ◽  
Vol 70 (4) ◽  
pp. 602-606 ◽  
Author(s):  
Philip Robinson ◽  
Mitsushi Okazawa ◽  
Tony Bai ◽  
Peter Paré

The degree of airway smooth muscle contraction and shortening that occurs in vivo is modified by many factors, including those that influence the degree of muscle activation, the resting muscle length, and the loads against which the muscle contracts. Canine trachealis muscle will shorten up to 70% of starting length from optimal length in vitro but will only shorten by around 30% in vivo. This limitation of shortening may be a result of the muscle shortening against an elastic load such as could be applied by tracheal cartilage. Limitation of airway smooth muscle shortening in smaller airways may be the result of contraction against an elastic load, such as could be applied by lung parenchymal recoil. Measurement of the elastic loads applied by the tracheal cartilage to the trachealis muscle and by lung parenchymal recoil to smooth muscle of smaller airways were performed in canine preparations. In both experiments the calculated elastic loads applied by the cartilage and the parenchymal recoil explained in part the limitation of maximal active shortening and airway narrowing observed. We conclude that the elastic loads provided by surrounding structures are important in determining the degree of airway smooth muscle shortening and the resultant airway narrowing.Key words: elastic loads, tracheal cartilage, airway smooth muscle shortening.


1990 ◽  
Vol 69 (3) ◽  
pp. 1033-1039 ◽  
Author(s):  
K. Ishida ◽  
P. D. Pare ◽  
T. Blogg ◽  
R. R. Schellenberg

To shorten in vivo, airway smooth muscle must overcome an elastic load provided by cartilage and lung parenchyma. We examined the effects of linear elastic loads (0.2-80 g/cm) on the active changes in porcine trachealis muscle length and tension in response to electrical field stimulation in vitro. Increasing elastic loads produced an exponential decrease in the shortening and velocity of shortening while causing an increase in tension generation of muscle strips stimulated by electrical field stimulation. Shortening was decreased by 50% at a load of 8 g/cm. At small elastic loads (less than or equal to 1 g/cm) contractile responses approximated isotonic responses (shortening approximately 60% of starting length), whereas at large loads (20 g/cm) responses approximated isometric responses with minimal shortening (20%). We conclude that elastic loading significantly alters the mechanical properties of airway smooth muscle in vitro, effects that are likely relevant to the loads against which the smooth muscle must contract in vivo.


1988 ◽  
Vol 65 (1) ◽  
pp. 57-64 ◽  
Author(s):  
G. L. Jones ◽  
P. M. O'Byrne ◽  
M. Pashley ◽  
R. Serio ◽  
J. Jury ◽  
...  

Airway hyperresponsiveness occurs after inhalation of O3 in dogs. The purpose of this study was to examine the responsiveness of trachealis smooth muscle in vitro to electrical field stimulation, exogenous acetylcholine, and potassium chloride from dogs with airway hyperresponsiveness after inhaled O3 in vivo and to compare this with the responsiveness of trachealis muscle from control dogs. In addition, excitatory junction potentials were measured with the use of single and double sucrose gap techniques in both groups of dogs to determine whether inhaled O3 affects the release of acetylcholine from parasympathetic nerves in trachealis muscle. Airway hyperresponsiveness developed in all dogs after inhaled O3 (3 ppm for 30 min). The acetylcholine provocative concentration decreased from 4.11 mg/ml before O3 inhalation to 0.66 mg/ml after O3 (P less than 0.0001). The acetylcholine provocative concentration increased slightly after control inhalation of dry room air. Airway smooth muscle showed increased responses to both electrical field stimulation and exogenous acetylcholine but not to potassium chloride in preparations from dogs with airway hyperresponsiveness in vivo. The increased response to electrical field stimulation was not associated with a change in excitatory junctional potentials. These results suggest that a postjunctional alteration in trachealis muscle function occurs after inhaled O3 in dogs, which may account for airway hyperresponsiveness after O3 in vivo.


1993 ◽  
Vol 183 (1) ◽  
pp. 101-113 ◽  
Author(s):  
K. M. Gilmour ◽  
C. P. Ellington

The amplitude and time course of muscle length changes were examined in vivo in tethered, flying bumblebees Bombus lucorum. A ‘window’ was cut in the dorsal cuticle and aluminium particles were placed on the exposed dorsal longitudinal muscle fibres. Muscle oscillations were recorded using high-speed video and a high-magnification lens. The amplitude of muscle length changes was 1.9 % (s.d.=0.5 %, N=7), corresponding to the commonly quoted strain of 1–3 % for asynchronous muscle. Higher harmonics, particularly the second, were found in the muscle oscillations and in the wing movements. The second harmonic for wing movements was damped in comparison to that for muscle length changes, probably as a result of compliance in the thoracic linkage. Inclusion of the second harmonic in the driving signal for in vitro experiments on glycerinated fibres generally resulted in a decrease in the work and power, but a substantial increase was found for some fibres.


2012 ◽  
Vol 303 (1) ◽  
pp. G1-G8 ◽  
Author(s):  
P.-A. Risse ◽  
L. Kachmar ◽  
O. S. Matusovsky ◽  
M. Novali ◽  
F. R. Gil ◽  
...  

Patients with cystic fibrosis (CF) often suffer from gastrointestinal cramps and intestinal obstruction. The CF transmembrane conductance regulator (CFTR) channel has been shown to be expressed in vascular and airway smooth muscle (SM). We hypothesized that the absence of CFTR expression alters the gastrointestinal SM function and that these alterations may show strain-related differences in the mouse. The aim of this study was to measure the contractile properties of the ileal SM in two CF mouse models. CFTR−/− and CFTR+/+ mice were studied on BALB/cJ and C57BL/6J backgrounds. Responsiveness of ileal strips to electrical field stimulation (EFS), methacholine (MCh), and isoproterenol was measured. The mass and the cell density of SM layers were measured morphometrically. Finally, the maximal velocity of shortening (Vmax) and the expression of the fast (+)insert myosin isoform were measured in the C57BL/6J ileum. Ileal hyperreactivity was observed in response to EFS and MCh in CFTR−/− compared with CFTR+/+ mice in C57BL/6J background. This latter observation was not reproduced by acute inhibition of CFTR with CFTRinh172. BALB/cJ CFTR−/− mice exhibited a significant increase of SM mass with a lower density of cells compared with CFTR+/+, whereas no difference was observed in the C57BL/6J background. In addition, in this latter strain, ileal strips from CFTR−/− exhibited a significant increase in Vmax compared with control and expressed a greater proportion of the fast (+)insert SM myosin isoform with respect to total myosin. BALB/cJ CFTR−/− ilium had a greater relaxation to isoproterenol than the CFTR+/+ mice when precontracted with EFS, but no difference was observed in response to exogeneous MCh. In vivo, the lack of CFTR expression induces a different SM ileal phenotype in different mouse strains, supporting the importance of modifier genes in determining intestinal SM properties.


1986 ◽  
Vol 61 (4) ◽  
pp. 1492-1498 ◽  
Author(s):  
N. L. Stephens ◽  
G. Morgan ◽  
W. Kepron ◽  
C. Y. Seow

We have reported previously that in ovalbumin-sensitized canine tracheal smooth muscle (TSM) the maximum ability to shorten is increased. This could account for the increased airway narrowing seen in vivo in allergic bronchoconstriction. It was associated with increased velocity of shortening. We now report that, by using an electromagnetic muscle lever system, quick releases were applied to control and sensitized TSM at 0.5-s intervals throughout the course of a lightly preloaded 10-s isotonic contraction. From the records obtained it is possible to determine that, early in contraction, shortening is brought about by relatively rapidly cycling [0.35 optimal muscle length units +/- 0.033/s (SE)] cross bridges. We also report that in the sensitized TSM it is the early bridges that increase their velocity by 26.6% (P less than 0.05) compared with similar bridges in muscles from control animals. Since 70% of the maximum shortening of the muscle occurs when early bridges are operative, it is likely that these bridges are responsible for the major part of the shortening. It is thus probable that increased allergic bronchoconstriction is produced by increased activity of early, rapidly cycling bridges. The bridges that are active late in the shortening show no difference between control and sensitized airway smooth muscles.


1996 ◽  
Vol 80 (6) ◽  
pp. 2243-2249 ◽  
Author(s):  
R. V. Baratta ◽  
M. Solomonow ◽  
G. Nguyen ◽  
R. D'Ambrosia

Three-dimensional relationships of load, length, and velocity of shortening of the tibialis anterior muscle in the cat were derived experimentally and fitted with an analytic model. Gravitational loads were applied to the isolated muscle, which arrived at an equilibrium with the passive forces before supramaximal tetanic stimulation was delivered to its nerve. Recordings of initial passive muscle length at equilibrium and length changes throughout the shortening phase up to the final length at active equilibrium were taken and numerically differentiated to obtain each load's instantaneous velocity. A three-dimensional surface was constructed by using instantaneous length and the corresponding velocity for each of several loads. Maximal velocity of shortening was shown to gradually decrease, occurring earlier in the shortening phase (at larger muscle lengths) as loads increased. Whereas load-velocity curves were hyperbolic for middle and short muscle lengths, they were nonmonotonic during shortening above the optimal length. The model was found to correlate well with the experimental data (R = 0.98) and allowed for prediction of both muscle performance boundaries and instantaneous shortening velocity for a given length across the physiological load spectrum, thus offering a realistic estimation of the contractile properties exhibited by the tibialis anterior muscle in functions similar to naturally occurring movements against gravitational loads, which are accelerated and decelerated during the movement.


1962 ◽  
Vol 202 (5) ◽  
pp. 931-939 ◽  
Author(s):  
Edmund H. Sonnenblick

Force-velocity relations were studied in the cat papillary muscle. As with skeletal muscle, a characteristic relation has been demonstrated between the velocity of shortening (V) and the force developed (Po). Two generalities have been shown to pertain. First, increasing initial muscle length increases the maximal developed force (Po) without a change in the maximal velocity of shortening (Vmax). Secondly, at any one muscle length, changes in frequency of contraction and chemical environment (increased calcium and norepinephrine) increase Vmax with a variable change in Po. Changes in Vmax thus help to characterize an inotropic intervention (altered contractility). Work and power, at any one muscle length, are functions of afterload, with maxima when the load is approximately 40% of isometric tension. With increasing initial muscle length, the work and power at any one afterload as well as the maximal work and power of the muscle are both increased. At constant initial length, positive inotropic interventions (increased frequency, increased calcium, and norepinephrine) increase the work at any one afterload as well as shift the maximal work potential to a higher afterload. Work performance thus depends on muscle length, the prevailing force-velocity curve, and the afterload at which the muscle is operating.


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