Combined Effect of Isoproterenol and Mechanical Oscillation on the Contractile Response of Mice Airway Smooth Muscle From Healthy and Asthmatic Subjects

2012 ◽  
Author(s):  
M. J. Jo-Avila ◽  
A. M. Al-Jumaily ◽  
J. Lu ◽  
L. Sobrevia
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Healthy Subjects ◽  
Contractile Response ◽  
Relaxation Response ◽  
Driving Mechanism ◽  
Airway Lumen ◽  
Mechanical Oscillations ◽  
Normal Breathing ◽  
Asthma Attack

The main driving mechanism during an asthma attack is the hyperconstriction of airway smooth muscle (ASM), which reduces the airway lumen and makes normal breathing difficult. The contraction can be relieved by using bronchodilator drugs such as Isoproterenol (ISO). This paper hypothesizes that mechanical oscillations may improve drug therapy when combined with ISO or used alone in asthmatic subjects. Preliminary results indicate that combining ISO with breathing equivalent mechanical oscillations tends to increase the relaxation response, as compared to ISO alone in airways from healthy subjects, but not in the same manner in asthmatic airways. The effect of superposed oscillations of 1% and 1.5% amplitude in the range 5–20 Hz applied over breathing equivalent mechanical oscillations was also assessed in the study.

Study of the Combined Effect of Isoproterenol and Mechanical Oscillation on the Contractile Response of Mice Airways From Healthy and Asthmatic Subjects (In Vivo)

2013 ◽  
Author(s):  
M. Jo-Avila ◽  
A. Al-Jumaily ◽  
J. Lu ◽  
L. Sobrevia
Keyword(s):  
Smooth Muscle ◽  
Drug Therapy ◽  
Airway Smooth Muscle ◽  
Contractile Response ◽  
Combined Effect ◽  
Driving Mechanism ◽  
Airway Lumen ◽  
Normal Breathing ◽  
Asthma Attack

The main driving mechanism during an asthma attack is the hyperconstriction of airway smooth muscle (ASM), which reduces the airway lumen and makes normal breathing difficult. The contraction can be relieved by using bronchodilator drugs such as Isoproterenol (ISO). This paper hypothesizes that superimposed length oscillations (SILO) may improve drug therapy when combined with ISO or used alone in asthmatic subjects. The aim of this study is to assess SILO patterns directly onto the airways of healthy and asthmatic subjects (mice), while they are under anaesthesia breathing spontaneously and pre-constricted (mimicking and asthmatic attack), and compared the response with the relaxation observed just with ISO.

Combined Effect of Isoproterenol and Mechanical Oscillation on the Contractile Response of Mice Airway Smooth Muscle

2011 ◽  
Author(s):  
M. J. Jo-Avila ◽  
A. M. Al-Jumaily ◽  
P. Mbikou ◽  
L. Sobrevia
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Contractile Response ◽  
Combined Effect ◽  
Relaxation Response ◽  
Preliminary Results ◽  
Mechanical Oscillation ◽  
Asthmatic Attack ◽  
Mechanical Oscillations

An asthmatic attack is instigated by hyperconstriction of airway smooth muscle (ASM). This can be relieved with bronchodilator medication such as Isoproterenol (ISO). This paper hypothesizes that mechanical oscillations may improve drugs therapy when combined with ISO. Preliminary results indicate that combining ISO with breathing equivalent mechanical oscillations trends to increase the relaxation response as compared with the use of ISO alone. The effect of superposed oscillations in the range of 10–30 Hz of frequency applied over breathing equivalent mechanical oscillations was also assessed in the study.

An Evolving Network Model of Airway Smooth Muscle Crossbridge Dynamics and Length Adaptation

2008 ◽  
Author(s):  
G. Ijpma ◽  
A. M. Al-Jumaily ◽  
S. P. Cairns
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Driving Mechanism ◽  
Deep Inspiration ◽  
Glassy Material ◽  
Physiological Loading ◽  
Normal Breathing ◽  
Contractile Forces ◽  
Filament Network

The main driving mechanism in asthmatic attacks is the contraction of airway smooth muscle (ASM). Physiological loading of ASM by normal breathing and deep inspiration has been shown to reduce ASM contractile force. Our research involves the development of a mathematical model to describe the dynamic behavior of ASM. In this model length adaptation is described by an evolving filament network of passive and active elements in parallel with a soft glassy material. Contractile forces are described by the evolving force length characteristics of some of the network links. It is envisaged that the model will bridge the gap between passive ASM dynamics and contractile dynamics. The model will be validated using experimental data from testing of ASM tissues in vitro.

Lysophosphatidic acid enhances contractility of isolated airway smooth muscle

1997 ◽  
Vol 83 (4) ◽  
pp. 1216-1222 ◽  
Author(s):  
M. L. Toews ◽  
E. E. Ustinova ◽  
H. D. Schultz
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Lysophosphatidic Acid ◽  
Contractile Response ◽  
Relaxation Response ◽  
Muscarinic Agonist ◽  
Minimal Effect ◽  
Adrenergic Agonist ◽  
Enhancing Effect ◽  
Cyclase Activator

Toews, M. L., E. E. Ustinova, and H. D. Schultz.Lysophosphatidic acid enhances contractility of isolated airway smooth muscle. J. Appl. Physiol.83(4): 1216–1222, 1997.—The effects of the simple phospholipid mediator lysophosphatidic acid (LPA) on the contractile responsiveness of isolated tracheal rings from rabbits and cats were assessed. In both species, LPA increased the contractile response to the muscarinic agonist methacholine, but LPA did not induce contraction on its own. Conversely, LPA decreased the relaxation response to the β-adrenergic-agonist isoproterenol in both species. Concentrations of LPA as low as 10−8 M were effective, and the effects of LPA were rapidly reversed on washing. Phosphatidic acid was much less effective, requiring higher concentrations and producing only a minimal effect. Contractions induced by serotonin and by substance P also were enhanced by LPA, but KCl-induced contractions were unaffected. LPA inhibited the isoproterenol-induced relaxation of KCl-precontracted rings, similar to its effects on methacholine-precontracted rings, and relaxation induced by the direct adenylyl cyclase activator forskolin was inhibited in a manner similar to that induced by isoproterenol. Epithelium removal did not alter the contraction-enhancing effect of LPA. The ability of LPA to both enhance contraction and inhibit relaxation of airway smooth muscle suggests that LPA could contribute to airway hypercontractility in asthma, airway inflammation, or other types of lung injury.

scholarly journals Adrenergic airway vascular smooth muscle responsiveness in healthy and asthmatic subjects

2001 ◽  
Vol 90 (2) ◽  
pp. 665-669 ◽  
Author(s):  
Jorge Brieva ◽  
Adam Wanner
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Dead Space ◽  
Healthy Subjects ◽  
Contractile Response ◽  
Mucosal Blood Flow ◽  
Forced Expiratory Volume ◽  
Baseline Values ◽  
The Mean

The purpose of the present study was to determine the responsiveness of airway vascular smooth muscle (AVSM) as assessed by airway mucosal blood flow (Q˙aw) to inhaled methoxamine (α1-agonist; 0.6–2.3 mg) and albuterol (β2-agonist; 0.2–1.2 mg) in healthy [ n = 11; forced expiratory volume in 1 s, 92 ± 4 (SE) % of predicted] and asthmatic ( n = 11, mean forced expiratory volume in 1 s, 81 ± 5%) adults. Mean baseline values for Q˙aw were 43.8 ± 0.7 and 54.3 ± 0.8 μl · min−1· ml−1of anatomic dead space in healthy and asthmatic subjects, respectively ( P < 0.05). After methoxamine inhalation, the maximal mean change in Q˙aw was −13.5 ± 1.0 μl · min−1· ml−1in asthmatic and −7.1 ± 2.1 μl · min−1· ml−1in healthy subjects ( P < 0.05). After albuterol, the mean maximal change in Q˙aw was 3.0 ± 0.8 μl · min−1· ml−1in asthmatic and 14.0 ± 1.1 μl · min−1· ml−1in healthy subjects ( P < 0.05). These results demonstrate that the contractile response of AVSM to α1-adrenoceptor activation is enhanced and the dilator response of AVSM to β2-adrenoceptor activation is blunted in asthmatic subjects.

Effects of mucosal removal on guinea-pig airway smooth muscle responsiveness

1986 ◽  
Vol 70 (6) ◽  
pp. 571-575 ◽  
Author(s):  
Christopher Murlas
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Airway Smooth Muscle ◽  
Contractile Response ◽  
Electrical Field Stimulation ◽  
Physiological Salt Solution ◽  
Induced Responses ◽  
Field Stimulation ◽  
Electrical Field ◽  
Airway Mucosa

1. The contractile response to histamine, acetylcholine (ACh), KCl or electrical field stimulation (EFS) was examined in paired tracheal rings (one of each being denuded by mucosal rubbing), which were mounted in muscle chambers filled with a continuously aerated physiological salt solution at 37°C. 2. Removal of the respiratory mucosa increased the sensitivity of airway muscle to ACh, histamine and EFS, but not to KCl. The hypersensitivity of denuded rings to histamine and EFS was greater than to ACh. Atropine reduced the histamine hypersensitivity observed. 3. Pretreating intact preparations with indomethacin augmented their responsiveness to EFS, histamine and ACh. 4. Indomethacin augmentation of histamine- and EFS-induced responses was greater in preparations without epithelium. 5. We conclude that the airway mucosa may be associated with a factor that reduces airway smooth muscle responsiveness to stimulation.

Specific reaginic antibody IgG1-induced changes of airway smooth muscle cells

1988 ◽  
Vol 65 (2) ◽  
pp. 767-775 ◽  
Author(s):  
M. Souhrada ◽  
J. F. Souhrada
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Contractile Response ◽  
Isometric Force ◽  
Airway Smooth Muscle Cells ◽  
Base Line ◽  
Dependent Relationship ◽  
Reaginic Antibody ◽  
Induced Changes ◽  
Igg1 Concentration

It was found that 1) an administration of both immunoglobulin G1 (IgG1) or immunized serum caused an immediate depolarization and an increase in the isometric force of airway smooth muscle (ASM) cells, followed by a sustained hyperpolarization and a return of the tone to the base-line values; 2) an IgG1 concentration-dependent relationship was found between a peak depolarization, a peak hyperpolarization, and a peak isometric force; for these events 50% effective dose (ED50) was found to be 0.17, 0.14, and 0.25 microgram/ml of IgG1, respectively; 3) both electrical and contractile responses to ovalbumin of ASM cells sensitized with IgG1 were also dependent on the concentration of IgG1; the ED50 values of this relationship were 0.27 and 0.25 micrograms/ml of IgG1, respectively; 4) amiloride (10(-8) to 10(-5) M) pretreatment and a sodium-deficient environment attenuated sensitized-induced electrical and contractile changes as well as the response of ASM to ovalbumin (0.1%); and 5) pretreatment of ASM with diphenhydramine (10(-5) M) or FPL 55712 (10(-6) M) had no effect on sensitization-induced changes in membrane potential but attenuated electrical and contractile response of ASM to ovalbumin (0.1%).

SP-induced contraction of airway smooth muscle in normal and allergen-sensitized rabbits: mechanism of action

1995 ◽  
Vol 78 (2) ◽  
pp. 428-432 ◽  
Author(s):  
G. N. Colasurdo ◽  
J. E. Loader ◽  
J. P. Graves ◽  
G. L. Larsen
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Indirect Effects ◽  
Contractile Response ◽  
Complex Interaction ◽  
Direct Effects ◽  
Response Curves ◽  
Cholinergic Neurotransmission ◽  
The Right

We studied the mechanisms involved in the airway smooth muscle (ASM) contraction to substance P (SP) in normal (control) and allergen-sensitized (immune) rabbits as well as immune rabbits exposed to allergen via the airways (immune challenged). Cumulative concentration-response curves to SP (1 x 10(-9) to 1 x 10(-4) M) were performed in ASM segments in the absence and presence of atropine (10(-5) M) in vitro. The maximal contractile response (g tension/g tissue) at 10(-4) M SP and ASM contractions at various concentrations of SP were expressed as means +/- SE. We found no difference in the contractile response to SP between control and immune animals. ASM segments obtained from immune-challenged rabbits were more responsive to SP. Atropine shifted to the right the concentration-response curves and decreased the maximal ASM contraction at 10(-4) M SP in all three groups; this effect, however, was greater in immune-challenged tissues. These findings demonstrate an increased contractile response to SP in immune-challenged animals mediated by a more pronounced facilitation of cholinergic neurotransmission. We conclude that the final ASM response to SP is the result of a complex interaction between direct effects on ASM and indirect effects through modulation of cholinergic neurotransmission.

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