Relation of Tissue Extensibility to Smooth Muscle Tone

1956 ◽  
Vol 185 (2) ◽  
pp. 302-308 ◽  
Author(s):  
J. W. Remington ◽  
R. S. Alexander
Keyword(s):  
Smooth Muscle ◽  
Critical Load ◽  
Muscle Tone ◽  
Load Removal ◽  
In Series ◽  
Load Release ◽  
Length Changes ◽  
Elastic Elements ◽  
Initial Viscosity

Isolated specimens of rabbit gut or bladder were subjected to fixed loads, length changes being recorded kymographically. The elongation curves showed two essential phases. First there was a rapid visco-elastic extension whose amount was directly related to load. Second, there was a sustained creep whose slope was less clearly dependent upon load. This creep appeared not to develop until a critical load value was exceeded. A stretch reduced the viscosity, as reflected in the initial extension of a succeeding stretch. This change could be reversed with long recovery intervals allowed after load removal. Load removal was followed by a brief viscoelastic recoil, and then a long term length retraction which had the same slope regardless of the amount of prior extension. The recoil was always less in amount than the previous visco-elastic extension. The recovery of the initial viscosity, with time, could not be related to the recovery in length. While acetylcholine or epinephrine could change the tissue length, they had no clear effect upon the amount or rate of initial extension, upon the late creep, or upon the late length retraction upon load release. The contractile elements of the muscle would seem to be in series with visco-elastic elements, and the elongation pattern of the latter dominantly controls the over-all tissue extensibility. Only in a few cases can the tissue extensibility be related to the amount of muscle contraction.

Structural changes and in situ aortic pressure-diameter relationship in long-term chemical-sympathectomized rats

1995 ◽  
Vol 269 (2) ◽  
pp. H407-H416 ◽  
Author(s):  
P. Lacolley ◽  
E. Glaser ◽  
P. Challande ◽  
P. Boutouyrie ◽  
J. P. Mignot ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Structural Changes ◽  
Muscle Tone ◽  
Pressor Response ◽  
Tracking System ◽  
Aortic Distensibility ◽  
Aortic Diameter ◽  
Smooth Muscle Relaxation

This study determined the effects of long-term chemical sympathectomy with guanethidine (GN) on the mechanical properties and composition of the distal abdominal aorta in Wistar rats. GN was daily administered for 3 mo (3M-GN, from 1 to 12 wk), 5 wk (5W-GN, from 7 to 12 wk), and 8 days (8D-GN, from 11 to 12 wk). All experiments were performed at 12 wk of age to avoid age differences at examination. We used a high-resolution echo-tracking system to determine in situ, in the systolic-diastolic range, the aortic diameter-, compliance-, and distensibility-pressure curves in anesthetized rats. We observed an equivalent significant fall in the tyramine pressor response in all conscious GN-treated rats. Blood pressure was not affected by sympathectomy after 8 days and 5 wk of treatment but was significantly reduced in 3M-GN rats. Chronic sympathetic denervation increased aortic diameter and compliance in 8D-GN rats, compared with those obtained at the same distending pressure in control rats, suggesting vascular smooth muscle relaxation. In contrast, in 5W-GN and 3M-GN rats, the distensibility pressure-curves were significantly shifted toward lower levels of distensibility and pressure, indicating a decreased aortic distensibility at the same level of arterial pressure. Sympathectomy produced a significant reduction in the content of elastin, one of the most distensible components of the arterial wall in 5W-GN and 3M-GN rats. These results suggest that intact sympathetic nerves are necessary to maintain normal functional and structural properties of large arteries in rat. The reduction in aortic distensibility, in long-term sympathectomized rats, could have resulted from complex interactions between local aortic denervation, change in the set point of distending pressure, and changes in aortic smooth muscle tone and/or wall composition.

scholarly journals Plasticity in canine airway smooth muscle.

1995 ◽  
Vol 105 (1) ◽  
pp. 73-94 ◽  
Author(s):  
V R Pratusevich ◽  
C Y Seow ◽  
L E Ford
Keyword(s):  
Smooth Muscle ◽  
Isometric Force ◽  
Strong Dependence ◽  
Smooth Muscles ◽  
Muscle Length ◽  
Relative Length ◽  
Length Range ◽  
Steady Level ◽  
In Series ◽  
Length Changes

The large volume changes of some hollow viscera require a greater length range for the smooth muscle of their walls than can be accommodated by a fixed array of sliding filaments. A possible explanation is that smooth muscles adapt to length changes by forming variable numbers of contractile units in series. To test for such plasticity we examined the muscle length dependence of shortening velocity and compliance, both of which will vary directly with the number of thick filaments in series. Dog tracheal smooth muscle was studied because its cells are arrayed in long, straight, parallel bundles that span the length of the preparation. In experiments where muscle length was changed, both compliance and velocity showed a strong dependence on muscle length, varying by 1.7-fold and 2.2-fold, respectively, over a threefold range of length. The variation in isometric force was substantially less, ranging from a 1.2- to 1.3-fold in two series of experiments where length was varied by twofold to an insignificant 4% variation in a third series where a threefold length range was studied. Tetanic force was below its steady level after both stretches and releases, and increased to a steady level with 5-6 tetani at 5 min intervals. These results suggest strongly that the number of contractile units in series varies directly with the adapted muscle length. Temporary force depression after a length change would occur if the change transiently moved the filaments from their optimum overlap. The relative length independence of the adapted force is explained by the reforming of the filament lattice to produce optimum force development, with commensurate changes of velocity and compliance.

Inhibition of dihydropyridine-sensitive calcium entry in hypoxic relaxation of airway smooth muscle

1995 ◽  
Vol 268 (2) ◽  
pp. L201-L206 ◽  
Author(s):  
C. Vannier ◽  
T. L. Croxton ◽  
L. S. Farley ◽  
C. A. Hirshman
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Muscle Tone ◽  
Bay K 8644 ◽  
O2 Concentration ◽  
Voltage Dependent ◽  
Progressive Hypoxia ◽  
Carbamyl Choline

Hypoxia dilates airways in vivo and reduces active tension of airway smooth muscle in vitro. To determine whether hypoxia impairs Ca2+ entry through voltage-dependent channels (VDC), we tested the ability of dihydropyridines to modulate hypoxia-induced relaxation of KCl- and carbamyl choline (carbachol)-contracted porcine bronchi. Carbachol- or KCl-contracted bronchial rings were exposed to progressive hypoxia in the presence or absence of 1 microM BAY K 8644 (an L-type-channel agonist). In separate experiments, rings were contracted with carbachol or KCl, treated with nifedipine (a VDC antagonist), and finally exposed to hypoxia. BAY K 8644 prevented hypoxia-induced relaxation in KCl-contracted bronchi. Nifedipine (10(-5) M) totally relaxed KCl- contracted bronchi. Carbachol-contracted bronchi were only partially relaxed by nifedipine but were completely relaxed when the O2 concentration of the gas was reduced from 95 to 0%. These data indicate that hypoxia can reduce airway smooth muscle tone by limiting entry of Ca2+ through a dihydropyridine-sensitive pathway, but that other mechanisms also contribute to hypoxia-induced relaxation of carbachol-contracted bronchi.

PGE2 release by bradykinin in human airway smooth muscle cells: involvement of cyclooxygenase-2 induction

1997 ◽  
Vol 273 (6) ◽  
pp. L1132-L1140 ◽  
Author(s):  
Linhua Pang ◽  
Alan J. Knox
Keyword(s):  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Arachidonic Acid Release ◽  
Human Airway Smooth Muscle ◽  
Short Term ◽  
Human Airway ◽  
Acid Release ◽  
Cox 2

Prostanoids may be involved in bradykinin (BK)-induced bronchoconstriction in asthma. We investigated whether cyclooxygenase (COX)-2 induction was involved in prostaglandin (PG) E2 release by BK in cultured human airway smooth muscle (ASM) cells and analyzed the BK receptor subtypes responsible. BK stimulated PGE2release, COX activity, and COX-2 induction in a concentration- and time-dependent manner. It also time dependently enhanced arachidonic acid release. In short-term (15-min) experiments, BK stimulated PGE2 generation but did not increase COX activity or induce COX-2. In long-term (4-h) experiments, BK enhanced PGE2 release and COX activity and induced COX-2. The long-term responses were inhibited by the protein synthesis inhibitors cycloheximide and actinomycin D and the steroid dexamethasone. The effects of BK were mimicked by the B2-receptor agonist [Tyr(Me)8]BK, whereas the B1 agonist des-Arg9-BK was weakly effective at high concentrations. The B2antagonist HOE-140 potently inhibited all the effects, but the B1 antagonist des-Arg9,(Leu8)-BK was inactive. This study is the first to demonstrate that BK can induce COX-2. Conversion of increased arachidonic acid release to PGE2 by COX-1 is mainly involved in the short-term effect, whereas B2 receptor-related COX-2 induction is important in the long-term PGE2 release.

scholarly journals Stromal cells from human long-term marrow cultures are mesenchymal cells that differentiate following a vascular smooth muscle differentiation pathway

Blood ◽  
1993 ◽  
Vol 82 (1) ◽  
pp. 66-76 ◽  
Author(s):  
MC Galmiche ◽  
VE Koteliansky ◽  
J Briere ◽  
P Herve ◽  
P Charbord
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Stromal Cells ◽  
Muscle Cells ◽  
Mesenchymal Cells ◽  
Myoid Cells ◽  
Marrow Cultures

In human long-term marrow cultures connective tissue-forming stromal cells are an essential cellular component of the adherent layer where granulomonocytic progenitors are generated from week 2 onward. We have previously found that most stromal cells in confluent cultures were stained by monoclonal antibodies directed against smooth muscle- specific actin isoforms. The present study was carried out to evaluate the time course of alpha-SM-positive stromal cells and to search for other cytoskeletal proteins specific for smooth muscle cells. It was found that the expression of alpha-SM in stromal cells was time dependent. Most of the adherent spindle-shaped, vimentin-positive stromal cells observed during the first 2 weeks of culture were alpha- SM negative. On the contrary, from week 3 to week 7, most interdigitated stromal cells contained stress fibers whose backbone was made of alpha-SM-positive microfilaments. In addition, in confluent cultures, other proteins specific for smooth muscle were detected: metavinculin, h-caldesmon, smooth muscle myosin heavy chains, and calponin. This study confirms the similarity between stromal cells and smooth muscle cells. Moreover, our results reveal that cells in vivo with the phenotype closest to that of stromal cells are immature fetal smooth muscle cells and subendothelial intimal smooth muscle cells; a cell subset with limited development following birth but extensively recruited in atherosclerotic lesions. Stromal cells very probably derive from mesenchymal cells that differentiate along this distinctive vascular smooth muscle cell pathway. In humans, this differentiation seems crucial for the maintenance of granulomonopoiesis. These in vitro studies were completed by examination of trephine bone marrow biopsies from adults without hematologic abnormalities. These studies revealed the presence of alpha-SM-positive cells at diverse locations: vascular smooth muscle cells in the media of arteries and arterioles, pericytes lining capillaries, myoid cells lining sinuses at the abluminal side of endothelial cells or found within the hematopoietic logettes, and endosteal cells lining bone trabeculae. More or less mature cells of the granulocytic series were in intimate contact with the thin cytoplasmic extensions of myoid cells. Myoid cells may be the in vivo counterpart of stromal cells with the above-described vascular smooth muscle phenotype.

scholarly journals Enteric Neuronal Damage, Intramuscular Denervation and Smooth Muscle Phenotype Changes as Mechanisms of Chagasic Megacolon: Evidence from a Long-Term Murine Model of Tripanosoma cruzi Infection

PLoS ONE ◽  
2016 ◽  
Vol 11 (4) ◽  
pp. e0153038 ◽  
Author(s):  
Camila França Campos ◽  
Silvia Dantas Cangussú ◽  
Ana Luiza Cassin Duz ◽  
Christiane Teixeira Cartelle ◽  
Maria de Lourdes Noviello ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Murine Model ◽  
Neuronal Damage ◽  
Chagasic Megacolon ◽  
Cruzi Infection

scholarly journals Constraint-Induced Movement Therapy After Injection of Botulinum Toxin Type A for a Patient With Chronic Stroke: One-Year Follow-up Case Report

2015 ◽  
Vol 95 (7) ◽  
pp. 1039-1045 ◽  
Author(s):  
Satoru Amano ◽  
Takashi Takebayashi ◽  
Keisuke Hanada ◽  
Atsushi Umeji ◽  
Kohei Marumoto ◽  
...  
Keyword(s):  
Case Report ◽  
Botulinum Toxin ◽  
Muscle Tone ◽  
Botulinum Toxin Type A ◽  
Type A ◽  
Movement Therapy ◽  
Chronic Stroke ◽  
Constraint Induced Movement Therapy ◽  
Arm Function

Background and Purpose Spasticity, an aspect of upper motor neuron syndrome, is a widespread problem in patients with stroke. To date, no study has reported the long-term (up to 1 year) outcomes of botulinum toxin (BTX) injection in combination with constraint-induced movement therapy in patients with chronic stroke. In this case report, the long-term (1 year) effects of the combination of BTX type A injection and constraint-induced movement therapy on spasticity and arm function in a patient with chronic stroke and arm paresis are described. Case Description The patient was a 66-year-old man who had had an infarction in the right posterior limb of the internal capsule 4 years before the intervention. At screening, the patient was not able to voluntarily extend his interphalangeal or metacarpophalangeal joints beyond the 10 degrees required for constraint-induced movement therapy. From 12 days after BTX type A injection, the patient received 5 hours of constraint-induced movement therapy for 10 weekdays. Outcomes All outcome measures (Modified Ashworth Scale, Fugl-Meyer Assessment, Action Research Arm Test, and amount of use scale of the Motor Activity Log) improved substantially over the 1-year period (before intervention to 1 year after intervention). Repeat BTX type A injections were not necessary because muscle tone and arm function did not worsen during the observation period. Discussion The improved arm function may have reflected improvements in volitional movements and coordination or speed of movements in the paretic arm as a result of a reduction in spasticity, a reduction of learned nonuse behaviors, or use-dependent plasticity after the combination of BTX type A injection and constraint-induced movement therapy. In addition, the possibility of an influence of the passage of time or the Hawthorne effect cannot be ruled out. If this approach proves useful in future controlled studies, it may reduce the rising medical costs of the treatment of stroke.

Bronchial Smooth Muscle Tone in Normal Subjects

CHEST Journal ◽  
1982 ◽  
Vol 81 (3) ◽  
pp. 396
Author(s):  
Elisabeth McIntyre ◽  
John H. Alpers ◽  
Richard E. Ruffin
Keyword(s):  
Smooth Muscle ◽  
Muscle Tone ◽  
Normal Subjects ◽  
Bronchial Smooth Muscle ◽  
Smooth Muscle Tone

Altered contractility of urinary bladder in diabetic rabbits: relationship to reduced Na+ pump activity

1996 ◽  
Vol 271 (6) ◽  
pp. C2045-C2052 ◽  
Author(s):  
S. Gupta ◽  
S. Yang ◽  
R. A. Cohen ◽  
R. J. Krane ◽  
I. Saenz De Tejada
Keyword(s):  
Smooth Muscle ◽  
Muscle Tone ◽  
Bladder Smooth Muscle ◽  
Na Pump ◽  
A 23187 ◽  
Normal Bladder ◽  
Diabetic Rabbit ◽  
Pump Activity ◽  
Diabetic Rabbits ◽  
Ionophore Monensin

We studied the effect of alloxan-induced diabetes on Na+ pump activity in isolated rabbit bladder strips. In addition, the effects of diabetes and the Na+ pump inhibitor ouabain on contractions induced by carbachol (CCh) and KCl were studied. In bladder strips from diabetic rabbits, ouabain-sensitive 86Rb+ uptake (a measure of Na+ pump activity) was approximately 50% less compared with strips from normal bladder. Diabetes also reduced the maximum contractions induced by CCh and KCl. Treatment of bladder strips with ouabain alone caused an acute concentration-dependent increase in tone. In contrast, longer incubation with ouabain inhibited CCh- and KCl-induced contractions in normal and diabetic bladders. Furthermore, differences in agonist-mediated contractions observed between normal and diabetic bladders were abolished in the presence of the maximally effective concentration of ouabain (10 microM). The ability of CCh to cause contraction in normal and diabetic rabbit bladders was also significantly inhibited by the Na+ ionophore monensin but not by the Ca2+ ionophore A-23187 or by depolarization with KCl. Monensin also inhibited KCl-induced contractions in normal bladder strips. These results indicate that 1) Na+ pump activity is an important modulator of bladder smooth muscle tone, 2) diabetes diminishes Na+ pump activity and inhibits agonist-induced contractions in bladder, and 3) an increase in intracellular Na+ concentration, secondary to inhibition of bladder smooth muscle Na+ pump activity, is associated with reduced responsiveness to contractile agonists. Diminished Na+ pump activity in diabetes may, in part, contribute to the development of bladder cystopathy.

Sign in / Sign up

Export Citation Format

Share Document