Mechanical properties of porcine intralobar pulmonary arteries

1988 ◽  
Vol 64 (4) ◽  
pp. 1537-1545 ◽  
Author(s):  
H. Ohtaka ◽  
J. C. Hogg ◽  
R. H. Moreno ◽  
P. D. Pare ◽  
R. R. Schellenberg
Keyword(s):  
Pulmonary Arteries ◽  
Pressure Change ◽  
Passive Tension ◽  
Active Tension ◽  
Balloon Inflation ◽  
Optimal Length ◽  
Active Volume ◽  
Calculated Length ◽  
Passive Pressure ◽  
Tension Curve

The isobaric and isovolumetric properties of intrapulmonary arteries were evaluated by placing a highly compliant balloon inside arterial segments. The passive pressure-volume (P-V) curve was obtained by changing volume (0.004 ml/s) and measuring pressure. The isobaric active volume change (delta V) or isovolumetric active pressure change (delta P) generated by submaximal histamine was measured at four different transmural pressures (Ptm's) reached by balloon inflation. The maximal delta P = 11.2 +/- 0.6 cmH2O (mean +/- SE) was achieved at 30.8 +/- 1.2 cmH2O Ptm and maximal delta V = 0.20 +/- 0.02 ml at 16.7 +/- 1.7 cmH2O Ptm. The P-V relationships were similar when volume was increased after either isobaric or isovolumetric contraction. The calculated length-tension (L-T) relationship showed that the active tension curve was relatively flat and that the passive tension at the optimal length was 149 +/- 11% of maximal active tension. These data show that 1) a large elastic component operates in parallel with the smooth muscle in intralobar pulmonary arteries, and 2) the change in resistance associated with vascular expansion of the proximal arteries is independent of the type of contraction that occurs in the more distal arterial segments.

The length-tension relationship of the dorsal longitudinal muscle of a leech

1975 ◽  
Vol 62 (1) ◽  
pp. 43-53
Author(s):  
JB Miller
Keyword(s):  
Body Wall ◽  
Longitudinal Muscle ◽  
Muscle Fibres ◽  
Passive Tension ◽  
Active Tension ◽  
Thin Filaments ◽  
Thick Filaments ◽  
Tension Curve ◽  
Cross Bridges ◽  
Relationship Of

The length-tension relationship of a preparation of the dorsal body wall of the leech Haemopis sanguisuga was determined. Passive tension is low except at very long lengths of the preparation, when it rises steeply. It is due mainly to the epidermis present in the preparation. The active tension curve is very flat, with tension being reduced only at very short and very long lengths. This shape is explained in the context of the myofilament arrangement of the muscle fibres. It may be that thin filaments can form cross-bridges with different thick filaments at different lengths of the preparation.

Increased responsiveness of jejunal longitudinal muscle in Trichinella-infected rats

1988 ◽  
Vol 254 (1) ◽  
pp. G124-G129 ◽  
Author(s):  
D. L. Vermillion ◽  
S. M. Collins
Keyword(s):  
Smooth Muscle ◽  
Muscle Function ◽  
Longitudinal Muscle ◽  
Trichinella Spiralis ◽  
Passive Tension ◽  
Active Tension ◽  
Maximum Tension ◽  
Longitudinal Smooth Muscle ◽  
Smooth Muscle Function

We examined in vitro changes in contractility of jejunal longitudinal muscle strips in rats infected with the nematode parasite Trichinella spiralis. Length-passive tension relationships were unchanged. However, muscle from infected rats on days 5 and 6 postinfection (PI) generated maximal active tension induced by carbachol at significantly less stretch (39.9 +/- 1.0 and 34.3 +/- 6.3%, respectively) than control tissues (66.0 +/- 2.3%). In infected rats on day 5 PI, the maximum tension generated by carbachol (1.6 +/- 0.4 g/mm2) and by 5-hydroxytryptamine (5-HTP) (2.6 +/- 0.1 g/mm2) was significantly greater than in control tissue (0.5 +/- 0.2 g/mm2). On removal of calcium from the medium, responses of muscle from control and infected rats were reduced in a proportionate manner. The increased responsiveness to carbachol and 5-HTP was maximal by day 5 PI and was associated with a decrease in the ED50 value for 5-HTP but not for carbachol. All changes were reversed by 23 days PI. These results indicate that T. spiralis infection in the rat is associated with alterations in jejunal longitudinal smooth muscle function.

Intravenous papain-induced cartilage softening decreases preload of tracheal smooth muscle

1989 ◽  
Vol 66 (4) ◽  
pp. 1694-1698 ◽  
Author(s):  
R. H. Moreno ◽  
P. D. Pare
Keyword(s):  
Mechanical Properties ◽  
Electrical Field Stimulation ◽  
Field Stimulation ◽  
Electrical Field ◽  
Optimal Length ◽  
Tracheal Cartilage ◽  
Passive Pressure ◽  
Volume Curve ◽  
Pressure Volume Curve ◽  
Trachealis Muscle

To study the interaction between tracheal cartilage and the trachealis muscle we measured trachealis muscle contraction in response to electrical field stimulation and methacholine in excised tracheal segments from control and papain-treated rabbits. Papain treatment softened the tracheal cartilage and altered the passive pressure volume curve of the tracheal segments at transmural pressures below 5 cmH2O. The transmural pressure required for maximal active changes in volume (isobaric contraction) with electrical field stimulation was increased in papain-treated animals. We conclude that tracheal cartilage provides a preload which stretches the trachealis muscle toward optimal length and that papain, by altering the elastic mechanical properties of cartilage, decreases this preload.

Pulmonary and systemic vascular smooth muscle mechanical characteristics in newborn sheep

1992 ◽  
Vol 263 (3) ◽  
pp. H881-H886 ◽  
Author(s):  
J. Belik ◽  
A. J. Halayko ◽  
K. Rao ◽  
N. L. Stephens
Keyword(s):  
Carotid Artery ◽  
Age Differences ◽  
Carotid Arteries ◽  
Mechanical Characteristics ◽  
Pulmonary Arteries ◽  
Developmental Differences ◽  
Lower Stress ◽  
Optimal Length ◽  
Vascular Muscle ◽  
Common Carotid Arteries

To investigate the hypothesis that the higher pulmonary vascular resistance in newborn sheep is the result of developmental differences in the vascular muscle mechanical properties, we evaluated pulmonary arteries from newborn and adult sheep and compared them with their respective systemic counterparts (common carotid arteries). The newborn pulmonary artery mechanical stress (13.0 +/- 1.4 mN/mm2) and shortening capacity (11.4 +/- 1.1% of optimal length) were lower (P less than 0.01) than in the adult (20.4 +/- 2.5 and 15.6 +/- 1.3, respectively). The adult carotid artery muscle developed a greater stress (97.6 +/- 18.5 mN/mm2) than the newborn (40.7 +/- 5.0; P less than 0.01), whereas no age differences in shortening capacity were observed (newborn = 19.4 +/- 1.7; adult = 18.4 +/- 1.5% of optimal length). The contraction half-time was similar for the pulmonary and carotid arteries and was not affected by age, whereas the relaxation half-times of the newborn pulmonary (30.7 +/- 2.9 s) and carotid artery (23.3 +/- 1.5) were greater than in the adult (24.9 +/- 2.9 and 14.6 +/- 1.4, respectively; P less than 0.01). The myosin contents of the pulmonary and carotid arteries, as an indicator of the tissue muscle mass, were similar and did not change with age. In conclusion, while the lower stress and shortening capacity of the newborn pulmonary arteries limit their maximum capacity to vasoconstrict, the significantly greater relaxation time of their vascular muscle, a new observation, may account for the higher resistance to blood flow after birth.

Effect of stretch on passive tension and contractility of isolated vascular smooth muscle

1962 ◽  
Vol 202 (5) ◽  
pp. 835-840 ◽  
Author(s):  
Harvey V. Sparks ◽  
David F. Bohr
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Standard Stimulus ◽  
Contractile Element ◽  
Passive Tension ◽  
Optimal Length ◽  
Length Variable

Helically cut strips of the wall of small branches of dog superior mesenteric artery were stretched in a stepwise fashion. Tension developed in response to stretch or to a standard stimulus (epinephrine or electricity) was recorded isometrically. The elastic diagram of the vessel is comparable to that reported by other investigators. Contraction in response to a standard stimulus increased with stretch, as much as 100% for a 10% increase in length. The increase in response continued until the strip reached a certain optimal length (variable from strip to strip), after which the response decreased with further stretch. When the strip was released in a stepwise fashion hysteresis was observed. Possible relationships of tension and length at the level of the contractile element are discussed together with ways in which the information presented here may relate to myogenic autoregulation.

Effect of Ischemia on the Length-Tension Diagram of Mammalian Skeletal Muscle

1956 ◽  
Vol 188 (1) ◽  
pp. 113-117 ◽  
Author(s):  
L. C. Senay ◽  
B. A. Schottelius
Keyword(s):  
Skeletal Muscle ◽  
Soft Tissue ◽  
Mammalian Skeletal Muscle ◽  
Passive Tension ◽  
Active Tension ◽  
Rapid Loss ◽  
The Difference ◽  
And Control ◽  
Contralateral Muscle

Ischemia was produced in the gastrocnemii of 13 rats by ligation and section of all soft tissue between knee and thigh. The contralateral muscle in each case served as a control. Isometric length-tension diagrams were obtained for both control and experimental muscles from 4 mm below resting length to 9 mm beyond resting length, stretch being imposed in 1-mm increments. In comparing the experimental and control length-tension diagrams, a 15% loss in active tension at resting length was observed in both the experimental and control muscles when the tension developed during an initial isometric tetanus was compared with tension developed at this length during the course of the length-tension diagram. The cause of this decrease is not certain but fatigue and changes in muscle extensibility were thought to play prominent roles. The active tension developed by the ischemic muscles was found to be less at all degrees of stretch, and in most instances this difference was significant. This tension loss in the ischemic muscles was not constant; plotting the difference between control and ischemic active tension revealed that from –4 mm to +2 mm of stretch the difference increased, while from +2 to +9 mm of stretch the tension loss decreased. This latter finding was further investigated by determining fatigue rates at selected degrees of stretch in ischemic and control muscles of 40 rats. These studies indicated that the ischemic muscles suffered a more rapid loss of active tension developed at degrees of stretch less than +2 mm but the control muscles had a more rapid active tension loss at lengths greater than +2 mm of stretch. An explanation for this is suggested. Development of contracture was thought to be the cause of the increase in the passive tension exhibited by the ischemic muscles.

Diaphragm in emphysematous hamsters: sarcomere adaptability

1983 ◽  
Vol 54 (6) ◽  
pp. 1635-1640 ◽  
Author(s):  
G. A. Farkas ◽  
C. Roussos
Keyword(s):  
Functional Residual Capacity ◽  
Sarcomere Length ◽  
Small Decrease ◽  
Optimal Length ◽  
Residual Capacity ◽  
Tension Curve ◽  
Sarcomere Number

We investigated whether the shift in the diaphragmatic length-tension curve of emphysematous animals was due to changes in either sarcomere number or sarcomere length. In vitro length-tension characteristics of the diaphragm were evaluated in control and emphysematous hamsters. Emphysema was induced by a single endotracheal instillation of elastase. Functional residual capacity, measured by means of a plethysmograph, was about twice that measured in emphysematous animals compared with control animals. Small diaphragmatic bundles were isolated and evaluated for their length-tension characteristics. The length-tension curve of diaphragms from emphysematous animals was displaced toward the left. Maximal tetanic tensions were similar in both groups, whereas optimal bundle length was significantly decreased in the emphysematous animals. Sarcomere number and sarcomere length at optimal length were then calculated for the diaphragmatic bundles. The bundles from emphysematous animals were found to have a significantly reduced number of sarcomeres, as well as a significantly decreased sarcomere length at optimal compared with control values. The total number of sarcomeres were also found to be significantly negatively correlated with the animal's functional residual capacity. From these results, we conclude that the decrease in diaphragmatic length, seen with hyperinflation, is due mainly to a loss of sarcomeres and possibly to a small decrease in sarcomere length measured at optimal bundle length.

Influence of nitric oxide on vascular resistance and muscle mechanics during tetanic contractions in situ

1999 ◽  
Vol 87 (1) ◽  
pp. 142-151 ◽  
Author(s):  
Bill T. Ameredes ◽  
Mark A. Provenzano
Keyword(s):  
Nitric Oxide ◽  
Vascular Resistance ◽  
Muscle Blood Flow ◽  
Muscle Mechanics ◽  
Peripheral Resistance ◽  
Passive Tension ◽  
Intramuscular Pressure ◽  
Active Tension ◽  
Plantaris Muscle

Studies of the effect of nitric oxide (NO) synthesis inhibition were performed in the isometrically contracting blood-perfused canine gastrocnemius-plantaris muscle group. Muscle blood flow (Q˙) was controlled with a pump during continuous NO blockade produced with either 1 mMl-argininosuccinic acid (l-ArgSA) or N G-nitro-l-arginine methyl ester (l-NAME) during repetitive tetanic contractions (50-Hz trains, 200-ms duration, 1/s). PumpQ˙ was set to match maximal spontaneousQ˙ (1.3–1.4 ml ⋅ min−1 ⋅ g−1) measured in prior, brief (3–5 min) control contraction trials in each muscle. Active tension and oxygen uptake were 500–600 g/g and 200–230 μl ⋅ min−1 ⋅ g−1, respectively, under these conditions. Within 3 min ofl-ArgSA infusion, vascular resistance across the muscle (Rv) increased significantly (from ∼100 to 300 peripheral resistance units; P < 0.05), whereas Rv increased to a lesser extent with l-NAME (from ∼100 to 175 peripheral resistance units; P < 0.05). The increase in Rv withl-ArgSA was unchanged by simultaneous infusion of 0.5–10 mMl-arginine but was reduced with 1–3 μg/ml sodium nitroprusside (41–54%). The increase in Rv withl-NAME was reversed with 1 mM ofl-arginine. Increased fatigue occurred with infusion ofl-ArgSA; active tension and intramuscular pressure decreased by 62 and 66%, whereas passive tension and baseline intramuscular pressure increased by 80 and 30%, respectively. These data indicate a possible role for NO in the control of Rv and contractility within the canine gastrocnemius-plantaris muscle during repetitive tetanic contractions.

Differential changes in ACh-, motilin-, substance P-, and K+-induced contractility in rabbit colitis

1999 ◽  
Vol 277 (1) ◽  
pp. G61-G68 ◽  
Author(s):  
Inge Depoortere ◽  
Gert van Assche ◽  
Theo Thijs ◽  
Karel Geboes ◽  
Theo L. Peeters
Keyword(s):  
Mechanical Properties ◽  
Smooth Muscle ◽  
Substance P ◽  
Contractile Activity ◽  
Passive Tension ◽  
Active Tension ◽  
Trinitrobenzenesulfonic Acid ◽  
Smooth Muscle Tissue ◽  
Structural Alterations ◽  
Time Profiles

To test the hypothesis that the changes in intestinal contractility, which accompany inflammation of the gut, are agonist specific, we compared the response of inflamed strips to substance P (SP), motilin, ACh, and K+ as a function of time. In parallel experiments, changes in the general mechanical properties (passive tension, optimal stretch) of the colitic tissue were evaluated. Colitis was induced by trinitrobenzenesulfonic acid, and rabbits were killed after 1, 2, 3, 5, or 8 days. Passive tension was increased starting from day 2 until day 8, and maximal active tension ( T max) was generated at less stretch from day 5. A 50% decrease in T max was observed for ACh and K+ between days 2 and 3 and for motilin and SP between days 3 and 5. For all compounds, T max returned to normal after 8 days. The pEC50value (negative logarithm of the concentration that induces 50% of the maximal contractile activity) for ACh was increased from day 3 until day 8 and for SP at day 3, whereas for motilin it was decreased at day 1. The changes in passive tension and optimal stretch indicate generalized structural alterations of smooth muscle tissue. However, the different time profiles of the changes in active tension and contractile potency for different contractile agents suggest that inflammation specifically affects receptor-mediated mechanisms.

scholarly journals Evidence that actomyosin cross bridges contribute to “passive” tension in detrusor smooth muscle

2010 ◽  
Vol 298 (6) ◽  
pp. F1424-F1435 ◽  
Author(s):  
Paul H. Ratz ◽  
John E. Speich
Keyword(s):  
Smooth Muscle ◽  
Actin Polymerization ◽  
Contractile Function ◽  
Cyclooxygenase Inhibitors ◽  
Passive Tension ◽  
Detrusor Smooth Muscle ◽  
Free Solution ◽  
Active Tension ◽  
Working Length ◽  
Cross Bridges

Contraction of detrusor smooth muscle (DSM) at short muscle lengths generates a stiffness component we termed adjustable passive stiffness (APS) that is retained in tissues incubated in a Ca2+-free solution, shifts the DSM length-passive tension curve up and to the left, and is softened by muscle strain and release (strain softened). In the present study, we tested the hypothesis that APS is due to slowly cycling actomyosin cross bridges. APS and active tension produced by the stimulus, KCl, displayed similar length dependencies with identical optimum length values. The myosin II inhibitor blebbistatin relaxed active tension maintained during a KCl-induced contraction and the passive tension maintained during stress-relaxation induced by muscle stretch in a Ca2+-free solution. Passive tension was attributed to tension maintaining rather than tension developing cross bridges because tension did not recover after a rapid 10% stretch and release as it did during a KCl-induced contraction. APS generated by a KCl-induced contraction in intact tissues was preserved in tissues permeabilized with Triton X-100. Blebbistatin and the actin polymerization inhibitor latrunculin-B reduced the degree of APS generated by a KCl-induced contraction. The degree of APS generated by KCl was inhibited to a greater degree than was the peak KCl-induced tension by rhoA kinase and cyclooxygenase inhibitors. These data support the hypothesis that APS is due to slowly cycling actomyosin cross bridges and suggest that cross bridges may play a novel role in DSM that uniquely serves to ensure proper contractile function over an extreme working length range.

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