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PubMed1998

IGF-I and/or growth hormone preserve diaphragm fiber size with moderate malnutrition.

Resistance to the anabolic effects of growth hormone (GH) occurs with severe caloric deficit. This study examined whether moderate caloric deficit (50% of daily intake for 7 days) in the adolescent rat exceeds a critical threshold for GH action and whether a combination of GH and insulin-like growth factor I (IGF-I) would have enhanced anabolic effects on the diaphragm (Dia). Five groups of rats (4 wk old) were studied: 1) control (Ctl), 2) nutritionally deprived (ND), 3) ND + GH, 4) ND + IGF-I, and 5) ND + GH + IGF-I. IGF-I was given by continuous infusion (200 microg/day). GH was injected subcutaneously (250 microg every 12 h). Contractile and fatigue properties of the Dia were determined in vitro. Quantitative histochemical methods were used to determine Dia fiber type proportions, cross-sectional areas, and succinate dehydrogenase activities. The body weight of Ctl rats increased 46% compared with 7% in ND animals, whereas that of ND rats receiving growth factors was intermediate. Serum IGF-I levels were reduced 54% in ND animals and maintained with the provision of growth factors. Dia fatigue resistance was improved in ND animals receiving growth factors. There were no differences in Dia contractile properties, fiber type proportions, or succinate dehydrogenase activities across groups. ND resulted in atrophy/growth arrest of all Dia fibers (20-32%) compared with Ctl. Administration of IGF-I and/or GH completely prevented atrophy/growth arrest of all Dia fibers. No additive or synergistic effects were noted. We propose that these growth factors may provide useful short-term adjunctive nutritional support in circumstances in which the provision of optimal nutrition may be delayed or inadequate.

Animals↗
PubMed1999

Influence of intercellular tissue connections on airway muscle mechanics.

Contraction of smooth muscle in visceral organs is modified by structures external to the muscle. Within muscle tissue itself, connective tissue plays an important role in force transference among the contractile cells. Connections arranged radially can affect contractile mechanics by limiting tissue expansion at short lengths. Previous work suggests that increased stiffness at extreme shortening is due to such radial constraints. Two approaches to further study of these effects are reported. To increase radial constraints, very thin Silastic bands were placed loosely about strips of canine trachealis muscle at rest length. The strips were allowed to shorten under light afterloads, expanding until restrained by the bands. Subsequent removal of the bands allowed increased shortening, with less increase in stiffness at short lengths. Related isometric effects were observed. To reduce constraints, muscle strips were partially digested with collagenase. Compared with control conditions, this treatment permitted further shortening, with less increase in stiffness at short lengths. These results emphasize the role of extracellular structures in determining mechanical function of smooth muscle.

Animals↗
PubMed1999

Alterations in diaphragm contractility after nandrolone administration: an analysis of potential mechanisms.

The aim of this study was to evaluate the potential mechanisms underlying the improved contractility of the diaphragm (Dia) in adult intact male hamsters after nandrolone (Nan) administration, given subcutaneously over 4 wk via a controlled-release capsule (initial dose: 4.5 mg. kg-1. day-1; with weight gain, final dose: 2.7 mg. kg-1. day-1). Control (Ctl) animals received blank capsules. Isometric contractile properties of the Dia were determined in vitro after 4 wk. The maximum velocity of unloaded shortening (Vo) was determined in vitro by means of the slack test. Dia fibers were classified histochemically on the basis of myofibrillar ATPase staining and fiber cross-sectional area (CSA), and the relative interstitial space was quantitated. Ca2+-activated myosin ATPase activity was determined by quantitative histochemistry in individual diaphragm fibers. Myosin heavy chain (MHC) isoforms were identified electrophoretically, and their proportions were determined by using scanning densitometry. Peak twitch and tetanic forces, as well as Vo, were significantly greater in Nan animals compared with Ctl. The proportion of type IIa Dia fibers was significantly increased in Nan animals. Nan increased the CSA of all fiber types (26-47%), whereas the relative interstitial space decreased. The relative contribution of fiber types to total costal Dia area was preserved between the groups. Proportions of MHC isoforms were similar between the groups. There was a tendency for increased expression of MHC2B with Nan. Ca2+-activated myosin ATPase activity was increased 35-39% in all fiber types in Nan animals. We conclude that, after Nan administration, the increase in Dia specific force results from the relatively greater Dia CSA occupied by hypertrophied muscle fibers, whereas the increased ATPase activity promotes a higher rate of cross-bridge turnover and thus increased Vo. We speculate that Nan in supraphysiological doses have the potential to offset or ameliorate conditions associated with enhanced proteolysis and disordered protein turnover.

Anabolic Agents↗
PubMed1999

Growth hormone restores aged diaphragm myosin composition and performance after chronic undernutrition.

The effects of growth hormone (GH) on diaphragm muscle myosin heavy chain (MHC) composition and mechanical performance were investigated in Fischer 344 male rats aged to senescence (24.5 mo of age). Chronic undernutrition (UN), refeeding (RF), and RF+GH were compared with ad libitum feeding by using a model of UN that produced a 50% decrease in body weight over a 12-mo period. The effect of aging was assessed by comparing MHC composition of ad libitum-fed rats at 12 and 24.5 mo of age. At senescence, significant decreases in slow type I (-23%) and fast type IIA (-31%) MHC had occurred with aging. Conversely, UN over this aging period increased types I (32-73%) and IIA (22-23%) MHC and decreased fast types IIB (32-54%) and IIX (30-31%) MHC. RF and RF+GH reversed these shifts back toward control values. At senescence, maximal specific force, maximal velocity, and specific power capacity were not different across treatment groups. During repetitive isotonic contraction trials, the diaphragms of UN rats maintained power production over time (54% of initial power at 60 s), whereas the power production of diaphragms of ad libitum-fed rats fell to 0% (P < 0.05). In comparison with UN rats, the diaphragms of RF and RF+GH rats produced 23 (not significant) and 11% (P < 0.05) of initial power, respectively, suggesting that RF+GH treatment restored performance characteristics after UN. We conclude that RF+GH can reverse alterations in MHC composition and mechanical performance produced by chronic UN in the aged rat diaphragm.

Animals↗
PubMed2000

Versatile, high-speed force transducer using a laser diode beam as an optical lever.

A force transducer with variable sensitivity and speed is described. Its moving element is a cantilever beam that projects vertically into a muscle bath. A brace constrains bending of the beam to a short, proximal "hinge." Rotation of the beam about the hinge is amplified 30-fold by an optical lever consisting of a laser diode beam reflected from a mirror on the cantilever to a photodiode pair. This design places the electrical components at a distance from the damp environment of the muscle bath. Large changes in sensitivity and speed can be obtained by substituting different cantilevers. Smaller changes can be made by varying the length of the hinge. A transducer with a 6-mm cantilever optimized for the study of single, skinned skeletal muscle fibers is described in detail. This device had a resonant frequency of 22 kHz and sensitivity such that the total root-mean-square noise in the circuit was more than 500-fold smaller than the expected maximum force. Variations of this device with orders of magnitude different sensitivities are also described.

Amplifiers, Electronic↗
PubMed2003

Mechanical state of airway smooth muscle at very short lengths.

Although the shortening of smooth muscle at physiological lengths is dominated by an interaction between external forces (loads) and internal forces, at very short lengths, internal forces appear to dominate the mechanical behavior of the active tissue. We tested the hypothesis that, under conditions of extreme shortening and low external force, the mechanical behavior of isolated canine tracheal smooth muscle tissue can be understood as a structure in which the force borne and exerted by the cross bridge and myofilament array is opposed by radially disposed connective tissue in the presence of an incompressible fluid matrix (cellular and extracellular). Strips of electrically stimulated tracheal muscle were allowed to shorten maximally under very low afterload, and large longitudinal sinusoidal vibrations (34 Hz, 1 s in duration, and up to 50% of the muscle length before vibration) were applied to highly shortened (active) tissue strips to produce reversible cross-bridge detachment. During the vibration, peak muscle force fell exponentially with successive forced elongations. After the episode, the muscle either extended itself or exerted a force against the tension transducer, depending on external conditions. The magnitude of this effect was proportional to the prior muscle stiffness and the amplitude of the vibration, indicating a recoil of strained connective tissue elements no longer opposed by cross-bridge forces. This behavior suggests that mechanical behavior at short lengths is dominated by tissue forces within a tensegrity-like structure made up of connective tissue, other extracellular matrix components, and active contractile elements.

Animals↗
PubMed2002

Changes in force-velocity properties of trachealis due to oscillatory strains.

The physically dynamic environment of the lung constantly modulates the mechanical properties of airway smooth muscle. In vitro experiments have shown that contractility of the muscle is compromised by oscillatory strains, perhaps through disruption of cross-bridge interaction and organization of the contractile filaments. To understand the mechanism by which oscillation affects contractility, functional changes of the muscle in terms of force-velocity relationship were assessed before and after imposition of length oscillation in both relaxed and activated states. The oscillation protocol was designed to reduce isometric force by 15-20%, followed by measurement of force-velocity properties. Maximal velocity and power changed by +8 and -14%, respectively, after oscillation applied in the relaxed state and changed by -15 and -25%, respectively, after oscillation applied during contraction. A simple model of reduced activation could not account for the results; neither could the results be explained satisfactorily by the current cross-bridge theory of contraction. The results, however, could be explained if the possibility of reorganization of the contractile filaments due to oscillatory strains was considered.

Animals↗
PubMed1993

Autografted minced muscle fragments do not affect muscle regeneration in partially excised rat gastrocnemius muscle.

The kinetics of the regeneration process following partial excision or mincing in the rat gastrocnemius muscle was compared using histological and physiological methods. Immediately following injury there was a marked decrease in the distance of shortening (DS) values during isotonic contraction, followed by a progressive increase until 2 weeks after injury. By 85 days the DS values attained those of control muscle during contraction against low loads (up to 50 g), and 80 and 62% of control values at 150 and 250 g, respectively. However, there was no difference in the DS values at 28 and 85 days after injury between muscles that were partially excised or when the removed part of the muscle was minced and placed in the injured site. It is concluded that the enrichment of an injured area of the gastrocnemius muscle with minced autografted muscle does not result in long-term improvement of the functional capacity of the regenerated muscle due to the addition of satellite cells and/or other factors in the minced tissue.

Animals↗
PubMed1984

Combined renovascular hypertension and diabetes in rats: a new preparation of congestive cardiomyopathy.

Myocardial function, electrophysiologic characteristics, and structure were studied in rats with both renovascular hypertension and streptozotocin-induced diabetes (HD). Ventricular papillary muscles from untreated rats with HD showed a marked slowing of isometric and isotonic contractions. Peak developed tension and peak shortening were preserved, except in one animal with findings of congestive heart failure. Transmembrane action potentials increased fivefold in duration. Myocardial interstitial fibrosis was frequently observed. Physiologic parameters of rats with HD treated by left nephrectomy, captopril, and insulin were very similar to those of age-matched controls. The mortality rate of rats with HD was 43% over 5 to 6 months in the first study. In a second study, spontaneously dying rats with HD were compared with those deliberately killed. A 55% mortality was observed over 7 months. Myocardial structural damage and histologic evidence of congestive heart failure were more frequent in spontaneously dying rats with HD. Combined renovascular hypertension and diabetes in rats appears to be a new preparation of congestive cardiomyopathy.

Action Potentials↗
PubMed1977

Altered performance of rat cardiac muscle follows changes in mechanical stress during relaxation.

We compared two sets of loading conditions for their effect on the mechanical performance of isolated rat trabecular muscle: (1) loading which approximated that of the intact ventricle; (2) nonphysiological afterloaded isotonic contractions. Improved performance, manifested by increased shortening and rate of shortening at constant load, was seen when lengthening occurred at light loads, as in the intact heart. In contrast, lengthening occurring at the same load against with shortening had taken place was followed by diminished performance. Viscous elements in series with the muscle could not account for this phenomenon. The results suggest the presence of an autoregulatory response of myocardium to mechanical stress during relaxation.

Animals↗
PubMed1982

The force-velocity relation and stepwise shortening in cardiac muscle.

A series of experiments was carried out to determine the effects of load variation on the character of stepwise shortening. We imposed afterloaded isotonic contractions on rat ventricular trabeculae, and measured the effect of load on pause duration, i.e., on the duration of the periods during which there was no sarcomere shortening. Sarcomere lengths were measured by optical diffraction. Increases of load brought about increases of pause duration; the relation was linear. The relation did not appear to depend on time during contraction, but did depend on sarcomere length: for a given load, pauses were longer at shorter sarcomere lengths. In a supplementary protocol in which we measured the dynamics of the central segment of the muscle during muscle isometric contraction, we found that the velocity of sarcomere shortening during the shortening step was approximately independent of load. These results provide a framework for interpretation of muscle force-velocity relations: diminished velocity at high load may be the result of increased pause durations.

Animals↗
PubMed1984

Mechanical properties of resting and active isolated coronary arteries.

Coronary arterial smooth muscle is myogenically active, is acted upon by a variety of modulating agents, and is subjected, in situ, to compression and distension by the myocardium. Its mechanical properties thus play a key role in the regulation of coronary blood flow. To describe these, we applied phase-plane analysis of shortening velocity vs. length and load clamping to strips of isolated coronary arteries made to contract by an increase in extracellular potassium concentration. At any load, length was larger in relaxed than in "resting" preparations. In addition, preloaded shortening was smaller than would be expected from the relation between active isometric force and muscle length. These suggest the occurrence of stretch-activation and shortening-inactivation. To judge from both phase-plane analysis and quick release experiments, shortening velocity depended on load as well as on time. Velocity decreased with increasing duration of contraction. Shortened coronary arteries resisted lengthening induced by loading and could transiently bear loads that considerably exceeded isometric force. This load-bearing capacity increased with increasing shortening. In conclusion, coronary arterial smooth muscle displays the classical relationship between length, force, and velocity. However, the nature of this relationship changes with duration of activity. In addition, it is greatly affected during changes in length or load, such as expected when the arterial wall is exposed to pulsatile blood flow and is surrounded by mechanically active muscle.

Animals↗
PubMed1986

Myocardial biochemical, contractile, and electrical performance after imposition of hypertension in young and old rats.

The effects of renovascular hypertension on the biochemical, contractile, and electrical performance of myocardial tissue from rats of various ages has been examined. Male Fischer rats, 2, 7, 12, and 17 months old, were made hypertensive by constriction of the left renal artery. Ten weeks after the onset of hypertension, left ventricular papillary muscles were isolated from those four groups when 5, 10, 15, and 20 months old, respectively. Mechanical performance and transmembrane electrical events were recorded simultaneously. Contractile protein enzyme activity was determined in the same hearts from which papillary muscles were used for acquisition of mechanical and electrical information. There was a slight increase in blood pressure in control groups as a function of age while blood pressure maintained a range of approximately 179-188 mm Hg for all hypertensive groups. Heart weight of control animals increased significantly from 5 months to 20 months of age from 539 +/- 26 to 1088 +/- 56 mg, representing an increase of 101%. In hypertensive animals, heart weight increased 50% in 5-month-, 15% in 10-month-, 50% in 15-month-, and 11.7% in 20-month-old animals. Although control groups revealed alterations in mechanical, electrical, and biochemical parameters that increased as a function of age, the magnitude of the biochemical, contractile, and electrical response to hypertension varied monotonically with the extent of myocardial hypertrophy, rather than age per se. Adaptation to the stress of hypertension was observed in each age group, and was revealed as prolongation of mechanical and electrical timing parameters, depression of the load-velocity relation, and contractile protein enzyme activity. Thus, the stress of hypertension, which was tolerated by the 10- and 20-month-old animals with lesser relative hypertrophy and lesser changes in measured parameters, may represent a differential adaptation to the stress of hypertension.

Action Potentials↗
PubMed1976

Responsiveness to glucagon in fetal hearts. Species variability and apparent disparities between changes in beating, adenylate cyclase activation, and cyclic AMP concentration.

Previous studies of the ability of the immature heart to respond to glucagon have yielded conflicting results. To test the possibility that the apparent discrepancies might be explained in part by species variability, isolated hearts of fetal mice and rats (13-22 days' gestational age) were studied under identical conditions in vitro. Changes in atrial rate and ventricular contractility were measured in spontaneously beating hearts exposed to glucagon, and activation of adenylate cyclase was assayed in cardiac homogenates. In mice of 16 days' gestational age or less, there was no change in heart rate in response to glucagon; at 17-18 days, minimal responsiveness was present; and after 19 days, 10muM glucagon caused an increase in spontaneous atrial rate of 30 +/- 4% (SEM) (P less than 0.001). Measurement of the extent and speed of volume displacement of the isotonically contracting hearts with a specially constructed capacitance transducer revealed that ventricular inotropic responsiveness also appeared after 17-19 days. Cardiac stores of glycogen were reduced in older hearts exposed to glucagon, but not in those aged less than 16 days. In contrast, glucagon failed to activate adenylate cyclase in homogenates of hearts of fetal mice at any age. Furthermore, glucagon failed to elicit an increase in the concentration of cyclic AMP in spontaneously beating hearts that developed tachycardia. Responses in hearts of fetal rats were distinctly different from those in mouse hearts: at no age was there any change in heart rate, strength of contraction, glycogen content, or adenylate cyclase activation. Thus, there are major species differences in cardiac pharmacological maturation. Although the mouse heart develops the ability to increase its rate and strength of contraction and to undergo glycogenolysis in response to glucagon well before birth, the rat heart does not. In addition, there is an apparent disparity in late fetal mouse hearts between the ability of glucagon to induce functional responses and its ability to stimulate adenylate cyclase and increase cyclic AMP levels. It is impossible, of course, to rule out absolutely the possibility that localized increases in a critical cyclic AMP pool were present but too small to measure in the entire tissue. Nevertheless, the most obvious interpretation of our results is that they are compatible with the hypothesis that glucagon may exert some of its hemodynamic effects independently from the adenylate cyclase-cyclic AMP system in the late-fetal mouse heart.

Adenylyl Cyclases↗
PubMed2000

Relative metabolic utilization of in situ rabbit soleus muscle: thermistor-based measurements and model.

Electrically conditioned skeletal muscle can provide the continuous power source for cardiac assistance devices. Optimization of the available sustained power from in vivo skeletal muscle requires knowledge of its metabolic utilization and constraints. A thermistor-based technique has been developed to measure temperature changes and to provide a relative estimate for metabolic utilization of in situ rabbit soleus muscle. The relative thermistor response, active tension and muscle displacement were measured during cyclic isometric and isotonic contractions across a range of muscle tensions and contraction durations. The thermistor response demonstrated linear relationships versus both contraction duration at a fixed muscle length and active tension at a fixed contraction duration (r(2)=0.90+/-0.14 and 0.70+/-0.21, respectively; means +/- s.d.). A multiple linear regression model was developed to predict normalized thermistor response, DeltaT, across a range of conditions. Significant model variables were identified using a backward stepwise regression procedure. The relationships for the in situ muscles were qualitatively similar to those reported for mammalian in vitro muscle fiber preparations. The model had the form DeltaT=C+at(c)F+bW, where the constant C, and coefficients for the contraction duration t(c) (ms), normalized active tension F and normalized net work W were C=-1.00 (P<0.001), a=5.97 (P<0.001) and b=2.12 (P<0.001).

Animals↗
PubMed1982

Pharmacological studies on supersensitization. VIII. Dissociation of induction of supersensitivity from presynaptic action of cocaine on isolated vas deferens of guinea pig.

Effects of cocaine on the isotonic contractions of isolated vas deferens of intact and reserpinized guinea pigs to acetylcholine were examined. Both cocaine-induced increase in sensitivity to acetylcholine and cocaine-induced increase in maximum response of Ca2+-contraction was attenuated remarkably by reserpine. However, cocaine-induced increases in acetylcholine- and K+-contractions in Ca2+-free Tyrode solution were not prevented by reserpine. Acetylcholine-contraction, but not K+-contraction, in the preparation exposed for 5 min to Ca2+-free Tyrode solution were inhibited by reserpine. Cocaine did not inhibit the cholinesterase activity of vas deferens of guinea pig. These results suggested that presynaptic mechanisms of cocaine-induced supersensitivity are excluded and that inhibitory effect of reserpine on cocaine-induced supersensitivity might be due to the inhibition of cocaine-induced increase in calcium-influx into smooth muscle cells of vas deferens.

Acetylcholine↗
PubMed1982

Pharmacological studies on supersensitization. IX. Non-specific supersensitivity of vas deferens of guinea pig induced by tripelennamine, N,N-dimethyl-N',N'-dibenzylethylenediamine and N,N-dibenzyl-N',N'-dimethyl-1,2-propanediamine.

Effects of tripelennamine, N,N-dimethyl-N',N'-dibenzylethylenediamine (DBED) and N,N-dibenzyl-N',N'-dimethyl-1,2-propanediamine (DBPD) on the isotonic contractions of isolated vas deferens of guinea pig were examined. These ethylenediamines, except DBPD, induced slight but significant increase in sensitivity of vas deferens to K+. Tripelennamine induced dose-dependent potentiation to epinephrine and norepinephrine, but tripelennamine-induced augmentation of acetylcholine-contractions was weak and dose-independent. DBED potentiated both catecholamines and acetylcholine in a dose-dependent way and in the same degree. The degree of DBPD-induced augmentation of epinephrine- and norepinephrine-induced contractions was dose-independent and much weaker than that of acetylcholine-contractions. Tripelennamine and DBED did not affect the contractile response to tyramine, while DBPD potentiated the contractile response to tyramine. These results suggest the following possibilities: 1) tripelennamine affects both amine uptake mechanism and beyond receptor mechanism of contractile processes and induced supersensitivity of various stimulants. 2) DBED affects mainly beyond receptor mechanism of contractile processes and augments the contractile responses to various stimulants. 3) The mechanism of DBPD-induced supersensitivity remained obscure, but the inhibition of the metabolic degradation of stimulants was proposed as one of the possible mechanism of supersensitization.

Acetylcholine↗
PubMed1983

Pharmacological studies on supersensitization. XII. Inhibitory effect of reserpine on tripelennamine-, N,N-dimethyl-N',N'-dibenzylethylenediamine- and N,N-dibenzyl-N',N'-dimethyl-1,2-propanediamine-induced supersensitivity of isolated vas deferens of guinea pig to acetylcholine.

Effects of tripelennamine, N,N-dimethyl-N',N'-dibenzylethylenediamine (DBED) and N,N-dibenzyl-N',N'-dimethyl-1,2-propanediamine (DBPD) on the isotonic contractions of isolated vas deferens of intact and reserpinized guinea pigs to acetylcholine were examined. Increase in sensitivity to acetylcholine induced by tripelennamine, DBED and DBPD was attenuated remarkably by reserpine. Tripelennamine- and DBED-induced increases in Ca2+-contractions were not affected by reserpine. Acetylcholine-contractions in Ca2+-free Tyrode solution were inhibited by reserpine, but K+-contractions in Ca2+-free Tyrode solution were not affected by reserpine. Tripelennamine- and DBED-induced increases in acetylcholine- and K+-contractions in Ca2+-free Tyrode solution were attenuated or abolished by reserpine. DBPD decreased cholinesterase activity of vas deferens of guinea pig, but DBED did not. These results suggest that, although the Ca2+-storage site utilized for acetylcholine-contraction is different from that for K+-contraction, tripelennamine- and DBED-induced increase in Ca2+-release from superficial Ca2+-binding sites induced by acetylcholine and K+ is inhibited by reserpine. It is also estimated that DBPD-induced supersensitivity to acetylcholine might be due to the inhibition of cholinesterase activity. However, the mechanism of inhibition of DBPD-induced supersensitivity by reserpine remained obscure.

Acetylcholine↗