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The modulatory role of prostaglandin E2 (PGE2) was examined in pony tracheal smooth muscle strips. Although exogenous PGE2 inhibited the contractile response to both electrical field stimulation (EFS) and acetylcholine (ACh) in a dose-dependent manner, the concentration required to inhibit the response to EFS (10 nM) was less than that required to inhibit the response to ACh (0.1 microM). Cyclooxygenase inhibition with aspirin or meclofenamate had no effect on either the response to EFS or to ACh even though PGE2 production was inhibited. Our results demonstrate that in ponies as in other species, exogenous PGE2 can inhibit the airway smooth muscle's response to EFS and ACh. However, the failure of cyclooxygenase inhibition to alter the response to EFS and ACh suggests that endogenous prostanoids do not exert a significant modulatory effect on pony tracheal smooth muscle in vitro.
OBJECTIVE: To characterize the physiological fatigue in bladder smooth muscles that can occur within 60 s of stimulation, which is closer to the duration of normal voiding. MATERIALS AND METHODS: Longitudinal and transverse strips of rat bladder were used; the muscles were mounted in an in vitro multi-muscle chamber, and the decline in contractile tension recorded during continuous electrical stimulation at frequencies of 5-30 Hz for 60 s. The effect of muscle length on fatigue was assessed by monitoring the decline in tension during 30 Hz stimulation at rest length, and at 60% and 100% stretched lengths of the bladder strips. To assess some of the factors involved in the development of fatigue, tension responses of fatigued muscles were monitored on exposure to 80 mm potassium or 1 microm bethanechol. RESULTS: In both longitudinal and transverse bladder strips stimulated at 30 Hz, peak contractile tension declined to 50% of original after approximately 33 s, and to 30% after 60 s of stimulation. After 10 s rest, 60% of the original tension was recovered. Increasing the frequency of fatigue stimulation from 5 to 30 Hz significantly increased the extent of the decline in tension and reduced the time to a 50% decrease in tension. Stretching the bladder strips from rest length to 100% stretched length significantly reduced the extent of tension decline and increased the time to a 50% decrease in tension. Exposure of fatigued muscles to high potassium or bethanechol generated more tension than electrical stimulation. CONCLUSION: Contractile fatigue occurs in both longitudinal and transverse strips of the bladder smooth muscles within the duration of normal voiding. Increasing the frequency of stimulation from 5 to 30 Hz increased the degree and rate of fatigue. Stretching the bladder strips from rest length by 60-100% reduced the degree and rate of fatigue. Bladder fatigue may be caused by decreased depolarization of the smooth muscle membranes, reduced release of acetylcholine from presynaptic nerve terminals, or by other yet undetermined mechanisms.
To determine if epithelium from immature airways can modulate the responsiveness of smooth muscle, we studied paired trachealis muscle strips from preterm sheep. The epithelium was removed from one strip and left undisturbed in the other. Concentration-effect (CE) curves to acetylcholine (ACh), KCl, and isoproterenol were obtained. To evaluate maturational effects, responses to ACh and isoproterenol were studied in trachealis strips from adult airways. Maximal stress (Po) to ACh increased after epithelium removal in preterm (P < 0.05) but not adult strips. Epithelium removal caused a leftward shift of the ACh CE curves in both preterm and adult strips (P < 0.001) and a decrease in the dose required to achieve a one-half maximal response (ED50) in both preterm (P < 0.005) and adult strips (P < 0.05). The magnitude of the change in Po as well as in the ED50 for ACh between preterms and adults was similar. Epithelium removal did not alter either the Po or the CE curves of preterm strips stimulated by KCl. Response to isoproterenol in precontracted strips was enhanced in the presence of an intact epithelium in both groups (P < 0.05). These data demonstrate that preterm airway epithelium is able to modulate the responsiveness of smooth muscle. Additionally, the magnitude of the effect is unchanged with maturation. We speculate that damage of airway epithelium from mechanical ventilation may contribute to the increased incidence of airway hyperreactivity observed in preterm infants.
The effects of prostaglandin (PG) E1, E2 and F2 alpha on isolated smooth muscles of rabbit bladder and urethra were studied by in vitro techniques for recording contractile activities. To examine the mechanism of PGs' effect, intracellular cyclic AMP content was also measured by radioimmunoassay. Spontaneous contractile force of muscle strips isolated from rabbit urinary bladder dome and base was increased dose-dependently by administration of PGE1, E2 or F2 alpha. Isolated muscle strips from bladder dome responded to PG more markedly than those from bladder base. The rank order of potency to induce contractile responses was PGF2 alpha greater than PGE2 greater than PGE1 in both dome and base muscles. Spontaneous contractile force of muscle strips isolated from rabbit urethra was increased dose-dependently by administration of PGF2 alpha, and, in contrast, was decreased dose-dependently by PGE1 or E2. These effects were not affected by pretreatment with atropine, phentolamine, propranolol and tetrodotoxin, but were significantly inhibited by pretreatment with verapamil, a Ca-antagonist. Cyclic AMP accumulation in urethral muscle strips significantly increased after administration of PGE1. These results demonstrated that contractile response of rabbit bladder smooth muscle to PG was mainly induced by Ca2+ influx and that cyclic AMP was related to the relaxation of rabbit urethral smooth muscle by PGE1.
Current review is focused on regulatory functions of myosin light chains from different muscle types. Special attention is paid to myosin light chains from striated muscles. The present review considers mainly the relevant data provided after 1986.
Certain forms of coronary artery disease do not respond to treatment with Ca2+ channel blockers, and a role for endothelin-1 (ET-1) in Ca2+ antagonist-insensitive forms of coronary vasospasm has been suggested; however, the signaling mechanisms involved are unclear. We tested the hypothesis that a component of ET-1-induced coronary smooth muscle contraction is Ca2+ antagonist-insensitive and involves activation of protein kinase C (PKC). Cell contraction was measured in smooth muscle cells isolated from porcine coronary artery, [Ca2+]i was measured in fura-2 loaded cells, and the cytosolic and particulate fractions were examined for PKC activity and reactivity with isoform-specific PKC antibodies using Western blot analysis. In Hank's solution (1 mmol/L Ca2+), ET-1 (10(-7) mol/L) caused a transient increase in [Ca2+]i (236+/-14 nmol/L) followed by a maintained increase in [Ca2+]i (184+/-8 nmol/L) and 35% cell contraction. The Ca2+ channel blockers verapamil and diltiazem (10(-6) mol/L) abolished the maintained ET-1-induced [Ca2+]i, but only partially inhibited ET-1-induced cell contraction to 18%. The verapamil-insensitive component of ET-1 contraction was inhibited by the PKC inhibitors calphostin C and epsilon-PKCV1-2. ET-1 caused translocation of Ca2+-dependent alpha-PKC and Ca2+-independent epsilon-PKC from the cytosolic to the particulate fraction that was inhibited by calphostin C. Verapamil abolished ET-1-induced translocation of alpha-PKC, but not that of epsilon-PKC. Phorbol 12-myristate 13-acetate (10(-6) mol/L), a direct activator of PKC, caused 22% cell contraction, with no increase in [Ca2+]i, and translocation of epsilon-PKC that was inhibited by calphostin C, but not by verapamil. KCl (51 mmol/L), which stimulates Ca2+ influx, caused 35% cell contraction and increase in [Ca2+]i (291+/-11 nmol/L) that were inhibited by verapamil, but not by calphostin C, and did not cause translocation of alpha- or epsilon-PKC. In Ca2+-free (2 mmol/L EGTA) Hank's solution, ET-1 caused 15% cell contraction, with no increase in [Ca2+]i, and translocation of epsilon-PKC that were inhibited by epsilon-PKC V1-2 inhibitory peptide. Thus, a significant component of ET-1-induced contraction of coronary smooth muscle is Ca2+ antagonist-insensitive and involves activation and translocation of Ca2+-independent epsilon-PKC, and may represent a signaling mechanism of Ca2+ antagonist-resistant forms of coronary vasospasm.
Spinal somatosensory evoked potentials (SSEPs) have been used to monitor spinal cord function during corrective scoliosis surgery. We report three cases in which direct epidural stimulation for measurement of SSEPs produced paraspinal muscle contraction, resulting in respiratory and metabolic acidosis. In two of the cases, SSEP-induced acidosis was observed even when only the first twitch of the train-of-four response was detectable after a second dose of muscle relaxant. In one of these two cases, the acidosis was abolished after a sufficient dose of vecuronium to ablate the twitch response. To prevent SSEP-induced respiratory and metabolic acidosis, we recommend that SSEPs should be measured only when profound neuromuscular blockade has been obtained.
We have recently shown (Eur. Respir. J. 1997;10:522-529) that in spontaneously breathing and actively expiring patients, static intrinsic positive end-expiratory pressure (PEEPi,st) can be corrected for expiratory muscle contraction by subtracting the average expiratory rise in gastric pressure (Pga,exp rise), calculated from three breaths just prior to an airway occlusion, from the end-expiratory airway pressure (Paw) of the first occluded inspiratory effort (PEEPi,st avg). However, since in some patients there is substantial variability in the intensity of expiratory muscle activity and hence in Pga,exp rise, this method may be inaccurate because the Pga,exp rise of breaths preceding airway occlusion may differ from that of the first postocclusion breath. In the present study, we introduced a new method consisting of synchronous subtraction of Pga,exp rise from Paw, both occurring during airway occlusion (PEEPi,st sub). PEEPi,st sub and PEEPi,st avg were each compared with the reference PEEPi,st (PEEPi,st ref), which was obtained during muscular paralysis and simulation of the spontaneous breathing pattern by the ventilator. We found that, in 25 critically ill patients, PEEPi,st sub (mean +/- SD, 5.3 +/- 2.6 cm H(2)O) was nearly identical to PEEPi,st ref (5.4 +/- 2.4 cm H(2)O). Their mean difference was -0.06 cm H(2)O with limits of agreement -0.96 to 0.84 cm H(2)O, indicating a strong agreement between these methods. In contrast, mean difference of PEEPi,st avg and PEEPi,st ref was 0.73 cm H(2)O with limits of agreement -3.97 to 5.43 cm H(2)O, indicating lack of agreement. Coefficient of variation of Pga,exp rise was 14.3 +/- 7.2% (range, 5.2 to 28.3%). There was a good correlation between the coefficient of variation of Pga,exp rise and the difference between PEEPi,st avg and PEEPi,st ref (r = 0.909; p < 0.001). We conclude that PEEPi,st can be accurately measured in spontaneously breathing patients by synchronous subtraction of Pga,exp rise from Paw during airway occlusion.
The influence of fusimotor activity, via the gamma-loop, on the reflex response of motor neurons to stretch or vibration of triceps surae muscles was investigated in decerebrated cats. Action potentials of single fusimotor neurons were recorded from fine branches cut from nerves innervating triceps surae muscles leaving their main nerve supply intact. Most of the examined fusimotor neurons were found to be coactivated with motor neurons during reflex contraction of the muscles. Week autogenetic inhibitory influence on the discharge of fusimotor neurons was established at the beginning of the reflex tension rise in the muscles. A decrease of the reflex motor signal leading to the so-called silent period may, on the ground of this finding, results partially from the transiently lowered fusimotor outflow to the contracting muscles. Investigation of the changes in fusimotor spike occurrence during the rising phase of reflex muscle contraction seemed to be valuable in the estimation of both the autogenetic reflex influence on these motoneurons and conditions required for servoassistance.
The motion of skinned muscle fibers in chemically controlled bathing solutions is examined to obtain information about the cross bridge cycle. The effects of an ATP regenerating system and ionic strength on both the transient and the steady response to step changes in load are compared. The transient is changed in characteristic ways by these factors, but the steady motion is unaffected. If changes in the transient reflect changes in the rates of "making" and "breaking" cross bridges, these results suggest that the rate of physiological contraction is limited by a slow transition in the unattached myosin molecule rather than the making and breaking of cross bridges per se.
Considerable attention has been directed to the characteristic force-velocity relation discovered by A. V. Hill in the study of muscle kinematics. Models of contractile process were tested on the basis of their compatibility with the Hill equation. However, almost all the isotonic data have been restricted to one length, l(0), the maximum length with almost no resting tension; the velocities measured are those initial values when the load begins to move. The force-velocity curve extrapolates to zero velocity for isometric tension, but only for the tension at that one length. Very few efforts have been made to study the profiles of the curves throughout the range of lengths over which shortening takes place. In examining the length region, l </= l(0), for an isotonically contracting muscle, not only is the force-velocity relation valid for the initial reference length, l(0), but also for any other length. The analysis in this report indicates that the constants a/P(0) and b/l(0) remain fixed throughout the length change of afterloaded isotonic shortening in the Rana pipiens sartorius muscles.
Animals decerebrated at the precollicular-premammillary body level exhibit spontaneous locomotion without any artificial stimulation. Our laboratory reported that the cardiovascular and autonomic responses at the onset of spontaneous locomotor events are evoked by central command, generated from the caudal diencephalon and the brain stem (Matsukawa K, Murata J, and Wada T. Am J Physiol Heart Circ Physiol 275: H1115-H1121, 1998). In this study, we examined whether central command and/or a reflex resulting from muscle afferents modulates arterial baroreflex function using a decerebrate cat model. The baroreflex was evoked by stimulating the aortic depressor nerve (ADN) at the onset of spontaneous muscle contraction (to test the possible influence of central command) and during electrically evoked contraction or passive stretch (to test the possible influence of the muscle reflex). When the ADN was stimulated at rest, heart rate and arterial blood pressure decreased by 40 +/- 2 beats/min and 11 +/- 1 mmHg, respectively. The baroreflex bradycardia was attenuated to 55 +/- 4% at the onset of spontaneous contraction. The attenuating effect on the baroreflex bradycardia was not observed at the onset and middle of electrically evoked contraction or passive stretch. The depressor response to ADN stimulation was identical among resting and any muscle interventions. The inhibition of the baroreflex bradycardia during spontaneous contraction was seen after beta-adrenergic blockade but abolished by muscarinic blockade, suggesting that the bradycardia is mainly evoked through cardiac vagal outflow. We conclude that central command, produced within the caudal diencephalon and the brain stem, selectively inhibits the cardiac component, but not the vasomotor component, of the aortic baroreflex at the onset of spontaneous exercise.
We analyse the Molecular Jet-hypothesis proposed by Morel & Bachouchi (1988, J. theor. Biol. 132, 83.). This hypothesis attempts to explain the movement of covaspheres that contain myosin heads attached to actin filaments. This movement occurs during muscle contraction. However, the hypothesis does not predict the velocity of covaspheres correctly. Therefore, we are studying additional aspects of the hypothesis.
Twenty-two human subjects performed sustained voluntary contractions of the mandibular elevator muscles firstly without and secondly with visual biofeedback. The level of electromyographic activity of the masseter muscle during the second clench exceeded that during the first clench by a mean of 36%. This differential indicates the ability of the subjects to override the central factors which normally limit muscle activity during a fatiguing contraction.
In migraine, the role of platelets is regarded as an important factor. We investigated plasma beta-thromboglobulin (BTG), platelet factor 4 (PF4), and 5-hydroxytryptamine (5-HT) in migraine patients and muscle contraction headache (MCH) patients during headache-free periods. The mean values of the plasma BTG, PF4, and 5-HT concentrations in the migraine group and the MCH group were significantly higher than those in healthy controls. The mean value of the plasma BTG concentration was significantly higher in the migraine group than in the MCH group, but the differences in the mean plasma PF4 and 5-HT concentrations between the two groups were not significant. Continuous platelet activation exists in both MCH patients and migraine patients. From the biochemical point of view, we have provided evidence for a similarity between migraine and MCH.
Chemical parametric excitation is presented as the fundamental mechanism of energy transfer. Together with the Franck-Condon principle, it provides a mechanically sound explanation for enzymatic reaction, nerve excitation, muscle contraction, and electron transfer at a basic level. Intermediate between macroscopic models of membrane asymmetry and molecular models, the new model rests on a systematic approach, proposed here, to organizational aspects of the energy transfer processes. In support, a derivation is given of the chemical analog of the Manley-Rowe power conservation relations for parametrically excited electrical networks. This extension to chemical systems indicates for the first time an explanation of power flow directionality and delegates a pumping role to the enzyme. The generalized Manley-Rowe relations are suggested to be a universal law of nature. In such case, nonlinearity could be attributable to the coupling of three systems by these generalized Manley-Rowe conditions relating flows/reactions/oscillations--even though separately each system might be described by linear (Onsager) relations.
The aim of this study was to determine if central GABA mechanisms are involved in the cardiac vagal withdrawal at the beginning of exercise in man. We tested whether GABA-enhancing effects of a benzodiazepine could be observed in the HR change (R-R interval) immediately following the onset of a brief (10s) isometric contraction (60 % maximum) of the biceps muscle. The difference between the change in R-R interval occurring during the same phase of respiration was compared for placebo (Pla) and 10 mg oral diazepam (Dz) treatment in a double blind, crossover trial. ECG, blood pressure, respiration and biceps muscle tension were recorded. The subjects breathed to a metronome and R-R interval measurements were plotted for early and late inspiration and early and late expiration. The mean values of the first late expiration R-R interval immediately following the start of contraction in early expiration were compared to the same measurements without contraction. Contractions initiated following diazepam treatment resulted in a significantly greater reduction in R-R interval (P < 0.05) implying that GABAergic suppression of cardiac vagal outflow may be responsible for contraction-induced tachycardia in man.