IN VIVO MUSCLE LENGTH CHANGES IN BUMBLEBEES AND THE IN VITRO EFFECTS ON WORK AND POWER

1993 ◽  
Vol 183 (1) ◽  
pp. 101-113 ◽  
Author(s):  
K. M. Gilmour ◽  
C. P. Ellington
Keyword(s):  
High Speed ◽  
Time Course ◽  
Second Harmonic ◽  
Muscle Length ◽  
Muscle Fibres ◽  
Bombus Lucorum ◽  
Length Changes ◽  
In Vitro Effects

The amplitude and time course of muscle length changes were examined in vivo in tethered, flying bumblebees Bombus lucorum. A ‘window’ was cut in the dorsal cuticle and aluminium particles were placed on the exposed dorsal longitudinal muscle fibres. Muscle oscillations were recorded using high-speed video and a high-magnification lens. The amplitude of muscle length changes was 1.9 % (s.d.=0.5 %, N=7), corresponding to the commonly quoted strain of 1–3 % for asynchronous muscle. Higher harmonics, particularly the second, were found in the muscle oscillations and in the wing movements. The second harmonic for wing movements was damped in comparison to that for muscle length changes, probably as a result of compliance in the thoracic linkage. Inclusion of the second harmonic in the driving signal for in vitro experiments on glycerinated fibres generally resulted in a decrease in the work and power, but a substantial increase was found for some fibres.

Tracheal smooth muscle mechanics in vivo

1990 ◽  
Vol 68 (1) ◽  
pp. 209-219 ◽  
Author(s):  
M. Okazawa ◽  
P. Pare ◽  
J. Road
Keyword(s):  
Smooth Muscle ◽  
Muscle Mechanics ◽  
Muscle Length ◽  
Base Line ◽  
Maximal Velocity ◽  
Velocity Of Shortening ◽  
Length Changes ◽  
Trachealis Muscle

We applied the technique of sonomicrometry to directly measure length changes of the trachealis muscle in vivo. Pairs of small 1-mm piezoelectric transducers were placed in parallel with the muscle fibers in the posterior tracheal wall in seven anesthetized dogs. Length changes were recorded during mechanical ventilation and during complete pressure-volume curves of the lung. The trachealis muscle showed spontaneous fluctuations in base-line length that disappeared after vagotomy. Before vagotomy passive pressure-length curves showed marked hysteresis and length changed by 18.5 +/- 13.2% (SD) resting length at functional residual capacity (LFRC) from FRC to total lung capacity (TLC) and by 28.2 +/- 16.2% LFRC from FRC to residual volume (RV). After vagotomy hysteresis decreased considerably and length now changed by 10.4 +/- 3.7% LFRC from FRC to TLC and by 32.5 +/- 14.6% LFRC from FRC to RV. Bilateral supramaximal vagal stimulation produced a mean maximal active shortening of 28.8 +/- 14.2% resting length at any lung volume (LR) and shortening decreased at lengths above FRC. The mean maximal velocity of shortening was 4.2 +/- 3.9% LR.S-1. We conclude that sonomicrometry may be used to record smooth muscle length in vivo. Vagal tone strongly influences passive length change. In vivo active shortening and velocity of shortening are less than in vitro, implying that there are significant loads impeding shortening in vivo.

Muscle length changes during swimming in scup: sonomicrometry verifies the anatomical high-speed cine technique.

1996 ◽  
Vol 199 (2) ◽  
pp. 459-463 ◽  
Author(s):  
D J Coughlin ◽  
L Valdes ◽  
L C Rome
Keyword(s):  
High Speed ◽  
Muscle Length ◽  
Fish Muscles ◽  
Muscle Shortening ◽  
Red Muscle ◽  
Independent Technique ◽  
Loop Technique ◽  
Length Changes ◽  
Work Loop

Recent attempts to determine how fish muscles are used to power swimming have employed the work loop technique (driving isolated muscles using their in vivo strain and stimulation pattern). These muscle strains have in turn been determined from the anatomical high-speed cine technique. In this study, we used an independent technique, sonomicrometry, to attempt to verify these strain measurements and the conclusions based on them. We found that the strain records measured from sonomicrometry and the anatomical-cine techniques were very similar. The ratio of the strain measured from sonomicrometry to that from the anatomical-cine technique was remarkably close to unity (1.046 +/- 0.013, mean +/- S.E.M., N = 15, for transducers placed on the muscle surface and corrected for muscle depth, and 0.921 +/- 0.028, N = 8, in cases where the transducers were inserted to the average depth of the red muscle). These measurements also showed that red muscle shortening occurs simultaneously with local backbone curvature, unlike previous results which suggested that white muscle shortening during the escape response occurs prior to the change in local backbone curvature.

BODY SIZE, MUSCLE POWER OUTPUT AND LIMITATIONS ON BURST LOCOMOTOR PERFORMANCE IN THE LIZARD DIPSOSAURUS DORSALIS

1993 ◽  
Vol 174 (1) ◽  
pp. 199-213 ◽  
Author(s):  
T. P. Johnson ◽  
S. J. Swoap ◽  
A. F. Bennett ◽  
R. K. Josephson
Keyword(s):  
Body Size ◽  
Body Mass ◽  
Power Output ◽  
Muscle Power ◽  
Muscle Length ◽  
Muscle Fibres ◽  
Dipsosaurus Dorsalis ◽  
Cycling Frequency ◽  
Length Changes

The power output of fast-glycolytic (FG) muscle fibres isolated from the iliofibularis (IF) muscle of desert iguanas (Dipsosaurus dorsalis) was measured at 35 sC using the oscillatory work-loop technique. To simulate cyclical muscle length changes during running, isolated fibre bundles were subjected to sinusoidal length changes and phasic stimulation during the strain cycle. At constant strain (12 %), the duration and timing (phase) of stimulation were adjusted to maximise power output. Using both hatchlings (4–8 g) and adults of varying sizes (15–70 g), the intraspecific allometries of IF length and contractile properties were described by regression analysis. The muscle length at which isometric force was maximum (L0, mm) increased geometrically with body mass (M, g) (L0=5.7M0.33). Maximum power output and the force produced during shortening showed no significant relationship to body size; work output per cycle (Wopt, J kg-1) under conditions required to maximise power did increase with body size (Wopt=3.7M0.24). Twitch duration (Td, ms), measured from the onset of force generation to 50 % relaxation, increased allometrically with body mass (Td=12.4M0.18). Limb cycling frequency during burst running (f, reported in the literature) and the frequency required to maximise power output in vitro (fopt) decreased with body size, both being proportional to body mass raised to the power 0.24. These findings suggest that limb cycling frequency may be limited by twitch contraction kinetics. However, despite corresponding proportionality to body size, limb cycling frequencies during burst running are about 20 % lower than the cycling frequencies required to maximise power output. Differences in the contractile performance of the IF in vitro and in vivo are discussed in relation to constraints imposed by gravitational forces and the design of muscular, nervous and skeletal systems.

Anti-obesity role of Aster glehni extract: in vivo and in vitro effects

Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
HM Lee ◽  
TG Ahn ◽  
CW Kim ◽  
HJ An
Keyword(s):  
In Vitro Effects

Comparison of Specific Antibody, D-Phe-Pro-Arg-CH2Cl and Aprotinin for Prevention of In Vitro Effects of Recombinant Tissue-Type Plasminogen Activator on Haemostasis Parameters

1987 ◽  
Vol 58 (03) ◽  
pp. 921-926 ◽  
Author(s):  
E Seifried ◽  
P Tanswell
Keyword(s):  
Specific Antibody ◽  
Plasma Concentrations ◽  
Fibrinolytic Therapy ◽  
Tissue Type ◽  
Control Value ◽  
Type Plasminogen Activator ◽  
In Vitro Effects ◽  
Fibrinolytic Parameters

SummaryIn vitro, concentration-dependent effects of rt-PA on a range of coagulation and fibrinolytic assays in thawed plasma samples were investigated. In absence of a fibrinolytic inhibitor, 2 μg rt-PA/ml blood (3.4 μg/ml plasma) caused prolongation of clotting time assays and decreases of plasminogen (to 44% of the control value), fibrinogen (to 27%), α2-antiplasmin (to 5%), FV (to 67%), FVIII (to 41%) and FXIII (to 16%).Of three inhibitors tested, a specific polyclonal anti-rt-PA antibody prevented interferences in all fibrinolytic and most clotting assays. D-Phe-Pro-Arg-CH2Cl (PPACK) enabled correct assays of fibrinogen and fibrinolytic parameters but interfered with coagulometric assays dependent on endogenous thrombin generation. Aprotinin was suitable only for a restricted range of both assay types.Most in vitro effects were observed only with rt-PA plasma concentrations in excess of therapeutic values. Nevertheless it is concluded that for clinical application, collection of blood samples on either specific antibody or PPACK is essential for a correct assessment of in vivo effects of rt-PA on the haemostatic system in patients undergoing fibrinolytic therapy.

Comparison of High Purity Factor IX Concentrates and a Prothrombin Complex Concentrate in a Canine Model of Thrombogenicity

1991 ◽  
Vol 66 (05) ◽  
pp. 609-613 ◽  
Author(s):  
I R MacGregor ◽  
J M Ferguson ◽  
L F McLaughlin ◽  
T Burnouf ◽  
C V Prowse
Keyword(s):  
High Purity ◽  
Time Course ◽  
Prothrombin Complex Concentrate ◽  
Degradation Products ◽  
Canine Model ◽  
Factor Ix ◽  
In Vitro Tests ◽  
Albumin Infusion

SummaryA non-stasis canine model of thrombogenicity has been used to evaluate batches of high purity factor IX concentrates from 4 manufacturers and a conventional prothrombin complex concentrate (PCC). Platelets, activated partial thromboplastin time (APTT), fibrinogen, fibrin(ogen) degradation products and fibrinopeptide A (FPA) were monitored before and after infusion of concentrate. Changes in FPA were found to be the most sensitive and reproducible indicator of thrombogenicity after infusion of batches of the PCC at doses of between 60 and 180 IU/kg, with a dose related delayed increase in FPA occurring. Total FPA generated after 100-120 IU/kg of 3 batches of PCC over the 3 h time course was 9-12 times that generated after albumin infusion. In contrast the amounts of FPA generated after 200 IU/kg of the 4 high purity factor IX products were in all cases similar to albumin infusion. It was noted that some batches of high purity concentrates had short NAPTTs indicating that current in vitro tests for potential thrombogenicity may be misleading in predicting the effects of these concentrates in vivo.

Studies on the mechanism of acute inhibition of thyroglobulin hydrolysis by iodine

1985 ◽  
Vol 108 (4) ◽  
pp. 511-517 ◽  
Author(s):  
Nandalal Bagchi ◽  
Birdie Shivers ◽  
Thomas R. Brown
Keyword(s):  
Time Course ◽  
Period 2 ◽  
Iodotyrosine Deiodinase ◽  
Rate Of Hydrolysis ◽  
Underlying Mechanisms ◽  
Excess Iodide ◽  
Sites Of Action ◽  
Hydrolysis Of

Abstract. Iodine in excess is known to acutely inhibit thyroidal secretion. In the present study we have characterized the time course of the iodine effect in vitro and investigated the underlying mechanisms. Labelled thyroid glands were cultured in vitro in medium containing mononitrotyrosine, an inhibitor of iodotyrosine deiodinase. The rate of hydrolysis of labelled thyroglobulin was measured as the proportion of labelled iodotyrosines and iodothyronines recovered at the end of culture and was used as an index of thyroidal secretion. Thyrotrophin (TSH) administered in vivo acutely stimulated the rate of thyroglobulin hydrolysis. Addition of Nal to the culture medium acutely inhibited both basal and TSH-stimulated thyroglobulin hydrolysis. The effect of iodide was demonstrable after 2 h, maximal after 6 h and was not reversible upon removal of iodide. Iodide abolished the dibutyryl cAMP induced stimulation of thyroglobulin hydrolysis. Iodide required organic binding of iodine for its effect but new protein or RNA synthesis was not necessary. The inhibitory effects of iodide and lysosomotrophic agents such as NH4C1 and chloroquin on thyroglobulin hydrolysis were additive suggesting different sites of action. Iodide added in vitro altered the distribution of label in prelabelled thyroglobulin in a way that suggested increased coupling in the thyroglobulin molecule. These data indicate that 1) the iodide effect occurs progressively over a 6 h period, 2) continued presence of iodide is not necessary once the inhibition is established, 3) iodide exerts its action primarily at a post cAMP, prelysosomal site and 4) the effect requires organic binding of iodine, but not new RNA or protein synthesis. Our data are consistent with the hypothesis that excess iodide acutely inhibits thyroglobulin hydrolysis by increasing the resistance of thyroglobulin to proteolytic degradation through increased iodination and coupling.

scholarly journals In Vitro Effects of Sulforaphane on Interferon-Driven Inflammation and Exploratory Evaluation in Two Healthy Volunteers

Molecules ◽  
2021 ◽  
Vol 26 (12) ◽  
pp. 3602
Author(s):  
Elena Genova ◽  
Maura Apollonio ◽  
Giuliana Decorti ◽  
Alessandra Tesser ◽  
Alberto Tommasini ◽  
...  
Keyword(s):  
Healthy Volunteers ◽  
Supportive Therapy ◽  
P Value ◽  
Type I ◽  
Interferon Signature ◽  
Interferon Stimulated Genes ◽  
Immune System Activation ◽  
In Vitro Effects

Interferonopathies are rare genetic conditions defined by systemic inflammatory episodes caused by innate immune system activation in the absence of pathogens. Currently, no targeted drugs are authorized for clinical use in these diseases. In this work, we studied the contribution of sulforaphane (SFN), a cruciferous-derived bioactive molecule, in the modulation of interferon-driven inflammation in an immortalized human hepatocytes (IHH) line and in two healthy volunteers, focusing on STING, a key-component player in interferon pathway, interferon signature modulation, and GSTM1 expression and genotype, which contributes to SFN metabolism and excretion. In vitro, SFN exposure reduced STING expression as well as interferon signature in the presence of the pro-inflammatory stimulus cGAMP (cGAMP 3 h vs. SFN+cGAMP 3 h p value < 0.0001; cGAMP 6 h vs. SFN+cGAMP 6 h p < 0.001, one way ANOVA), restoring STING expression to the level of unstimulated cells. In preliminary experiments on healthy volunteers, no appreciable variations in interferon signature were identified after SFN assumption, while only in one of them, presenting the GSTM1 wild type genotype related to reduced SFN excretion, could a downregulation of STING be recorded. This study confirmed that SFN inhibits STING-mediated inflammation and interferon-stimulated genes expression in vitro. However, only a trend towards the downregulation of STING could be reproduced in vivo. Results obtained have to be confirmed in a larger group of healthy individuals and in patients with type I interferonopathies to define if the assumption of SFN could be useful as supportive therapy.

scholarly journals Uptake and Distribution of Administered Bone Marrow Mesenchymal Stem Cell Extracellular Vesicles in Retina

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 730
Author(s):  
Biji Mathew ◽  
Leianne A. Torres ◽  
Lorea Gamboa Gamboa Acha ◽  
Sophie Tran ◽  
Alice Liu ◽  
...  
Keyword(s):  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Extracellular Vesicles ◽  
Time Course ◽  
Ganglion Cells ◽  
Ex Vivo ◽  
Dependent Manner ◽  
Paracrine Effects

Cell replacement therapy using mesenchymal (MSC) and other stem cells has been evaluated for diabetic retinopathy and glaucoma. This approach has significant limitations, including few cells integrated, aberrant growth, and surgical complications. Mesenchymal Stem Cell Exosomes/Extracellular Vesicles (MSC EVs), which include exosomes and microvesicles, are an emerging alternative, promoting immunomodulation, repair, and regeneration by mediating MSC’s paracrine effects. For the clinical translation of EV therapy, it is important to determine the cellular destination and time course of EV uptake in the retina following administration. Here, we tested the cellular fate of EVs using in vivo rat retinas, ex vivo retinal explant, and primary retinal cells. Intravitreally administered fluorescent EVs were rapidly cleared from the vitreous. Retinal ganglion cells (RGCs) had maximal EV fluorescence at 14 days post administration, and microglia at 7 days. Both in vivo and in the explant model, most EVs were no deeper than the inner nuclear layer. Retinal astrocytes, microglia, and mixed neurons in vitro endocytosed EVs in a dose-dependent manner. Thus, our results indicate that intravitreal EVs are suited for the treatment of retinal diseases affecting the inner retina. Modification of the EV surface should be considered for maintaining EVs in the vitreous for prolonged delivery.

Metabolism and cardiovascular effects of leukotrienes in warm- and cold-acclimated American bullfrogs (Rana catesbeiana)

1991 ◽  
Vol 260 (5) ◽  
pp. R834-R838
Author(s):  
C. A. Herman ◽  
G. A. Charlton ◽  
R. L. Cranfill
Keyword(s):  
Time Course ◽  
Rana Catesbeiana ◽  
Cardiovascular Effects ◽  
Leukotriene C4 ◽  
Gamma Glutamyl Transpeptidase ◽  
Leukotriene D4 ◽  
Inactivation Mechanism ◽  
Glutamyl Transpeptidase

Sulfidopeptide leukotrienes are important mediators in mammals, but much less is known of their metabolism and action in nonmammalian vertebrates. This study examines the cardiovascular effects of leukotrienes on blood pressure and heart rate and compares the metabolism of leukotrienes in vivo and in vitro in warm- and cold-acclimated bullfrogs. Leukotriene C4 (LTC4) is more potent than leukotriene D4 (LTD4) and leukotriene E4 (LTE4) in eliciting hypotension. The leukotrienes are more potent in warm-acclimated animals. Conversion of [3H]LTC4 to [3H]LTD4 occurs rapidly in warm-acclimated bullfrogs, with 15.2 +/- 1.7% of the [3H]LTC4 remaining at 1.5 min. Conversion is slower in vivo in cold-acclimated frogs, with 20.2 +/- 1.7% of the [3H]LTC4 remaining by 6 min. In blood taken from warm-acclimated frogs, conversion of [3H]LTC4 to [3H]LTD4 occurs more rapidly at 22 than at 5 degrees C. This pattern is similar in blood taken from cold-acclimated frogs, suggesting that no modification of gamma-glutamyl transpeptidase occurs at low temperature. [3H]LTE4 production is not observed in vivo or in vitro during the time course of the experiments. The rapid metabolism of LTC4 to LTD4 may represent an inactivation mechanism in amphibians. The cardiovascular effects of LTC4 in vivo may be much greater than current measurements indicate because of rapid conversion of LTC4 to the less potent LTD4.

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