Influence of aldosterone on isometric tension development in the rat heart

1963 ◽  
Vol 204 (6) ◽  
pp. 1001-1004 ◽  
Author(s):  
William C. Ullrick ◽  
Robert L. Hazelwood
Keyword(s):  
Heart Muscle ◽  
Rat Heart ◽  
Isolated Rat Heart ◽  
Isometric Tension ◽  
Muscle Performance ◽  
Tension Development ◽  
Tension Time ◽  
Isometric Twitch

Isometric twitch curves were recorded from preparations of rat heart trabeculae carneae removed from normal or adrenalectomized animals, or from normal animals injected for 3 days with saline or with 3 µg/day of d-aldosterone. Preparations from normal and from adrenalectomized animals were stimulated for 60 min in aldosterone-free Ringer's solution, or for 30 min in aldosterone-free Ringer's followed by 30 min in Ringer's containing 3 x 10–4 µg/ml of d-aldosterone. For a number of preparations from adrenalectomized animals the concentration of aldosterone was increased to 3 x 10–1 µg/ml. Regardless of treatment, all preparations were stimulated for a total of 1 hr at a rate of approximately 395/min; subsequently the recorded twitch curves were analyzed for peak tension development and for tension-time area. Although adrenalectomy tended to lower these variables of in vitro heart muscle performance, aldosterone, either administered in vivo or added directly to the isolated muscle bath, was without influence. It is concluded that aldosterone in the concentrations used does not alter the isometric tension characteristics of isolated rat heart muscle.

Myocardial mechanics predict hemodynamic performance during normal function and alcohol-induced dysfunction in rats

1991 ◽  
Vol 261 (6) ◽  
pp. H1880-H1888
Author(s):  
J. M. Capasso ◽  
P. Li ◽  
P. Anversa
Keyword(s):  
Pressure Rise ◽  
Normal Function ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Papillary Muscles ◽  
Least Squares Regression ◽  
Tension Development ◽  
Myocardial Mechanics

To determine whether mechanical evaluation of muscle tissue removed from the myocardium can be employed as a direct indicator of cardiac contractile performance in situ, isometric and isotonic parameters of muscle mechanics in vitro were correlated with in vivo global functional characteristics of the same heart. Twelve-month-old animals maintained on standard food and water were employed as representative of normal cardiac function. Animals of identical age with left ventricular (LV) dysfunction induced by oral alcohol (30%) ingestion from 4 to 12 mo were utilized to represent depressed cardiac performance. Accordingly, 24 h after the establishment of the hemodynamic profile for a control or experimental heart, the LV posterior papillary muscle was removed from the same heart and examined isometrically and isotonically. Least squares regression analysis was employed to establish a correlation coefficient and P values between various in vitro and in vivo parameters. Hemodynamic measurements were performed under chloral hydrate anesthesia and LV pump performance was evaluated with respect to aortic and ventricular pressures and the rates of rise and decay of the LV pressure trace. Papillary muscles were evaluated with respect to timing parameters of the isometric and isotonic twitch, the first derivative of isometric tension development, and the speed of muscle shortening at increasing physiologic loads. LV peak rate of pressure rise and decay were then correlated with the various isometric and isotonic properties. Myocardial mechanics and hemodynamics revealed depressed function in the papillary muscles and hearts from alcoholic rats. Moreover, significant correlations were found between the LV rate of pressure change (peak +dP/dt and -dP/dt) and both isometric and isotonic twitch measurements.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals The Platinum(II) Complexes Induced Oxidative Stress of Isolated Rat Heart

2017 ◽  
Vol 18 (2) ◽  
pp. 111-117
Author(s):  
Katarina Radonjic ◽  
Isidora Stojic ◽  
Vladimir Zivkovic ◽  
Ivan Srejovic ◽  
Nevena Jeremic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transition Metal ◽  
Metal Complexes ◽  
Transition Metal Complexes ◽  
Rat Heart ◽  
Clinical Success ◽  
Chemotherapeutic Agents ◽  
Isolated Rat Heart

AbstractInterest for the clinical application of transition metal complexes as chemotherapeutic agents initially started with discovery of cisplatin. Despite the remarkable clinical success, cisplatin treatment is limited due to its resistance and side effects. Over the last 40 years, numerous transition metal complexes were synthesized and investigated in vitro and in vivo in order to establish a metallopharmaceutical that will exert less toxicity and equal or higher potency. We have compared the cardiotoxicity of 2 platinum complexes, one ligand, and a starting salt for complex synthesis using an experimental model of an isolated, perfused rat heart according to the Langendorfftechnique. The cardiotoxicity was assessed by comparison of oxidative stress induced following the perfusion of the following compounds: Dichloro(1,2-diaminocyclohexane)platinum(II), cisplatin, potassium-tetra-chloroplatinum(II) and 1,2-diaminocyclohexane, which were perfused at increasing concentrations from 10−8to 10−4M for 30 minutes. The oxidative stress was assessed by determination of superoxide anion radical, hydrogen peroxide, thiobarbituric acid reactive substances, and nitric oxide from the coronary venous effluent. Our results showed that the levels of oxidative stress parameters were not significantly affected by perfusion with all the tested compounds and were not dose-dependent. These results could be of importance to further investigations concerning the effects of platinum-based potential anticancer drugs on the heart.

Development of myocardial dysfunction in endotoxin shock

1985 ◽  
Vol 248 (6) ◽  
pp. H818-H826 ◽  
Author(s):  
J. L. Parker ◽  
H. R. Adams
Keyword(s):  
Heart Muscle ◽  
Isolated Heart ◽  
Myocardial Dysfunction ◽  
Isotonic Saline ◽  
Endotoxin Shock ◽  
Left Ventricular ◽  
Saline Control ◽  
Tension Development

Isolated heart muscle preparations were used to investigate the onset and development of myocardial inotropic dysfunction during endotoxin shock in guinea pigs. Left atrial muscles were removed from separate groups of animals at increasing time intervals after administration of either 4 mg/kg purified Escherichia coli endotoxin (shock groups) or an equivalent volume of isotonic saline (control groups). Peak developed contractile tension (CT) and maximal rate of tension development (+dT/dtmax) were significantly depressed in shock tissues as early as 2 h postendotoxin (P less than 0.01), with the magnitude of the contractile deficit progressively increasing during 4, 6, and 12 h postendotoxin. Contractility remained significantly depressed (P less than 0.001) at 16 and 24 h postendotoxin but progressively recovered toward control levels during 16, 24, 48, and 72 h postendotoxin. Shock-induced myocardial dysfunction was characterized by altered contractile responsiveness to low-Ca2+ medium (0.5 mM), gentamicin (4 mM), and hypoxia; altered inotropic reactivity to these interventions followed similar temporal development as the postendotoxin changes in basal contractile parameters. Left ventricular papillary muscles obtained at 16 h postendotoxin corroborated the shock-induced contractile depression observed in atria. These studies provide evidence for early and progressive intrinsic myocardial dysfunction in endotoxin shock and demonstrate that this dysfunction can be unmasked through the study of in vitro atrial and ventricular heart muscle preparations isolated from in vivo shocked animals.

Cardiac function and phosphorylation of contractile proteins

1983 ◽  
Vol 302 (1108) ◽  
pp. 83-90 ◽  
Keyword(s):  
Light Chain ◽  
Rat Heart ◽  
Troponin I ◽  
Contractile Proteins ◽  
Perfused Heart ◽  
Tension Development ◽  
C Protein ◽  
Perfused Hearts

The primary regulation of cardiac contractility is probably through changes in the level of cytoplasmic free Ca 2+ . In the stimulation of contraction by catecholamines, secondary controls may be present at the level of the contractile proteins. Troponin-I, a subunit of the troponin complex of the thin filament, and C-protein, a thick filament component, are both phosphorylated in perfused hearts in response to catecholamines over time courses similar to that for the increase in contraction. Both proteins are also phosphorylated rapidly in vitro by cyclic-AMP-dependent protein kinase. Phosphorylation of troponin-I causes a decrease in the sensitivity of both cardiac myofibrillar ATPase and tension development of skinned fibre preparations to Ca 2+ , and also an increase in the rate of dissociation of Ca 2+ from isolated troponin. These results support the hypothesis that the role of phosphorylation of cardiac troponin-I is to contribute to the increased rate of relaxation of the heart that is observed with catecholamines. C-protein is phosphorylated to a maximum of 4-5 mol phosphate per mole protein both in vivo and in vitro . At present, however, the functions of both C-protein itself and its phosphorylation are unknown. Dephosphorylation of these contractile proteins after catecholamine stimulation is slow in perfused heart, although the rate can be increased by cholinergic agents. Phosphorylase, in contrast, is rapidly dephosphorylated under these circumstances. Phosphoprotein phosphatases relatively specific for phosphorylase have been identified in rat heart, whereas troponin-I appears to be dephosphorylated by general phosphatases. These observations account for the different rates of dephosphorylation of phosphorylase and the contractile proteins, but do not explain the slow dephosphorylation of the latter. In control perfused hearts myosin P-light chain was 50 % phosphorylated, and this was not changed by perfusion with positive inotropic agents or by short-term ischaemia. It was also unchanged during long-term hormonal modifications. Perfusions with 32 P 1 in rat heart give a half-time for the turnover of phosphate bound to the P-light chain of 2-4 min, showing that the myosin light chain kinase and phosphatase are active in the heart. It is hypothesized that under control conditions the kinase is already fully active, and that an increase in cytoplasmic Ca 2+ cannot therefore cause further activation of the enzyme.

Substrate regulation of mitochondrial oxidative phosphorylation in hypercapnic rabbit muscle

1992 ◽  
Vol 72 (2) ◽  
pp. 521-528 ◽  
Author(s):  
S. Nioka ◽  
Z. Argov ◽  
G. P. Dobson ◽  
R. E. Forster ◽  
H. V. Subramanian ◽  
...  
Keyword(s):  
Oxidative Phosphorylation ◽  
Intracellular Ph ◽  
Isometric Tension ◽  
Muscle Performance ◽  
Oxidative Enzymes ◽  
Rabbit Muscle ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Atp Production

Endurance muscle performance is highly dependent on ATP production from mitochondrial oxidative phosphorylation. To study the role of the mitochondrial oxidative enzymes in muscle fatigue, we analyzed the relationship between the concentrations of substrates associated with ATP synthesis and the muscle performance of electrically stimulated rabbit muscle under CO2-induced acidosis. Two different conditions of pacing-induced muscle performance were produced in the gastrocnemius and soleus muscle groups in anesthetized rabbits by stimulating the sciatic nerve submaximally at two frequencies. Phosphorus nuclear magnetic resonance was used to measure ATP, phosphocreatine, and Pi and to provide data for a calculation of intracellular pH and free ADP. To induce acidosis, the animal was ventilated with 20% CO2. The administration of CO2 effectively reduced the intracellular pH from 6.9 to 6.7 and reduced the isometric tension-time integral (TTI) to below half the value measured in normocapnia at the low pacing frequency. A twofold increase in the pacing frequency resulted in a doubling of the TTI in normocapnia and a tripling of TTI in hypercapnia. The increases in TTI corresponded with increases in free ADP and Pi concentrations. Under the various conditions, all free ADP values were near the in vitro Michaelis-Menten constant (Km) of ADP. The Michaelis-Menten relationship of the oxidative phosphorylative enzymes was applied to the change in substrate concentrations with respect to TTI. From this relationship we observed that the in vivo Km of free ADP was 26 microM, which is close to the in nitro Km, and that Km and maximal reaction velocity did not change under hypercapnia and increased pacing frequency.(ABSTRACT TRUNCATED AT 250 WORDS)

Glycogen mobilization and work in the rat heart

1961 ◽  
Vol 200 (5) ◽  
pp. 999-1003 ◽  
Author(s):  
Robert L. Hazelwood ◽  
William C. Ullrick
Keyword(s):  
Rat Heart ◽  
Work Performance ◽  
Glycogen Content ◽  
Isolated Rat Heart ◽  
Muscle Preparation ◽  
Glucose Content ◽  
Tension Time ◽  
Isometric Twitch ◽  
Glycogen Stores ◽  
Work Done

Glycogen mobilization was studied in isolated rat heart trabeculae carneae stimulated to contract isometrically. Glycogen content of stimulated and nonstimulated muscle preparations was determined, as was glucose content of the fluid bathing the muscles. Isometric twitch curves were integrated over periods of stimulation and the results, in milligram seconds of tension time, used as an index of work performance. Relationships between work performance, 48-hr fasting, hypophysectomy, and mobilization of glycogen were investigated. The amount of glycogen mobilized by the isolated tissue was correlated with initial glycogen content but not with work performance. There was no correlation between initial glycogen content and work done by the tissue. These experiments indicate that the isolated cardiac muscle preparation relies on substrate(s) other than carbohydrate as an immediate source of energy. Heart preparations from 48-hr fasted and from hypophysectomized animals showed significantly greater work performance than did preparations from normal animals, but depletion of glycogen stores again appeared to be related to initial glycogen content and not to work done.

scholarly journals In vivo measurement of intrauterine pressure by telemetry: a new approach for studying parturition in mouse models

2010 ◽  
Vol 42 (2) ◽  
pp. 310-316 ◽  
Author(s):  
Stephanie L. Pierce ◽  
William Kutschke ◽  
Rafael Cabeza ◽  
Sarah K. England
Keyword(s):  
Mouse Models ◽  
Accurate Method ◽  
Isometric Tension ◽  
Mouse Uterus ◽  
New Approach ◽  
In Vivo Measurement ◽  
Intrauterine Pressure

Transgenic and knockout mouse models have proven useful in the study of genes necessary for parturition—including genes that affect the timing and/or progression of labor contractions. However, taking full advantage of these models will require a detailed characterization of the contractile patterns in the mouse uterus. Currently the best methodology for this has been measurement of isometric tension in isolated muscle strips in vitro. However, this methodology does not provide a real-time measure of changes in uterine pressure over the course of pregnancy. Recent advances have opened the possibility of using radiotelemetric devices to more accurately and comprehensively study intrauterine pressure in vivo. We tested the effectiveness of this technology in the mouse, in both wild-type (WT) mice and a mouse model of defective parturition (SK3 channel-overexpressing mice), after surgical implant of telemetry transmitters into the uterine horn. Continuous recordings from day 18 of pregnancy through delivery revealed that WT mice typically deliver during the 12-h dark cycle after 19.5 days postcoitum. In these mice, intrauterine pressure gradually increases during this cycle, to threefold greater than that measured during the 12-h cycle before delivery. SK3-overexpressing mice, by contrast, exhibited lower intrauterine pressure over the same period. These results are consistent with the outcome of previous in vitro studies, and they indicate that telemetry is an accurate method for measuring uterine contraction, and hence parturition, in mice. The use of this technology will lead to important novel insights into changes in intrauterine pressure during the course of pregnancy.

Role of sarcoplasmic reticulum in loss of load-sensitive relaxation in pressure overload cardiac hypertrophy

1994 ◽  
Vol 266 (1) ◽  
pp. H68-H78 ◽  
Author(s):  
C. R. Cory ◽  
R. W. Grange ◽  
M. E. Houston
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Hypertrophy ◽  
Atpase Activity ◽  
Pressure Overload ◽  
Fold Increase ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Tension Development ◽  
Sequestration Potential

The loss of load-sensitive relaxation observed in the pressure-overloaded heart may reflect a strategy of slowed cytosolic Ca2+ uptake to yield a prolongation of the active state of the muscle and a decrease in cellular energy expenditure. A decrease in the potential of the sarcoplasmic reticulum (SR) to resequester cytosolic Ca2+ during diastole could contribute to this attenuated load sensitivity. To test this hypothesis, both in vitro mechanical function of anterior papillary muscles and the SR Ca2+ sequestration potential of female guinea pig left ventricle were compared in cardiac hypertrophy (Hyp) and sham-operated (Sham) groups. Twenty-one days of pressure overload induced by coarctation of the suprarenal, subdiaphragmatic aorta resulted in a 36% increase in left ventricular mass in the Hyp. Peak isometric tension, the rate of isometric tension development, and the maximal rates of isometric and isotonic relaxation were significantly reduced in Hyp. Load-sensitive relaxation were significantly reduced in Hyp. Load-sensitive relaxation quantified by the ratio of a rapid loading to unloading force step in isotonically contracting papillary muscle was reduced 50% in Hyp muscles. Maximum activity of SR Ca(2+)-adenosinetriphosphatase (ATPase) measured under optimal conditions (37 degrees C; saturating Ca2+) was unaltered, but at low free Ca2+ concentrations (0.65 microM), it was decreased by 43% of the Sham response. Bivariate regression analysis revealed a significant (r = 0.84; P = 0.009) relationship between the decrease in SR Ca(2+)-ATPase activity and the loss of load-sensitive relaxation after aortic coarctation. Stimulation of the SR Ca(2+)-ATPase by the catalytic subunit of adenosine 3',5'-cyclic monophosphate-dependent protein kinase resulted in a 2.6-fold increase for Sham but only a 1.6-fold increase for Hyp. Semiquantitative Western blot radioimmunoassays revealed that the changes in SR Ca(2+)-ATPase activity were not due to decreases in the content of the Ca(2+)-ATPase protein or phospholamban. Our data directly implicate a role for decreased SR function in attenuated load sensitivity. A purposeful downregulation of SR Ca2+ uptake likely results from a qualitative rather than a quantitative change in the ATPase and possibly one of its key regulators, phospholamban.

Reduced high-energy phosphate levels in rat hearts. I. Effects of alloxan diabetes

1976 ◽  
Vol 230 (6) ◽  
pp. 1744-1750 ◽  
Author(s):  
TB Allison ◽  
SP Bruttig ◽  
Crass MF ◽  
RS Eliot ◽  
JC Shipp
Keyword(s):  
Oxidative Metabolism ◽  
Oxygen Delivery ◽  
Rat Heart ◽  
High Energy ◽  
Diabetic Rat ◽  
High Energy Phosphate ◽  
Atp Production ◽  
Rat Hearts

Significant alterations in heart carbohydrate and lipid metabolism are present 48 h after intravenous injection of alloxan (60 mg/kg) in rats. It has been suggested that uncoupling of oxidative phosphorylation occurs in the alloxanized rat heart in vivo, whereas normal oxidative metabolism has been demonstrated in alloxan-diabetic rat hearts perfused in vitro under conditions of adequate oxygen delivery. We examined the hypothesis that high-energy phosphate metabolism might be adversely affected in the alloxan-diabetic rat heart in vivo. Phosphocreatine and ATP were reduced by 58 and 45%, respectively (P is less than 0.001). Also, oxygen-dissociation curves were shifted to the left by 4 mmHg, and the rate of oxygen release from blood was reduced by 21% (P is less than 0.01). Insulin administration normalized heart high-energy phosphate compounds. ATP production was accelerated in diabetic hearts perfused in vitro with a well-oxygenated buffer. These studies support the hypothesis that oxidative ATP production in the alloxan-diabetic rat heart is reduced and suggest that decreased oxygen delivery may have a regulatory role in the oxidative metabolism of the diabetic rat heart.

scholarly journals Thyroid hormone increases beta‐catenin levels through PI3K in rat heart in vivo and in vitro

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Marcela Sorelli Carneiro‐Ramos ◽  
Gabriela Placoná Diniz ◽  
Maria Luiza Morais Barreto‐Chaves ◽  
Anselmo Sigari Moriscot
Keyword(s):  
Thyroid Hormone ◽  
Rat Heart ◽  
Beta Catenin
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