Altered Ca2+ handling and myofilament desensitization underlie cardiomyocyte performance in normothermic and hyperthermic heat-acclimated rat hearts

2007 ◽  
Vol 103 (1) ◽  
pp. 266-275 ◽  
Author(s):  
Omer Cohen ◽  
Hifa Kanana ◽  
Ronen Zoizner ◽  
Chaya Gross ◽  
Uri Meiri ◽  
...  
Keyword(s):  
Mechanical Performance ◽  
Ryanodine Receptors ◽  
Pool Size ◽  
Force Generation ◽  
Isolated Hearts ◽  
Rat Hearts ◽  
Metabolic Performance ◽  
And Control ◽  
Negative Inotropic Response ◽  
Beating Frequency

Heat acclimation (AC) improves cardiac mechanical and metabolic performance. Using cardiomyocytes and isolated hearts from 30-day and 2-day acclimated rats (AC and AC-2d, 34°C), we characterized cellular contractile mechanisms under normothermic (37°C) and hyperthermic (39–42°C) conditions. To determine contractile responses, Ca2+ transients (Ca2+ T), sarcoplasmic reticulum (SR) Ca2+ pool size (fura-2/indo-1 fluorescence), force generation [amplitude systolic motion (ASM)], L-type Ca2+ channels [dihydropyridine receptor (DHPR)], ryanodine receptors (RyRs), and total (PLBt) and phosphorylated phospholamban [serine phosphorylated (PLBs) and theonine phosphorylated (PLBtr)] proteins and transcripts were measured (Western blot, RT-PCR). Cardiac mechanical performance was measured using a Langendorff system. We demonstrated that AC and AC-2d increased Ca2+ T amplitude (148% and 147%, respectively) and twitch force (180% and 130%, respectively) and desensitized myofilaments, as indicated by a rightward shift in the ASM-Ca2+ relationships, despite no change in SR Ca2+ pool size. Hence, generation of higher Ca2+ T underlies greater force development in AC and AC-2d myocytes. In isolated hearts, ryanodine administration eliminated differences between AC and control (C) hearts, implying an important role for RyRs in that acclimation phase. Increased expression of DHPR and RyRs, and decreased PLBs/PLBt in AC hearts only, suggest that different pathways increase force generation in the AC-2d vs. AC myocytes. At basal beating rates, hyperthermia (39–41°C) enhanced pressure generation in AC hearts. C hearts failed to restitute pressure beyond 39°C. Increased beating frequency produced negative inotropic response. In C cardiomyocytes, hyperthermia elevated basal cytosolic Ca2+ and tension, Ca2+ T, and ASM. AC myocytes enhanced Ca2+ T but showed myofilament desensitization, suggesting its involvement in cardiac protection against hyperthermia. Collectively, both Ca2+ turnover and myofilament responsiveness are important adaptive acclimatory targets during normothermic and hyperthermic conditions.

The Effect of Adrenaline-Induced Endogenous Lipolysis upon the Mechanical and Metabolic Performance of Ischaemically Perfused Rat Hearts

1977 ◽  
Vol 53 (6) ◽  
pp. 513-521
Author(s):  
R. W. Brownsey ◽  
R. V. Brunt
Keyword(s):  
Heart Rate ◽  
Mechanical Performance ◽  
Slight Reduction ◽  
Marked Rise ◽  
Tension Development ◽  
Mechanical Responses ◽  
Resting Tension ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Metabolic Performance

1. The isolated perfused non-working rat heart, subjected to low coronary flow, has been used to study the effects of myocardial ischaemia on both the mechanical and metabolic performance of the heart. 2. In this preparation, adrenaline initially increased developed tension and heart rate, followed shortly thereafter by marked deterioration in mechanical performance to levels below those observed in the control state. These latter responses occurred simultaneously with stimulation of endogenous myocardial lipolysis. The rate of release of non-esterified fatty acids was positively correlated with both the decline in developed tension and the rise in resting tension. 3. The anti-lipolytic agent nicotinic acid had no effect on the initial mechanical responses of the heart to adrenaline but prolonged the period of enhanced tension development after adrenaline and reduced the degree of later deterioration in performance, in addition to blocking lipolytic stimulation. 4. Hearts from rats fed on a diet rich in animal fat contained larger triglyceride reserves and exhibited greater rates of non-catecholamine-stimulated lipolysis than hearts from normally fed rats. During ischaemic perfusion such hearts showed a more marked rise in resting tension and decline in heart rate than hearts from normally fed animals. Such hearts also had an increased incidence of arrhythmias and a slight reduction in developed tension. The initial responses of these hearts from fat-fed rats to adrenaline were also depressed as compared with normal hearts. Hearts from fat-fed rats showed a greater tendency to deteriorate in performance after adrenaline, particularly with falling heart rates and the onset of ventricular fibrillation. 5. We suggest that these results indicate that myocardial lipolysis makes a significant contribution to the adrenaline-induced deterioration in performance seen in these ischaemically perfused rat hearts.

Pantothenate kinase and control of CoA synthesis in heart

1984 ◽  
Vol 246 (4) ◽  
pp. H532-H541 ◽  
Author(s):  
J. D. Robishaw ◽  
J. R. Neely
Keyword(s):  
Pantothenic Acid ◽  
Cysteine Synthase ◽  
Pantothenate Kinase ◽  
Isolated Hearts ◽  
Low Concentrations ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
And Control ◽  
Perfused Hearts ◽  
Oxidation Of Glucose

Control of coenzyme A (CoA) synthesis was studied in isolated perfused rat hearts. The data obtained support the hypothesis that phosphorylation of pantothenic acid by pantothenate kinase is the flux-generating reaction in the pathway of CoA synthesis. This reaction operated in the cell far removed from its thermodynamic equilibrium; it was saturated with substrates under all conditions studied; and the concentration of substrate changed in the opposite direction to flux when flux was altered. The reaction was subject to control by external factors associated with oxidation of glucose, pyruvate, or palmitate. CoA synthesis from 4'-phosphopantothenic acid was not inhibited by glucose and pyruvate, suggesting that pantothenate kinase is the only reaction in the pathway that is controlled in isolated hearts. Maximum rates of CoA synthesis in perfused hearts with pantothenate kinase stimulation were dependent on a supply of exogenous cysteine. Perfusate [14C]cysteine was incorporated into intermediates of this pathway and CoA. When protected from oxidation to cystine by low concentrations of dithiothreitol, 0.1 mM cysteine in the perfusate resulted in maximum rates of CoA synthesis. Evidence was obtained that indicates that addition of cysteine relieves a substrate limitation at the 4'-phosphopantothenyl cysteine synthase reaction.

Israel’s Ground Forces in the Occupied Territories

2020 ◽  
Vol 35 (2) ◽  
pp. 37-57
Author(s):  
Eyal Ben-Ari ◽  
Uzi Ben-Shalom
Keyword(s):  
High Intensity ◽  
Force Generation ◽  
Institutional Autonomy ◽  
Multiple Forms ◽  
The West ◽  
Occupied Territories ◽  
Media Monitoring ◽  
Israel Defense Forces ◽  
And Control ◽  
Over Time

The Israel Defense Forces (IDF) routinely rotate ground forces in and out of the Occupied Territories in the West Bank. While these troops are trained for soldiering in high-intensity wars, in the Territories they have long had to carry out a variety of policing activities. These activities often exist in tension with their soldierly training and ethos, both of which center on violent encounters. IDF ground forces have adapted to this situation by maintaining a hierarchy of ‘logics of action’, in which handling potentially hostile encounters takes precedence over other forms of policing. Over time, this hierarchy has been adapted to the changed nature of contemporary conflict, in which soldiering is increasingly exposed to multiple forms of media, monitoring, and juridification. To maintain its public legitimacy and institutional autonomy, the IDF has had to adapt to the changes imposed on it by creating multiple mechanisms of force generation and control of soldierly action.

scholarly journals Exercise Training Preserves Ischemic Preconditioning in Aged Rat Hearts by Restoring the Myocardial Polyamine Pool

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Weiwei Wang ◽  
Hao Zhang ◽  
Guo Xue ◽  
Li Zhang ◽  
Weihua Zhang ◽  
...  
Keyword(s):  
Exercise Training ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Polyamine Metabolism ◽  
Aged Rat ◽  
Isolated Hearts ◽  
Age Related ◽  
Rat Hearts ◽  
Myocardial Ischemia Reperfusion

Background. Ischemic preconditioning (IPC) strongly protects against myocardial ischemia reperfusion (IR) injury. However, IPC protection is ineffective in aged hearts. Exercise training reduces the incidence of age-related cardiovascular disease and upregulates the ornithine decarboxylase (ODC)/polyamine pathway. The aim of this study was to investigate whether exercise can reestablish IPC protection in aged hearts and whether IPC protection is linked to restoration of the cardiac polyamine pool.Methods. Rats aging 3 or 18 months perform treadmill exercises with or without gradient respectively for 6 weeks. Isolated hearts and isolated cardiomyocytes were exposed to an IR and IPC protocol.Results. IPC induced an increase in myocardial polyamines by regulating ODC and spermidine/spermine acetyltransferase (SSAT) in young rat hearts, but IPC did not affect polyamine metabolism in aged hearts. Exercise training inhibited the loss of preconditioning protection and restored the polyamine pool by activating ODC and inhibiting SSAT in aged hearts. An ODC inhibitor,α-difluoromethylornithine, abolished the recovery of preconditioning protection mediated by exercise. Moreover, polyamines improved age-associated mitochondrial dysfunctionin vitro.Conclusion. Exercise appears to restore preconditioning protection in aged rat hearts, possibly due to an increase in intracellular polyamines and an improvement in mitochondrial function in response to a preconditioning stimulus.

Metabolite utilization by isolated embryonic rat hearts in vitro

Development ◽  
1972 ◽  
Vol 28 (2) ◽  
pp. 235-245
Author(s):  
Steven J. Cox ◽  
David L. Gunberg
Keyword(s):  
Metabolic Pathways ◽  
Maximum Rate ◽  
Contractile Activity ◽  
Cardiac Contraction ◽  
Anaerobic Conditions ◽  
Isolated Hearts ◽  
Rat Hearts ◽  
Aerobic And Anaerobic ◽  
Aerobic And Anaerobic Conditions

Isolated hearts from 11-, 12- and 13-day rat embryos were incubated in a simple defined salt solution to which was added a variety of single substrates. Utilization of the added substrate was determined by comparing the contractile rates of the hearts in the presence and absence of the compound being tested. Of all the compounds tested only those involved in the Embden-Meyerhof glycolytic pathway were capable of maintaining cardiac contraction at a maximum rate in the 11-day heart. This was accomplished under both aerobic and anaerobic conditions. Although glycolysis remained important, the 12- and 13-day hearts exhibited a shift in dependence towards other metabolic pathways. This conclusion was based on the observations that anaerobic glycolysis could no longer maintain maximum heart rates and that a variety of non-glycolytic compounds could be utilized for contractile activity by the 12- and 13-day organs.

Adenosine antagonism decreases metabolic but not functional recovery from ischemia

1991 ◽  
Vol 260 (1) ◽  
pp. H193-H200 ◽  
Author(s):  
D. A. Angello ◽  
J. P. Headrick ◽  
N. M. Coddington ◽  
R. M. Berne
Keyword(s):  
Functional Recovery ◽  
Left Ventricular ◽  
Low Flow ◽  
Ischemia And Reperfusion ◽  
Constant Flow ◽  
Hemodynamic Parameters ◽  
Isolated Hearts ◽  
Rat Hearts ◽  
Adenosine Antagonism ◽  
Developed Pressure

The effect of adenosine receptor antagonism on function and metabolism was examined in isolated hearts during low flow ischemia and reperfusion. Isovolumic rat hearts perfused at constant flow were subjected to 30 min of ischemia followed by 30 min of reperfusion. Infusion of vehicle or 10 microM 8-phenyltheophylline (8-PT) was initiated 10 min before ischemia and maintained throughout reperfusion. 8-PT infusion had no significant effects on hemodynamic parameters or metabolism preischemia. During ischemia, left ventricular developed pressure declined to approximately 15% of preischemic values in control and 8-PT hearts, and ATP and PCr decreased to approximately 73 and 60% of preischemic values. Inorganic phosphate (Pi) increased to 353 = 41 and 424 +/- 53% of preischemic values in control and 8-PT hearts, respectively. After reperfusion, function recovered to greater than 95% of preischemic levels in control and 8-PT hearts. Unlike control hearts, recovery of metabolites was significantly different during reperfusion in 8-PT hearts (P less than 0.05); ATP, phosphocreatine, and Pi recovered to 82 +/- 8, 71 +/- 8, and 281 +/- 27% of preischemic values, respectively. Venous purine washout was significantly greater (P less than 0.05) during reperfusion in 8-PT hearts (327 +/- 113 nmol) than in control hearts (127 +/- 28 nmol). Blockade of adenosine receptors appears to adversely affect metabolic but not functional recovery in the ischemic-reperfused myocardium.

Heat stress protects aged hypertrophied and nonhypertrophied rat hearts against ischemic damage

1997 ◽  
Vol 273 (3) ◽  
pp. H1333-H1341 ◽  
Author(s):  
R. N. Cornelussen ◽  
A. V. Garnier ◽  
M. M. Vork ◽  
P. Geurten ◽  
R. S. Reneman ◽  
...  
Keyword(s):  
Heat Stress ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Control Treatment ◽  
Sham Operation ◽  
Hsp 70 ◽  
Rat Hearts ◽  
Developed Pressure ◽  
And Control ◽  
Postischemic Recovery

To explore the effects of heat stress (HS) in aged hypertrophied and nonhypertrophied rat hearts, postischemic recovery was investigated 15 mo after aortic constriction (AoB) or sham operation (Sham). Twenty-four hours after HS (42 degrees C; 15 min) or control treatment (normothermia), global ischemia was induced for 20 min in isolated AoB hearts and for 20 or 30 min in Sham hearts. After HS, postischemic recovery after 20-min ischemia in AoB hearts and 30-min ischemia in Sham hearts, respectively, was significantly better than in corresponding controls. In AoB hearts, cardiac output (CO), left ventricular developed pressure (LVDP), and the positive maximal first derivative of left ventricular pressure (+dP/dtmax) recovered to 33 +/- 26 (means +/- SD), 87 +/- 5, and 72 +/- 12%, respectively, after HS and to 5 +/- 8, 22 +/- 39, and 17 +/- 29% of preischemic values, respectively, in controls. Postischemic arrhythmias were significantly reduced in HS hypertrophied hearts, but creatine kinase (CK) loss was not reduced. In Sham hearts subjected to 30 min ischemia, CO, LVDP, and +dP/dtmax recovered to 20 +/- 20, 75 +/- 8, and 59 +/- 15%, respectively, after HS and to 3 +/- 8, 21 +/- 32, and 16 +/- 32% of preischemic values, respectively, in controls. Duration of arrhythmias and CK loss were not reduced in the heated hearts. When Sham hearts were subjected to only 20-min ischemia, functional recovery was not different in HS and control hearts, indicating that HS pretreatment extends the ischemic interval before irreversible injury occurs in the heart. In all HS Sham hearts, the myocardial 72-kDa HS protein (HSP 70) content was significantly increased. However, in HS AoB hearts, HSP 70 levels were not significantly different from the values in the control hearts. These results indicate that HS pretreatment induces cardioprotection in aged hypertrophied and nonhypertrophied rat hearts, which, however, cannot be unequivocally related to increased HSP 70 tissue contents.

scholarly journals Fundamentals of Force-Controlled Friction Riveting: Part II—Joint Global Mechanical Performance and Energy Efficiency

Materials ◽  
2018 ◽  
Vol 11 (12) ◽  
pp. 2489 ◽  
Author(s):  
Gonçalo Pina Cipriano ◽  
Lucian Blaga ◽  
Jorge dos Santos ◽  
Pedro Vilaça ◽  
Sergio Amancio-Filho
Keyword(s):  
Energy Efficiency ◽  
Mechanical Response ◽  
Mechanical Performance ◽  
Tensile Force ◽  
Optimization Approach ◽  
Additional Energy ◽  
Efficient Manner ◽  
Control Optimization ◽  
Friction Parameters ◽  
And Control

The present work investigates the correlation between energy efficiency and global mechanical performance of hybrid aluminum alloy AA2024 (polyetherimide joints), produced by force-controlled friction riveting. The combinations of parameters followed a central composite design of experiments. Joint formation was correlated with mechanical performance via a volumetric ratio (0.28–0.66 a.u.), with a proposed improvement yielding higher accuracy. Global mechanical performance and ultimate tensile force varied considerably across the range of parameters (1096–9668 N). An energy efficiency threshold was established at 90 J, until which, energy input displayed good linear correlations with volumetric ratio and mechanical performance (R-sq of 0.87 and 0.86, respectively). Additional energy did not significantly contribute toward increasing mechanical performance. Friction parameters (i.e., force and time) displayed the most significant contributions to mechanical performance (32.0% and 21.4%, respectively), given their effects on heat development. For the investigated ranges, forging parameters did not have a significant contribution. A correlation between friction parameters was established to maximize mechanical response while minimizing energy usage. The knowledge from Parts I and II of this investigation allows the production of friction riveted connections in an energy efficient manner and control optimization approach, introduced for the first time in friction riveting.

Dissociation of hypoxia-induced calcium gain and rise in resting tension in isolated rat hearts

1988 ◽  
Vol 254 (4) ◽  
pp. H678-H685
Author(s):  
W. G. Nayler ◽  
J. S. Elz ◽  
D. J. Buckley
Keyword(s):  
Perfusion Defect ◽  
Creatine Phosphate ◽  
Ventricular Muscle ◽  
Isolated Hearts ◽  
Resting Tension ◽  
Rat Hearts ◽  
Early Increase ◽  
Butanedione Monoxime ◽  
Tension Generation ◽  
Isolated Rat

When isolated hearts are perfused with substrate-free hypoxic buffer for prolonged periods of time, resting tension and tissue Ca increase. These two events may be interrelated. Isolated rat hearts were used to establish whether the hypoxia-induced increase in tissue Ca can be dissociated from the rise in resting tension. Tension generation was inhibited at the start of hypoxic perfusion by adding 2,3-butanedione monoxime (BDM, 30 mM). In other experiments the Ca2+ in the hypoxic buffer was reduced from 1.3 to 0.1 mM. After 30-120 min of hypoxia, ventricular muscle was assayed for ATP, creatine phosphate, Ca, and Na, and the perfusion defect was established. Resting tension was recorded before and throughout the hypoxic perfusion. Sixty minutes of perfusion with 1.3 mM Ca2+ glucose-free hypoxic buffer caused the tissue Ca to increase (P less than 0.01). Resting tension increased by 7.9 +/- 0.6 g (P less than 0.01). Sixty minutes of perfusion with 0.1 mM Ca2+ glucose-free hypoxic buffer failed to cause an increase in tissue Ca, but resting tension increased (P less than 0.01). During perfusion with glucose-free hypoxic buffer containing 2.6 mM Ca2+ and 30 mM BDM, resting tension remained low for up to 120 min, but after 60 min Ca accumulation occurred. After 120 min of BDM-hypoxic perfusion, tissue Ca reached 11.8 +/- 0.9 mumol/g dry wt. With or without BDM, hypoxia caused an early increase in tissue Na ahead of any increase in tissue Ca.(ABSTRACT TRUNCATED AT 250 WORDS)

Isovolumetric performance of isolated ground squirrel and rat hearts at low temperature

1984 ◽  
Vol 247 (4) ◽  
pp. R722-R727 ◽  
Author(s):  
D. R. Caprette ◽  
J. B. Senturia
Keyword(s):  
Low Temperature ◽  
Ground Squirrel ◽  
Mechanical Performance ◽  
Cell Communication ◽  
Ventricular Myocardium ◽  
Ground Squirrels ◽  
Rat Hearts ◽  
Pulsus Alternans ◽  
Rate Of Increase ◽  
Developed Pressure

The effects of low temperature on mechanical performance of the isolated left ventricles of the 13-lined ground squirrel (a hibernator) and the rat (a nonhibernator) were studied. In addition, low-temperature performance of hearts from summer-active, winter-hibernating, and winter-active ground squirrels were compared. By measuring pressure (P) generated against a balloon inserted into the left ventricle, maximum developed pressure (DP) and maximum rate of increase of P (peak dP/dt) were determined over a temperature range of 5–20 degrees C. The DP and dP/dt of the rat ventricle exhibited significantly greater reduction in magnitude at reduced temperature, compared with those of ground squirrel ventricle. Rat, but not ground squirrel, hearts exhibited arrhythmias of various kinds, including extra-systoles, tachycardia, pulsus alternans, and periods of asystole. Hearts from winter-active ground squirrels developed greater pressures than those from winter-hibernating and summer-active animals. This evidence suggests that disruption of cell communication in the nonhibernator ventricular myocardium plays an important role in the failure of the nonhibernator heart at low body temperatures. Contractility of the seasonal hibernator's heart is influenced by both season and hibernation itself, possibly through shifts in myocardial metabolism. However, seasonal adaptations appear not to be required to confer the special resistance of the seasonal hibernator's heart to the deleterious effects of low temperature.

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