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Biomedical subjects

H Gesser

Publications and source records attributed to H Gesser.

At least 19 recordsLinked to original sources
PubMed2006

Force development at elevated [Mg2+]o and [K+]o in myocardium from the freshwater turtle (Trachemys scripta) and influence of factors associated with hibernation.

The effects of high [Mg(2+)](o) on force development were examined for heart muscle of freshwater turtle. Plasma [Mg(2+)] during hibernation may increase drastically and like plasma [K(+)] approach values as high as 10 mM. Each experiment performed at either 20 or 5 degrees C involved four ventricular preparations of which one pair was exposed to 10, and one to 1 mMMg(2+). One preparation of each pair was furthermore exposed to 10 mM K(+), whereas the other was maintained at 2.5 mM K(+). During oxygenation, high relative to low [Mg(2+)](o) displayed a weak tendency to reduce twitch force; a tendency that was not reduced by elevations of [Ca(2+)](o). Severe hypoxia accentuated the negative effect of high [Mg(2+)](o). This effect disappeared, however, when hypoxia was combined with acidosis obtained by 24 mM lactic acid. In comparison to [Mg(2+)](o), high [K(+)](o) strongly depressed force development under both oxygenation and hypoxia, but no consistent interplay between the two ions was revealed. The negative inotropic effects of both high [Mg(2+)](o) and high [K(+)](o) were reduced or eliminated by 10 muM adrenaline. In conclusion the cardiac effects of elevations in [Mg(2+)](o) appear to be small during hibernation, in particular when considering the concomitant adrenergic stimulation and acidosis.

Acidosis↗
PubMed2004

Regulation of mitochondrial energy production in cardiac cells of rainbow trout (Oncorhynchus mykiss).

In skinned rat cardiac fibres, mitochondrial affinity for endogenous ADP generated by creatine kinase and Ca2+-activated ATPases is higher than for exogenous ADP added to the surrounding medium, suggesting that mitochondria are functionally coupled to creatine kinase and ATPases. Such a coupling may be weaker or absent in ectothermic vertebrate cardiac cells, because they typically have less elaborate intracellular membrane structures, higher glycolytic capacity and lower working temperature. Therefore, we examined skinned cardiac fibres from rainbow trout at 10 degrees C. The apparent mitochondrial affinity for endogenous ADP was obtained by stimulation with ATP and recording of the release of ADP into the surrounding medium. The apparent affinity for endogenous ADP was much higher than for exogenous ADP suggesting a functional coupling between mitochondria and ATPases. The apparent affinity for exogenous ADP and ATP was increased by creatine or an increase in Ca2+-activity, which should increase intrafibrillar turnover of ATP to ADP. In conclusion, ADP seems to be channelled from creatine kinase and ATPases to mitochondria without being released to the surrounding medium. Thus, despite difference in structure, temperature and metabolic capacity, trout myocardium resembles that of rat with regard to the regulation of mitochondrial respiration.

Adenosine Diphosphate↗
PubMed2003

Creatine kinase and mitochondrial respiration in hearts of trout, cod and freshwater turtle.

The importance of the creatine kinase system in the cardiac muscle of ectothermic vertebrates is unclear. Mammalian cardiac muscle seems to be structurally organized in a manner that compartmentalizes the intracellular environment as evidenced by the substantially higher mitochondrial apparent Km for ADP in skinned fibres compared to isolated mitochondria. A mitochondrial fraction of creatine kinase is functionally coupled to the mitochondrial respiration, and the transport of phosphocreatine and creatine as energy equivalents of ATP and ADP, respectively, increases the mitochondrial apparent ADP affinity, i.e. lowers the Km. This function of creatine kinase seems to be absent in hearts of frog species. To find out whether this applies to hearts of ectothermic vertebrate species in general, we investigated the effect of creatine on the mitochondrial respiration of saponin-skinned fibres from the ventricle of rainbow trout, Atlantic cod and freshwater turtle. For all three species, the apparent Km for ADP appeared to be substantially higher than for isolated mitochondria. Creatine lowered this Km in trout and turtle, thus indicating a functional coupling between mitochondrial creatine kinase and respiration. However, creatine had no effect on Km in cod ventricle. In conclusion, the creatine kinase-system in trout and turtle hearts seems to fulfil the same functions as in the mammalian heart, i.e. facilitating energy transport and communication between cellular compartments. In cod heart, however, this does not seem to be the case.

Adenosine Diphosphate↗
PubMed2002

Mechanical efficiency of the trout heart during volume and pressure-loading: metabolic implications of the stiffness of the ventricular tissue.

In the mammalian heart the metabolic costs of pressure loading exceed those of volume loading. As evidence suggests that the opposite may be true in fish, we evaluated the metabolic costs of volume and pressure loading in the isolated trout heart and compared the results with the mammalian heart based on the biomechanical properties of cardiac muscle. The highest power output (2.33+/-0.32 mW g(-1), n=5) appeared at the highest preload pressure tested (0.3 kPa) and at an afterload of 5 kPa. At a higher afterload, power did not increase because stroke volume fell. The highest mechanical efficiency (20.7+/-2.0%, n=5) was obtained at a preload of 0.15 kPa and an afterload of 5 kPa. Further increases in preload or afterload did not increase mechanical efficiency, probably because of increases in ventricular wall stress which increased the oxygen consumed disproportionately more than the stroke work. Under pressure unloading (25% decrease in power output), mechanical efficiency was significantly higher in comparison with volume unloading. Given that stiffness of the ventricular tissue is larger in trout than in rat papillary muscles, it is suggested that the increased strain during volume loading is energetically disadvantageous for stiff muscles like those of trout, but it is advantageous when muscle stiffness is lower as it occurs in the rat papillary muscle.

Anaerobiosis↗
PubMed2002

Oxygen consumption and force development in turtle and trout cardiac muscle during acidosis and high extracellular potassium.

Relative to species such as rainbow trout, freshwater turtle shows a high tolerance to challenges involving acidosis and increases in extracellular K+. Therefore, the effects of acidosis or high K+ on twitch force and oxygen consumption were examined in ventricular ring preparations from these two species. The oxygen consumption associated with force development was estimated by net oxygen consumption (oxygen consumption during twitch force development minus that during rest). For turtle, elevation of CO2 from 2% (pH 7.7) to 12% (pH 6.9) in the gas equilibrating the muscle bath decreased twitch force by 20% without any effects on oxygen consumption. Decreasing pH from 7.7 to 6.9 with 22 mM lactic acid had similar effects. For trout, CO2-induced acidosis decreased twitch force by approximately 60%. Furthermore, force development became energetically less efficient as it fell disproportionately more than net oxygen consumption. This was not observed for lactic acidosis. For trout but not for turtle, acidosis resulted in an increase in oxygen consumption during rest. An increase in extracellular K+ from 2.5 mM to 10 mM depressed force and oxygen consumption proportionately for both species. Adrenaline (10 microM) increased twitch force for both species and oxygen consumption for trout; it attenuated the effects of high extracellular K+. Neither adrenaline nor high K+ influenced the ratio of force to net oxygen consumption. As opposed to high extracellular K+, acidosis appears to increase the energetic cost of contractility, particularly for the trout heart.

Acidosis↗
PubMed2001

Effects of high extracellular [K+] and adrenaline on force development, relaxation and membrane potential in cardiac muscle from freshwater turtle and rainbow trout.

Increases in extracellular K(+) concentrations reduced the twitch force amplitude of heart muscle from the freshwater turtle (Trachemys scripta elegans) and rainbow trout (Oncorhynchus mykiss). Adrenaline augmented twitch force amplitude and reduced the relative influence of [K(+)]. In the absence of adrenaline, high [K(+)] had less effect in reducing twitch force in turtle than in trout, whereas the reverse was true in the presence of adrenaline. Under anoxic conditions, twitch force was lower in 10 mmol l(-1) than in 2.5 mmol l(-1) K(+) in both preparations, but adrenaline removed this difference. A further analysis of turtle myocardium showed that action potential duration was shorter and resting potential more positive in high [K(+)] than in low [K(+)]. Adrenaline restored the duration of the action potential, but did not affect the depolarisation, which may attenuate Na(+)/Ca(2+) exchange, participating in excitation/contraction coupling. The contractile responses in the presence of adrenaline were, however, similar in both high and low K(+) concentrations when increases in extracellular Ca(2+) were applied to increase the demand on excitation/contraction coupling. The possibilities that adrenaline counteracts the effects of high [K(+)] via the sarcoplasmic reticulum or sarcolemmal Na(+)/K(+)-ATPase were examined by inhibiting the sarcoplasmic reticulum with ryanodine (10 micromol l(-1)) or Na(+)/K(+)-ATPase with ouabain (0.25 or 3 mmol l(-)). No evidence to support either of these possibilities was found. Adrenaline did not protect all aspects of excitation/contraction coupling because the maximal frequency giving regular twitches was lower at 10 mmol l(-1) K(+) than at 2.5 mmol l(-1) K(+).

Action Potentials↗
PubMed1999

Influence of inorganic phosphate and energy state on force in skinned cardiac muscle from freshwater turtle and rainbow trout.

Inorganic phosphate, which increases in the hypoxic cardiac cell, depresses force development. The cardiac muscle of freshwater turtle maintains a remarkably high contractility during hypoxia; this may involve a low sensitivity to phosphate. Therefore, freshwater turtle and rainbow trout were compared with regard to Ca(2+)-activated force in skinned atrial trabeculae in a bath containing 3 mM ATP buffered by 15 mM creatine phosphate in the presence of creatine kinase. For turtle, an increase in phosphate from 0 mM to either 6 mM or 12 mM reduced maximal force by 50% and 80% respectively, whereas the Ca2+ activity eliciting half maximal force (Ca0.5) was increased by 70% in 6 mM and could not be reliably recorded in 12 mM. For trout, the effects of phosphate were less pronounced. An increase from 0 mM to 12 mM did not affect maximal force significantly, but elevated Ca0.5 by 70%. Hypoxia increases ADP as creatine phosphate is shifted to creatine, therefore, creatine phosphate was changed from 15 mM to 3 mM and creatine from 0 mM to 12 mM. After these changes, the elevation of phosphate from 0 mM to 12 mM had no significant effects for either turtle or trout. In conclusion, the high performance of turtle cardiac muscle during hypoxia does not involve a low sensitivity of the contractile system to phosphate. In addition, the effect of increased phosphate seems to be offset by a concomitant increase in ADP.

Adenosine Diphosphate↗
PubMed1999

Ca(2+) uptake in the sarcoplasmic reticulum from the systemic heart of octopod cephalopods.

We have measured Ca(2+) uptake in crude homogenates of heart tissue, as well as cell shortening and ionic currents in isolated myocytes exposed to caffeine, to characterize Ca(2+) uptake in the sarcoplasmic reticulum (SR) of the systemic heart of octopus. The maximal rate of SR Ca(2+) uptake in crude homogenates of octopus heart was 43+/-4 (mean +/- s.e.m., N=7), compared with 28+/-2 nmol min(-)(1 )mg(-)(1) protein (N=4) in homogenates of rat heart. The Ca(2+)-dependency of SR Ca(2+) uptake was similar for the two species, with a Ca(2+) activity at half-maximal uptake rate (pCa(50)) of 6.04+/-0.02 for octopus and 6.02+/-0.05 for rat. Exposure of isolated myocytes to 10 mmol l(-)(1) caffeine resulted in cell shortening to 53+/-2 % of the resting cell length and an inward trans-sarcolemmal ionic current. The charge carried by this current was 3.28+/-0.70 pC pF(-)(1) (mean +/- s.e.m., N=5) corresponding to extrusion of 34.0+/-0.7 amol Ca(2+ )pF(-)(1) from the cell by Na(+)/Ca(2+) exchange. This is approximately 50 times more than the Ca(2+) carried by the Ca(2+) current elicited by a 200 ms depolarization from -80 to 0 mV and corresponds to an increase in the total intracellular [Ca(2+)] of 404+/-86 (&mgr;)mol l(-)(1) non-mitochondrial volume due to Ca(2+) release from the SR. Thus, we find that at 20 degrees C in the SR both Ca(2+) content and Ca(2+) uptake rate in the systemic heart of octopus are comparable with or larger than the corresponding values obtained in the rat heart. These results support the argument that the SR may play an important role in the regulation of contraction in the systemic heart of cephalopods.

Journal Article↗
PubMed1997

Ca2+ activated myosin-ATPase in cardiac myofibrils of rainbow trout, freshwater turtle, and rat.

The Ca(2+)-activated myosin-ATPase and its dependence on hypoxia were assessed in freshwater turtle, rainbow trout, and in some cases rat. At 20 degrees C and pH 7.3, the maximal ATPase activity was (mean +/- SEM): turtle 0.040 +/- 0.003, trout 0.090 +/- 0.005, and rat 0.12 +/- 0.004 mmol*min-1*g-1 myofibrillar dry weight. The turnover number was about three times lower for turtle than for trout. Trout is typically active at lower temperatures than turtle, and its myosin-ATPase activity was about three times lower at 10 degrees than at 20 degrees C. Addition of 12 mM phosphocreatine showed that the myosin-ATPase activity covered by myofibrillar creatine kinase was 22 +/- 2% for turtle, 14 +/- 2% for trout, and 69 +/- 5% for rat. At pH 6.8 relative to 7.3, the maximal M-ATPase activity was the same, whereas the Ca(2+)-sensitivity decreased, and more so for trout than for turtle. This difference disappeared, when trout myocardium was examined at 10 degrees C. P(i) (15 mM) affected neither maximal activity nor Ca(2+)-sensitivity. ADP, however, reduced maximal myosin-ATPase activity, and more so in trout than in turtle. In conclusion, the "slow"-type myosin, the low sensitivity of acidification and ADP, and the high creatine kinase/myosin-ATPase ratio in turtle relative to trout accord with the well-known ability of turtle myocardium to work during hypoxia. However, the difference in living temperature between turtle and trout obscures the situation (e.g. inclusion of rat data suggests that the creatine kinase/myosin-ATPase ratio is related to temperature.

Adenosine Diphosphate↗
PubMed1996

Cardiac force and high-energy phosphates under metabolic inhibition in four ectothermic vertebrates.

Isometric twitch tension of ventricular preparations stimulated at 0.2 Hz fell over 30 min of anoxia by a fraction decreasing in the order rainbow trout, cod, eel, and freshwater turtle. Drops in the estimated cytoplasmic energy state were related to larger tension losses for trout than for the other species, possibly due to larger changes in free phosphate. Anoxic energy degradation was slower for turtle than for the other species. Anoxia combined with glycolytic inhibition (1 mmol/l iodoacetate) enhanced the decrease in twitch tension for a drop in energy state and enlarged the increase in ADP/ATP relative to that in creatine/phosphocreatine to an extent inversely related to the creatine kinase activity. Furthermore, it increased resting tension to an extent possibly related to myosin-adenosinetriphosphatase (ATPase) activity and lowered the content of phosphorylated adenylates in trout and turtle myocardium. The results indicate that species differences in performance of the metabolically challenged myocardium depend on energy-degrading processes, e.g., myosin-ATPase activity, phosphate release, creatine kinase activity, and efflux/degradation of ADP and AMP, and that glycolysis offers protection due to its cytoplasmic localization.

Adenosine Diphosphate↗
PubMed1994

Creatine kinase, energy-rich phosphates and energy metabolism in heart muscle of different vertebrates.

Maximal activities of creatine kinase, pyruvate kinase and cytochrome oxidase and total concentrations of creatine and phosphorylated adenylates were measured in cardiac muscle of hagfish, eight teleost species, frog, turtle, pigeon and rat. The ratio of creatine kinase to cytochrome oxidase with cytochrome oxidase as a rough estimate of aerobic capacity and cellular "energy turnover", was increased in myocardia of hagfish, turtle and crucian carp. These myocardia are likely to be frequently exposed to oxygen deficiency. In agreement with this, they possess a high relative glycolytic capacity as indicated by a high pyruvate kinase/cytochrome oxidase ratio. The creatine kinase/cytochrome oxidase ratio for the other myocardia varied within a factor of 2, except the value for cod myocardium which was below the others. Total creatine varied among species and was high in active species such as herring, pigeon and rat but also high in crucian carp. The variation in total concentration of phosphorylated adenylates was considerably less than the variation in total creatine. The high creatine kinase/cytochrome oxidase ratio in myocardia likely to be challenged by hypoxia may represent an enhanced efficiency for both "spatial" and "temporal" buffering of phosphorylated adenylates to attenuate the impact of a depressed energy liberation. As to the differences in total creatine, this factor influences not only the cellular energy distribution but possibly also contractility via an effect on the free phosphate level.

Animals↗
PubMed1989

Force frequency relation in the myocardium of rainbow trout. Effects of K+ and adrenaline.

Isolated heart ventricular preparations from rainbow trout were electrically stimulated to contraction. Following a temporary change in stimulation rate from 0.2 Hz to a higher value, the force fell to a minimum after which it increased and levelled off. Upon the return to 0.2 Hz a further transient increase in force appeared. The latter two responses were stimulated by an increased extracellular K+, which is known to inactivate the Na+ channel. The initial negative inotropic effect, in contrast to the two subsequent positive effects, was associated with a parallel decrease in amplitude of the action potential measured in 15 mM K+, used as an index of the Ca2+ influx. One micromolar (1 microM) ryanodine did not affect either the negative or the positive responses due to an increase in stimulation rate, but depressed the force developed after prolonged periods of rest. Ten micromolar (10 microM) adrenaline strongly inhibited the positive effects of an elevation of frequency. An elevation of extracellular Na+ from 141 to 166 mM had a similar effect. In conclusion, the positive effects occurring in 15 mM K+ do not seem to depend on the initial Na+ current. They may nevertheless depend on changes of the cellular Na+ balance as suggested by the effects of adrenaline, K+ and Na+. The functional role of the sarcoplasmic reticulum is unclear.

Animals↗
PubMed1989

Sarcoplasmic reticulum, potassium, and cardiac force in rainbow trout and plaice.

The role played by the sarcoplasmic reticulum in force development and in cellular Ca2+ balance and its dependence on extracellular K+ were examined in heart ventricular tissue of rainbow trout and plaice. Compared with the steady-state twitch at a stimulation rate of 0.2 Hz, a 30-s rest led to a similar increase in twitch force in trout heart, regardless of whether [K+] was 2.5 or 5 mM. At 5 mM (but not at 2.5 mM) post-rest potentiation increased with increasing rest periods (from 30 to 900 s). These post-rest potentiations were removed or transformed into a loss of force by 10 microM ryanodine or 8 mM caffeine. In the plaice heart, where the sarcoplasmic reticulum is claimed to be sparse, the post-rest potentiation and the influence of ryanodine were small. The Ca2+ uptake measured during 5 min with 45Ca in the trout heart was higher in 5 than in 2.5 mM K+, regardless of the concomitant stimulation rate. This effect of K+ was removed by 10 microM ryanodine. The twitch force after 5 min of rest correlated significantly with the Ca2+ uptake, whereas the twitch force developed at a rate of 0.2 or 1.0 Hz did not. In conclusion, an elevation of K+ appears to stimulate the Ca2+ uptake of the sarcoplasmic reticulum. The twitch force after prolonged rest seems to relate to the Ca2+ contained in this organelle, whereas this does not apply to the twitch force developed at more physiological rates (0.2 or 1 Hz).

Animals↗
PubMed1988

Action potential, force and function of the sarcoplasmic reticulum in the anaerobic trout heart.

The electromechanical coupling mechanism was studied in anaerobic heart ventricle strips of rainbow trout which had been electrically stimulated to contraction at 12 contractions/min. The twitch force fell immediately upon the onset of anaerobiosis (5 mM sodium cyanide and N2). The duration and overshoot of the action potential were reduced, the duration only transiently however, since a recovery to the pre-anaerobic level occurred later on. A change of extracellular Ca2+ from 1.25 to 5 mM during anaerobiosis caused a prompt increase in twitch force, whereas the action potential duration and overshoot decreased, the former, again only for a short time. The action potential, measured in 14 mM K+ to block the initial sodium current, was not significantly affected by anaerobiosis, although the accompanying twitch force values were more than halved. The negative effects of anaerobiosis on contractility were not influenced by either ryanodine or caffeine, whereas they were reduced at an elevated extracellular concentration of Ca2+. The results suggest that the regulation of the cytoplasmic Ca activity of the trout heart is well maintained under anaerobic conditions although the contractility is strongly reduced.

Action Potentials↗
PubMed1987

Electrical and mechanical activity in heart tissue of flounder and rainbow trout during acidosis.

1. Twitch force and voltage across the sarcolemma were measured in heart tissue of flounder and rainbow trout. 2. For the trout heart, hypercapnia was followed by a loss of force and an action potential prolongation. 3. This was also observed for the flounder heart, but only initially. 4. About 5 min after the onset of hypercapnia, an increase in force and a shortening of the action potential occurred in the flounder heart. 5. After about 30 min of hypercapnia a decrease in force and a prolongation of the action potential slowly appeared. 6. These results can be interpreted in terms of a species-dependent effect of acidosis on the cellular Ca2+ handling and the influence of intracellular Ca2+ on the action potential.

Acidosis↗
PubMed1987

Extracellular Ca2+, force, and energy state in cardiac tissue of rainbow trout.

The importance of ATP and phosphocreatine (PCr) concentrations for myocardial force development was examined in electrically paced ventricular strips from rainbow trout. Three metabolic situations were studied involving either an aerobic block (N2, 5 mM NaCN), both an aerobic and a glycolytic block (1 mM iodoacetate), or no metabolic inhibitors. Increasing extracellular Ca2+ from 1.25 to 5 mM enhanced twitch-force development in all of these situations but caused no change in resting force or ATP and PCr content, except for the noninhibited preparations for which PCr increased. Anaerobiosis caused a decrease in the PCr concentration together with a fall in twitch force and an increase in resting force. Notably the changes in the contractile system associated with a given reduction in PCr were smaller in the absence than in the presence of iodoacetate. The results show that an increased Ca2+ availability stimulates the twitch-force development also at markedly lowered levels of high-energy phosphates. A maintained Ca2+ regulation appears to be one important reason for this. Furthermore, glycolysis seems to protect contractility in a way not reflected in the level of high-energy phosphates.

Adenosine Triphosphate↗
PubMed1984

Contractility and 45Ca fluxes in heart muscle of flounder at a lowered extracellular NaCl concentration.

The twitch force of isolated electrically paced ventricular strips of flounder, Platichthys flesus L., increased after lowering the extracellular sodium chloride concentration by 50 mmol l-1. This response was markedly reduced by replacing the sodium chloride with either Tris-HCl or sucrose, so that osmolarity was unchanged. The 45Ca efflux decreased and the 45Ca influx increased when the extracellular sodium concentration Nao+ was lowered. In contrast, changing only the osmolarity had no observable effect on these fluxes. An increased resting tension appeared in strips exposed to a Na+-, Ca2+-free solution. This was transient at an unchanged osmolarity but became permanent at an osmolarity lowered by 100 mosmol l-1. These results suggest that both a lowered Nao and a lowered osmolarity have a positive inotropic effect, due respectively to an increased cellular uptake of Ca2+ and a redistribution of cellular Ca2+.

Animals↗