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Biomedical subjects

B Wohlfart

Publications and source records attributed to B Wohlfart.

At least 55 records · Page 3Linked to original sources
PubMed1991

The action of 2,3-butane-dionemonoxime on the inotropic state in guinea-pig myocardium.

Isolated papillary muscles from guinea-pig right ventricles were used (temperature 33 degrees C, stimulation frequency 0.5 Hz). Isometric twitch and action potentials were recorded. Upon addition of 2,3-butane-dionemonoxime (BDM) (2 mM) the peak twitch force was reduced from 4.17 +/- 0.4 mN/mm2 to 1.68 +/- 0.3 mN/mm2 (n = 9, P less than 0.001). The time course of the isometric twitch was slightly altered. Time to peak tension (TPT) was reduced by 12.0 +/- 3% (n = 9, P less than 0.001) whereas time to half relaxation (THR) was left unaffected. The rate of rise of force was reduced by 35 +/- 3.2 mN/mm2s i.e. 46 +/- 3%. The action potential duration and amplitude was not significantly changed by the drug. The shape of the curve relating peak twitch force of an extra beat to the preceding test interval, i.e. mechanical restitution, was affected by 2 mM 2,3-butane-dionemonoxime. The curve reached its maximum faster after addition of the drug. Maximum postextrasystolic potentiation (force in response to the prepreceding test interval) was 3.2 +/- 0.4 mN/mm2 in 2 mM 2,3-butane-dionemonoxine and 7.6 +/- 0.7 mN/mm2 in control (n = 6). However the percentage potentiation was very similar in control (82%) and in presence of 2,3-butane-dionemonoxime (91%). Peak twitch force in relation to peak force of the preceding potentiated contraction during decay of postextrasystolic potentiation was analysed. There was a linear relation between the variables, the slope being 0.34 +/- 0.04 in control and 0.30 +/- 0.02 in 2,3-butane-dionemonoxime. This suggests that the drug is without an action on the fraction of calcium recirculating within the cell.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1990

Effects of low temperature on contraction in papillary muscles from rabbit, rat, and hedgehog.

During hibernation the body temperature may fall to only a few degrees above 0 degree C. The heart of the hedgehog continues to function whereas the hearts of nonhibernating mammals stop beating. The present study was performed to investigate and compare the mechanical responses to hypothermia in rabbits, rats, and hedgehogs. Isometric force was recorded from papillary muscles mounted in an organ bath and effects of hypothermia on the mechanical restitution curve were also compared. A reduction of bath temperature from 35 degrees C caused an increase in peak developed force. Maximum force was seen at 20 degrees C in the rabbit, 15 degrees C in the rat, and 10 degrees C in the hedgehog preparations. In all the species there was a similar prolongation of time to peak force and of time from peak to half-relaxation as temperature was lowered. An increase in resting force and after-contractions were recorded in the rabbit and rat muscles at temperatures below 15 and 10 degrees C, respectively. The rabbit and rat preparations became inexcitable at temperatures below 10 and 5 degrees C, respectively. The hedgehog papillary muscle, on the other hand, still contracted at 0 degree C and did not show increased resting force nor after-contractions. The results are consistent with the hypothesis that there is a calcium overload in cardiac cells from rabbit and rat at low temperatures but there is no calcium overload in the hedgehog muscle during hypothermia.

Animals↗
PubMed1990

Mechanical restitution at different temperatures in papillary muscles from rabbit, rat, and hedgehog.

Mechanical restitution curves, i.e., peak isometric force as a function of the duration of the preceding test interval, were investigated in papillary muscles from rabbit, rat, and hedgehog. Peak force of rabbit papillary muscle increased with prolongation of the test interval from about 0.3 s to about 1.0 s and for longer intervals peak force declined (called type I mechanical restitution). On the other hand, in rat and hedgehog, papillary muscles' force reached a maximum value at intervals of 30-120 s (called type II mechanical restitution). When temperature was decreased from 35 to 15 degrees C, maximum force of type I mechanical restitution shifted from 1.0 to 10 s, whereas maximum force of type II restitution did not change significantly. Type II mechanical restitution consisted of two different phases, designated phase A and phase B, respectively. As temperature was decreased from 35 to 0 degree C in the hedgehog preparation, the two phases became even more separated. At 35 degrees C, the rising part of mechanical restitution in the rabbit muscle could not be distinguished from phase A of the hedgehog preparation and was also very similar to phase A of the rat muscle. Phase A is thus present in both type I and type II mechanical restitution, but phase B is a special feature of type II mechanical restitution. Phase A and phase B might be a manifestation of activator calcium originating from two different sources, e.g., the sarcoplasmic reticulum and the sarcolemma.

Animals↗
PubMed1990

Analysis of the inotropic mechanism of enoximone in guinea pig ventricular muscle.

Force and action potentials were recorded in guinea pig papillary muscles. The peak force was 131.8 +/- 3.3% of control at 2 microM and 144.4 +/- 2.0% at 4 microM enoximone. Enoximone (2 microM) increased the rate of rise of force (131.0 +/- 4.9%) and time from peak to half-relaxation (106 +/- 1.1%). The time to peak twitch force shortened (96.7 +/- 0.6%). The action potential duration decreased at 2 microM (96.4 +/- 1.2%) and 4 microM (92.8 +/- 1.4%) enoximone. The action potential amplitude was 106.7 +/- 0.8% in 2 microM and 112.6 +/- 0.6% in 4 microM enoximone. The peak twitch force in response to a test stimulus given after varied intervals (i.e., mechanical restitution) was increased at all test intervals, whereas the time to full restitution was not affected at any concentration. The force in response to the preceding test interval (postextrasystolic potentiation) was also increased. Maximum potentiation was 11.9 +/- 3.0 mN/mm2 in controls, 15.9 +/- 3.3 mN/mm2 in 2 microM enoximone, and 17.02 +/- 3.2 mN/mm2 in 4 microM enoximone. During the decay of postextrasystolic potentiation, there was a linear relationship between the peak force of the postpotentiated contraction and peak force of the potentiated contraction. The slope of the line increased from 0.34 to 0.43 (n = 12, p less than 0.001) by enoximone (2 microM). The results suggest that enoximone exerts its positive inotropic effect by (a) increasing calcium inflow during the action potential and/or (b) reducing calcium outflow, thereby increasing the recirculation of activator calcium.

Action Potentials↗
PubMed1990

ST changes in relation to heart rate during bicycle exercise in patients with coronary artery disease.

Exercise test on cycle ergometer and coronary angiography were performed on 190 patients with chest pain. Volunteers with a normal thallium scintigraphy (n = 47) served as controls. The load started at 20 W and increased at a rate of 10 W min-1 until exhaustion or symptoms. Conventional 12-lead ECGs were recorded by means of computer before, during and after exercise. Minimum ST amplitude 60 ms after the STJ point (ST60) at end of work with a cut-off level of -1.10 mm had a sensitivity of 69% (52/75) and a specificity of 89% (37/42) when individuals with a normal resting ECG were considered. ST80 and sum of ST60 in left ventricular leads had slightly lower values of sensitivity and specificity. Changes in ST60 during exercise discriminated less well between the groups. Final heart rate during exercise (less than 148 min-1) had a sensitivity of 88% (53/60) and a specificity of 89% (42/47). The change in heart rate during exercise (less than 66 min-1) had a sensitivity of 50/60 (only patients without beta-blockers were considered). The best discrimination was obtained by defining a test score (TS) according to the linear equation TS = 2.95-0.23 x HRE-0.301 X ST60 where a positive value indicates a positive test and a negative value a negative test. Sensitivity and specificity were 21/23 (91%) and 40/42 (95%), respectively. The test score was also calculated in those patients having significant coronary disease and an abnormal resting ECG (no bundle branch block, no beta-blockers) and this yielded a sensitivity of 30/34.

Adult↗
PubMed1990

Inotropic mechanisms of amrinone in papillary muscles from guinea-pig hearts.

Isometric force and action potentials were recorded in papillary muscles from guinea-pigs (temperature 33 degrees C, stimulation frequency 0.5 Hz). Amrinone (1 mM) increased peak twitch force (to 220% of control, n = 12) and rate of rise of force (to 221% of control, n = 12), while time from peak to half-relaxation was markedly reduced (to 70% of control). The time to peak force was not significantly changed. Action potential at 50% repolarization was shortened (93.3% of control, n = 8), whereas plateau voltage became more positive. Peak twitch force in response to a test stimulus after a varied interval, i.e. mechanical restitution, was increased at all intervals by the drug. However, the time to full mechanical restitution (1.5 s) was not affected. Forces in response to the test interval preceding the previous contraction (post-extrasystolic potentiation) were analysed. Maximum potentiation was 16.0 mN mm-2 (2.7 +/- 0.4%) before and 22.6 mN mm-2 (1.7 +/- 0.1%) after addition of the drug, i.e., the relative potentiation was diminished in the presence of the drug. The test interval for optimum potentiation was shortened from 370 to 320 ms (P less than 0.05, n = 12) in 1 mM amrinone. During decay of post-extrasystolic potentiation peak force of the post-potentiated contraction was linearly related to force of the potentiated contraction. The slope of this line (which is believed to monitor recirculation of activator calcium) was increased by amrinone from 0.37 to 0.50 (P less than 0.01, n = 12).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1990

Force production following transient potential changes in voltage-clamped myocardium.

Inter-relationships between force, membrane voltage and currents were studied in ferret and guinea-pig papillary muscles using the single sucrose gap technique (37 degrees C). The preparations were held at -90 or -40 mV and depolarized (excited) to 0 mV for 180 ms at 1.0 Hz. At regular intervals the shape of a single clamp pulse (called '1') was varied and its effects were investigated during the same test cycle and in two subsequent test cycles ('2' and '3'). Peak force of contraction 1 (F1) increased with the duration of the test clamp up to 90 ms and was constant thereafter. F1 increased with clamp amplitude (V1) between -30 and 10 mV and decreased at greater amplitudes. This relation was similar to the relation between peak second inward current (I1) and V1. The peak force of contractions 2 and 3 rose with the clamp duration and clamp amplitudes of cycle 1. The relation between F3 and F2 was linear (slope 0.40), except at the lowest and highest F2 values where there was a small deviation. There was an inverse relation between I2 and F2. The results support the idea that increased duration or amplitude of the voltage clamp pulse leads to a greater calcium entry which is manifested in the following potentiated contraction. The relation between F3 and F2 implies that about 40% of calcium recirculates between the contractions. The inverse relationship between F2 and I2 indicates that the second inward current is regulated by release from the sarcoplasmic reticulum via negative feedback.

Animals↗
PubMed1988

Hypothermic effects on action potential and force production of hedgehog and guinea pig papillary muscles.

Action potentials and isometric force were recorded in papillary muscles from guinea pigs and summer hedgehogs at different temperatures between 37 and 0 degrees C. The action potential of the hedgehog was of a lower amplitude (mean 83 +/- 6 mV) than that of the guinea pig (mean 110 +/- 5 mV). The action potential duration at 50% repolarization was 22 +/- 2 msec in the hedgehog as compared to 105 +/- 11 msec in the guinea pig. Moreover, there was no distinct plateau phase of the hedgehog action potential. Lowering temperature prolonged the action potential duration in the two preparations by about the same percentage. However, the guinea pig preparation became progressively less excitable below 20 degrees C. Lowered temperature produced a positive inotropic effect in the guinea pig, whereas this effect was very slight in the hedgehog heart. Postextrasystolic potentiation was seen in the guinea pig but not in the hedgehog preparation. It is suggested that this difference between the preparations may be due to a greater relative amount of activator calcium in the hedgehog heart. The difference in cold tolerance between the preparations may reflect a difference in chemical composition of the sarcolemma.

Action Potentials↗
PubMed1987

A simple model for demonstration of STT-changes in ECG.

This study is based on the idea that the STT part of the electrocardiogram in a small segment of the heart wall can be accurately constructed by calculating the difference between one subendocardial and one epicardial action potential. The following simulations were performed on computer and graphically presented. Endocardial ischaemia producing depression of the ST segment, downward sloping of the ST segment and negative T waves. Epicardial injury causing either a real or a pseudo ST elevation. Abnormal conduction between endocardium and epicardium (Increased delay between endocardial and epicardial excitation or reversed excitation path) producing discordant R and T waves. Analysis of STT changes are discussed on the background of these simulations. The proposed model for a segmental ECG was extrapolated to the whole heart by considering the contribution from each of 8 segments to a resultant heart vector.

Action Potentials↗
PubMed1987

Effects of neuropeptide Y (NPY) on isolated guinea-pig heart.

Neuropeptide Y (NPY) is present in nerve fibres throughout the mammalian heart. We have elucidated the effects of NPY on the isolated papillary muscle and heart (Langendorff) from the guinea-pig. The paced papillary muscle was studied with regard to duration of the action potential, peak force, maximum rate of force development, time to peak force, and time from peak force to half relaxation; all these parameters were identical whether or not NPY (5 X 10(-7) M) was present in the medium. When a stimulation with trains of pulses was superimposed, the paced papillary muscle exhibited enhanced contractions. This increase in contractility was not observed in the presence of the beta-adrenoceptor antagonist propranolol (10(-6) M) and was thus considered to be adrenergically mediated. The latter (adrenergic) response was markedly attenuated by NPY. Since NPY did not interfere with the response to exogenous noradrenaline (NA) it is suggested that the peptide exerts a pre-junctional inhibitory affect on adrenergic nerve-mediated positive inotropy. Neuropeptide Y did not influence the electrocardiogram from the spontaneously beating heart (Lagendorff), nor did the peptide modify the positive chronotropic effect of exogenously applied NA. In conclusion, the results indicate that NPY is without effect on the heart muscle proper but that the sympathetic terminals of the heart possess pre-junctional receptors for NPY (and/or related peptides) related to suppression of stimulated NA release.

Action Potentials↗
PubMed1987

Analysis of the inotropic effect of prenalterol in papillary muscles from guinea-pig hearts.

The inotropic effects of prenalterol were studied in papillary muscles isolated from the right ventricle of guinea-pig hearts. Force production and action potential were recorded. The preparations were paced at 0.4 Hz (at 31-32 degrees C) under isometric conditions. Prenalterol, in concentration 0.1 microM did not change the action potential duration whereas the peak force and the maximum rate of force development increased by 40.3 and 36.3%, respectively. Time to peak force was slightly shortened (-3.0%) and so was the time from peak force to half relaxation (-5.2%). A predetermined stimulus protocol was used for assessment of the recirculation fraction of activator calcium. At selected times an extra contraction was introduced in order to obtain contractile potentiation. Force of the subsequent two test contractions (after fixed intervals) was analysed. Prenalterol slightly reduced the decay of the postextrasystolic potentiation measured in the two test contractions. It is suggested that the inotropic effect of prenalterol is due to an intensified calcium influx during the action potential, and to some extent to more efficient re-utilization of released calcium. There seems to be a more rapid release of calcium from troponin C giving rise to a shortened time to peak force and an enhanced relaxation.

Action Potentials↗
PubMed1984

Velocity of sarcomere shortening in rat cardiac muscle: relationship to force, sarcomere length, calcium and time.

The relation between force and velocity was determined in sixteen trabeculae of rat right ventricle as a function of time during a twitch, of sarcomere length and of external Ca2+ concentration, [Ca2+]o. The trabeculae were studied in modified Krebs-Henseleit solution at 25 degrees C. Force was measured with a semiconductor strain gauge. Sarcomere length was measured with a laser diffraction system. A servomotor system was used in which control could be switched between sarcomere length, muscle length and force. Force-velocity relations were derived from load clamps and from contractions in which sarcomere length was initially held constant followed by a quick release and slower release of the sarcomeres at controlled velocity. Force-velocity relations were fitted by Hill's equation (Hill, 1938), (Po-P) b = (P+a) V, where P = force, V = velocity, Po = isometric force in mN/mm2 and a and b are constants. For [Ca2+]o = 2.5 mM, with both interventions the values (mean +/- S.D.) were: b = 1.00 +/- 0.45 micron/s; a = 9.52 +/- 5.60 mN/mm2; Vo measured = 13.6 +/- 3.0 micron/s; Vo calculated = 13.4 +/- 3.4 micron/s; Po measured = 96.5 +/- 25.0 mN/mm2; Po calculated = 119.3 +/- 34.5 mN/mm2. Vo rose with [Ca2+]o to a maximum at [Ca2+]o = 1.2 mM when Po was about 50% of maximum, while Po rose with [Ca2+]o to a maximum at above 2.5 mM. Vo rose with time during the twitch to a maximum at 25 ms following onset of contraction; Po was then about 50% of the maximum that was obtained at 120 ms. Vo increased with sarcomere length from zero at a sarcomere length of 1.6 micron to a maximum at 1.85 micron. Between 1.85 micron and 2.3 micron, Vo was constant. At 1.85 micron, Po was about 60% of maximum Po. These results are compatible with the hypothesis that Vo is more sensitive than Po to the amount of Ca2+ bound to the contractile proteins, and that Vo reaches a maximal value with an amount of Ca2+ bound to the contractile proteins at which Po has obtained only about 50% of its maximal value.

Animals↗
PubMed1983

Cardiac action potential duration and contractility in the intact dog heart.

The maximum rate of rise of left ventricular pressure (DP) and action potential duration (a.p.d.) were measured in closed-chest anaesthetized dogs with atrioventricular dissociation and beta-adrenergic blockade. Right ventricular stimulation was carried out with protocols consisting of a conditioning 'priming' period and a test period. When a single test stimulus was introduced at varying intervals after the priming period, DP was found to be maximal at 800-1000 ms. With this single test stimulus fixed at the optimum, DP was found to be a variable inverse function of the a.p.d. of the same beat; no positive correlation could be found between DP and a.p.d. When a second test stimulus at the optimum interval was introduced after the first, the DP (DP2) was found to be strongly dependent on that elicited by the first test stimulus (DP1); the relationship was positive, linear, independent of the method used to vary DP, and independent of whether DP1 was depressed or potentiated. The slope of the relationship was less than 1.0 and the line passed through the point where DP2 = DP1; this is the point of continuous stimulation at the optimum interval in a steady state. This result is consistent with the hypothesis that the coefficient relating DP1 to DP2, at constant a.p.d. of the first test pulse (AP1), is an index of the proportion of the activator of contraction stored during relaxation of test beat 1 which is released again on beat 2. In order to test the hypothesis that the remaining contractility depended on the action potential of test beat 1, AP1 was varied by changing the intervals between the priming stimuli. In order to determine the relationship between DP2 and AP1 it was necessary to carry out multiple regression analysis because DP2 was already known to be strongly dependent on DP1 (point 3 above), i.e. DP2 = BDP(DP1) + BAP(AP1 - D). This analysis yielded highly significant positive values for the coefficients BDP and BAP. This result is compatible with the postulate that a.p.d. influences the amount of the activator of contraction entering the intracellular store, but that this activator is not available for release to the contractile proteins until the next depolarization.

Action Potentials↗
PubMed1982

Mechanical restitution of the rat papillary muscle.

The experiments were performed on isometrically contracting rat papillary muscles paced at 1.0 Hz and at a temperature of 37 degrees C. The contractile response of a test contraction continuously rose when the duration of the preceding stimulus interval was gradually increased from 0.2 s. A maximum value was seen at intervals of 60--120 s. This phenomenon was called mechanical restitution of the papillary muscle. The insertion of a priming beat before the test contraction in order to increase the amount of contractile calcium elevated the mechanical restitution curve but it did not change the maximum contractile force seen after 60--120 s intervals. Lowering the extracellular calcium concentration from 2.0 mM to 1.0 mM, however, depressed this maximum contractile force to about 50%. The mechanical restitution is thought to reflect inflow of activator calcium to a cellular store, from which it is later released in response to the action potential. By using two test contractions a simple method is described to estimate the recirculating fraction of activator calcium between beats in this preparation. In 11 preparations the recirculating fraction of activator calcium was 0.72 +/- 0.03 (mean +/- SE). The results are consistent with the view that the same model of metabolism of activator calcium as previously proposed for rabbit papillary muscles is also applicable to the rat heart.

Action Potentials↗
PubMed1982

Electrical and mechanical responses of the intact rabbit heart in relation to the excitation interval. A comparison with the isolated papillary muscle preparation.

Experiments were performed on anesthetized open thorax rabbits with complete heart block and on isolated papillary muscles from rabbit hearts. Both preparations were basically paced at 1.0 Hz. Two consecutive test stimuli (denoted 1 and 2, respectively) were applied at various intervals. Action potentials were recorded; using suction electrodes in the intact heart and microelectrodes in the isolated tissue. Peak rate of rise of left ventricular pressure (DP) and of isometric force (DF, in vitro) were taken as measures of the contractile response. Action potential duration (AP), at 50% repolarization, were longer in vivo (175 ms) than in vitro (130 ms). AP and DP (DF) of the test contractions were similarly related to the test pulse intervals in the two preparations. DP2 was significantly correlated with DP1 and AP1 (r: 0.92-0.96). The regression coefficient for the dependence of DP2 on DP1 was significantly greater in vivo (0.61) than in vitro (0.21). This was interpreted to mean that recirculation of activator calcium from one heart beat to another was greater in vivo than in vitro. The isolated tissue would therefore be more dependent on calcium entering during the action potential. This could explain the greater postextrasystolic potentiation in vitro than in vivo (255% and 141% of steady state-responses, respectively).

Action Potentials↗