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Biomedical subjects

M J Lab

Publications and source records attributed to M J Lab.

At least 73 records · Page 4Linked to original sources
PubMed1981

Inosine as a selective inotropic agent on ischaemic myocardium?

Intravenous infusion of inosine (15 mg.kg-1.min-1) to the open-chested pig resulted in hypotension, coronary vasodilatation and slightly increased myocardial contractility. Following coronary occlusion, the action of inosine to increase myocardial contractility was apparently selective. Regional myocardial performance of ischaemic myocardium was increased significantly relative to nonischaemic. The selectivity of inotropic action was not mimicked by glucose-insulin-potassium. It is concluded that the selectivity is multifactoral and that the inotropic, vasodilatory and metabolic actions of the nucleoside contribute to the apparent selectivity.

Animals↗
PubMed1981

The action-potential duration and contractile response of the intact heart related to the preceding interval and the preceding beat in the dog and cat.

1. Simultaneous measurements were made in anaesthetized dogs of monophasic action potentials from the right ventricle and of the maximum rate of rise of left ventricular pressure (dP(lv)/dt(max)). Atrio-ventricular dissociation was induced and the heart paced via right ventricular electrodes.2. A control period of steady pacing was followed by a test stimulus after a variable interval called the ;test-pulse interval'. The duration of the action potential of the test beat (measured at 70% repolarization) increased with test-pulse interval and reached an approximately steady value at intervals of 1.0-1.5 sec. This constitutes the ;electrical restitution curve'.3. An increase in the frequency of stimulation prior to the introduction of the test pulses caused a downward displacement of the electrical restitution curve.4. Stimulation at 2 Hz and paired pulse stimulation at 1 Hz (same number of stimuli per min) were introduced prior to the test pulses and produced very similar electrical restitution curves.5. For a constant frequency of stimulation in the control period, adrenaline produced downward displacement of the restitution curve.6. It is concluded that there is no obvious relationship between the restitution of the action potential duration and of the contractile response. We suggest therefore that electrical and mechanical restitution occur through separate processes, the former through time-dependent recovery in membrane conductances and the latter through time-dependent increase in availability of intracellular calcium for release.7. Contractions were introduced with a test-pulse interval shorter than the optimum, and were followed by a second test pulse fixed at the optimum interval of 0.8-1.0 sec. The second test beats were potentiated (post-extrasystolic potentiation). In isolated ejecting cat hearts, there was an optimum interval for the first test pulse to produce the greatest potentiation of the second test beat. This interval was 0.2-0.3 sec, and was shortened by an increase in frequency of stimulation prior to the first test beat.8. The interval preceding the first test pulse was then varied within a range (0.8-2.0 sec) which did not produce potentiation. These first test pulses were sometimes preceded by one extrasystole. The timing of this extrasystole was altered to vary the post-extrastolic potentiation of the first test pulse.9. Multiple regression analysis, carried out between dP(lv)/dt(max) of the second test pulse (DP(2), the dependent variable) and the action potential duration (AP(1)) and dP(lv)/dt(max) (DP(1)) of the first test pulse (independent variables) yielded correlation coefficients between 0.88 and 0.99. Each determination of the coefficient included data from beats with and without post-extrasystolic potentiation.10. It is postulated that the coefficient relating DP(2) to DP(1) in the multiple regression analysis (mean value 0.75) is an index of the proportion of calcium stored during relaxation which is released again on the next beat.11. When the decay of post-extrasystolic potentiation was examined in consecutive beats at the optimum interval, the action potential durations of these beats were found to be nearly constant. A plot of dP(lv)/dt(max) of each beat against dP(lv)/dt(max) of the previous beat yielded a curvilinear relationship which was less steep than that relating DP(2) to DP(1) in the two test pulse analysis; this was attributed to inconstancy of calcium ion entry during the action potential.

Action Potentials↗
PubMed1980

Transient depolarisation and action potential alterations following mechanical changes in isolated myocardium.

The effects of induced changes in muscle length on the action potential of frog ventricular strips and cat papillary muscle have been studied. When the frog preparation was stretched near the onset of contraction, the action potential duration shortened whereas a stretch during peak activity produced minimal change. Action potentials of cat papillary muscle do not alter with stretch at any time. By contrast, release of both preparations at a time when tension was near its peak, prolonged repolarisation or produced a transient depolarisation. The ECG changes corroborated the action potential changes. The release produced a deactivation of contraction which correlated with the transient depolarisation when the contraction and potential were expressed as ratios of the undisturbed measurements. Possible explanations for the results are discussed in terms of active and passive mechanisms that can relate to mechanical and electrical phenomena simultaneously. The mechanically induced transient depolarisations are clinically relevant, for regional ischaemia produces electrical and mechanical inhomogeneities which would cause contraction-excitation feedback interactions and thus electrophysiological abnormalities.

Action Potentials↗
PubMed1979

An audiovisual teaching model of the muscle spindle.

Students in biology and medicine often have difficulty in visualizing the structure, function and disease of complex integrated body systems. One example in neurophysiology is the muscle spindle and Golgi tendon organ. A model is described which demonstrates the properties of these two muscle receptors. The model combines mechanical elements, which can change their length to represent muscle contraction, with an electronic representation of the passage of action potentials along 'nerves', indicated by light-emitting diodes and loudspeakers. The model has been in use for some years as a supplement to conventional teaching methods. In a recent questionnaire about the model, a group of medical students responded favourably. We suggest that models such as this are valuable teaching aids.

Audiovisual Aids↗
PubMed1979

An automatic cardiac action potential duration meter.

The duration of a cardiac action potential (AP) is measured from the beginning of its upstroke to the end of its asymptotic repolarization phase: the end being given by a point in proportion to the AP amplitude. If the resting potential, AP amplitude, as well as the duration, alter simultaneously, frequent accurate measurements can be extremely tedious. A fully automatic AP duration meter has thus been constructed to cope with these difficulties while measuring within about 2% on a beat-to-beat basis. It is suitable either for brief sampling of AP durations when recording with microelectrodes, which may impale cells intermittently, or for continuous monitoring, as with suction electrodes on intact beating hearts in situ. For example, the device can faithfully track changes in duration during periods of regional myocardial ischemia in intact ventricles in situ while the AP alters its base line, upstroke velocity, amplitude, and duration.

Action Potentials↗
PubMed1978

Monophasic action potentials, electrocardiograms and mechanical performance in normal and ischaemic epicardial segments of the pig ventricle in situ.

Few studies report simultaneous electrical and mechanical recordings from the epicardium of intact beating hearts in situ during ischaemia. We use suction to apply transducers and electrodes to areas of the epicardium. This interferes little with its behaviour and allows: i) free mobility over the surface; ii) simultaneous tridirectional length changes to be recorded and summed for an overall impression of mechanical behaviour, iii) detection of changes in direction of movement; iv) simultaneous recordings of monophasic action potential and epicardial ECG. During ischaemia we can detect impaired contraction with dyskinesis and a change in direction of epicardial forces. The action potential duration shortens and we have noted impaired conduction, inexitability and recordings consistent with re-entry leading to ventricular fibrillation.

Action Potentials↗
PubMed1978

Mechanically dependent changes in action potentials recorded from the intact frog ventricle.

The wall of the ventricle contracts inhomogeneously during an isovolumic beat of an isolated, intact frog ventricle. Some epicardial segments actually lengthen while the pressure is rising. Almost simultaneously, the early repolarization phase of the monophasic action potential recorded from such a segment is accelerated, compared to the same phase for an isotonic beat in which the segment shortens. Segment lengthening during the isovolumic beat also may be seen during the late repolarization phase when, in contract to the above, it produces an afterdepolarization. These electrical changes disappear when isotonic contraction is restored. Corroborative findings were obtained from microelectrode and insulated gap recordings from isolated frog ventricular strip. Both electrical changes can be seen clearly when the segment is lengthened by intraventricular injections of Ringer's solution. There also is a short transition period toward the end of the action potential plateau when lengthening produces neither depolarization nor repolarization. The accelerated repolarization is manifest as a shortening of the Q-T interval in the ventricular electrogram. In all experimental preparations, the afterdepolarizations reached threshold for a propagated action potential. This mechanism may explain the generation of extrasystoles in myocardial ischemia.

Action Potentials↗