Biomedical subjects
J C Cowan
Publications and source records attributed to J C Cowan.
The effects of ventricular end-diastolic and systolic pressures on action potential and duration in anaesthetized dogs.
1. Although it is known that mechanical events in the heart influence the duration of the cardiac action potential, there is no quantitative information on the effects of independent changes in ventricular end-diastolic and systolic pressures. 2. Experiments were carried out on open-chest anaesthetized dogs in which the autonomic nervous influences on the heart were prevented and monophasic action potentials were recorded form the epicardial surface of the left ventricle. The duration of these action potentials was taken as the interval from the upstroke to the point of 90% repolarization. 3. Elevation of left ventricular peak systolic pressure, at constant end-diastolic pressure, significantly shortened the monophasic action potential. 4. Elevation of end-diastolic pressure at constant peak systolic pressure significantly lengthened the monophasic action potential. 5. Responses were not dependent on release of noradrenaline from sympathetic nerve terminals because they persisted after administration of bretylium tosylate. They were also not due to myocardial ischaemia because they persisted when coronary perfusion pressure was maintained at a constant high level. 6. Simultaneous recordings of changes in myocardial segment length showed the expected responses to changes in ventricular pressures: increases in shortening in response to increases in diastolic pressure and no consistent effect from changes in systolic pressure. 7. These investigations demonstrate the independent effects of changes in systolic and end-diastolic pressures on cardiac action potential duration. This effect is likely to be an effect of the mechanical events, i.e. contraction-excitation feedback. This response may be mediated through changes in myocardial fibre tension, the consequent changes in fibre shortening, or both.
Cardiac rupture after thrombolytic therapy: the use of aprotinin to reduce blood loss after surgical repair.
Emergency cardiac surgery after recent thrombolytic therapy is associated with increased blood loss. A patient underwent emergency repair of a ruptured left ventricle after intravenous streptokinase treatment for acute coronary occlusion. High dose aprotinin was given during the operation to reduce the expected blood loss. Surgical repair was successful without bleeding complications. Total postoperative blood loss was 365 ml.
Comparison of unipolar and bipolar ventricular paced evoked responses.
OBJECTIVES: To study the differences between endocardial bipolar and unipolar ventricular paced evoked responses and surface electrocardiograms. PATIENTS: 10 patients with conduction system disease awaiting insertion of a permanent pacemaker were studied with temporary ventricular pacing from the right ventricular apex. MAIN OUTCOME MEASURE: Comparison of the durations of the QRS complexes and QTa and QTe intervals of the endocardial bipolar paced evoked response and the surface electrocardiogram with those of the reference unipolar paced evoked response. RESULTS: By comparison with the unipolar reference, the mean durations of the QRS complexes of the bipolar signal and the surface electrocardiogram were 41.8% and 132.1% respectively. The mean QTa interval was 85.9% and 112.2% respectively and the mean QTe interval was 86.9% and 109.5% respectively. All these differences were significant. The amplitudes of the unipolar QRS complexes and T waves were significantly larger than those recorded in the bipolar configuration. CONCLUSIONS: Differences between the unipolar and bipolar ventricular paced evoked responses are significant. The time course of the unipolar signal is closer to that of the surface electrocardiogram. This indicates that the unipolar paced evoked response does not reflect local electrophysiological events, as has been suggested previously.
The fall of John Thomas.
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Torsades de pointes ventricular tachycardia and terodiline.
We report five patients (four women, one man; mean age 74 years, range 55-87) taking terodiline who had torsades de pointes ventricular tachycardia associated with prolongation of the QT interval. The QT interval was normal before the introduction of terodiline in three patients and returned to normal after terodiline withdrawal in four. Atrioventricular conduction disturbance or bradycardia were evident in all patients. Terodiline should be prescribed with caution to elderly patients.
Contraction-excitation feedback in an ejecting whole heart model--dependence of action potential duration on left ventricular diastolic and systolic pressures.
STUDY OBJECTIVE: Contraction-excitation feedback may play a role in arrhythmogenesis in heart failure. The aims of this study were to determine whether contraction-excitation feedback has a significant effect on action potential duration within a physiological range of pressures, and to investigate the individual effects of left ventricular end diastolic and peak systolic pressures on action potential duration. DESIGN: A new model was developed for studying contraction-excitation feedback in a physiologically ejecting isolated heart preparation. Hearts were perfused via the left atrium, ejecting against an aortic afterload. By varying left atrial and aortic pressures, left ventricular end diastolic pressure and left ventricular peak systolic pressure were controlled independently. Intracellular potentials were recorded from the epicardium. EXPERIMENTAL MATERIAL: Hearts (n = 33) were obtained from guinea pigs weighing 300-350 g. MEASUREMENTS AND MAIN RESULTS: Increasing left ventricular end diastolic pressure from 0.3 to 1.1 kPa (2.2 to 8.3 mm Hg), at constant left ventricular peak systolic pressure, shortened action potential duration by 11.3(SEM 1.5) ms (p less than 0.0005). Action potential duration achieved a new steady state within 30 s of a change in end diastolic pressure. The changes were fully reversible. The effects of left ventricular peak systolic pressure variation at constant left ventricular end diastolic pressure were less marked. Increasing left ventricular peak systolic pressure from 10.3 to 13.1 kPa (75 to 100 mm Hg) shortened action potential duration by 2.1(0.7) ms (p less than 0.01). Reduction of aortic pressure below 8 kPa had variable effects on action potential duration, reflecting the development of ischaemia. CONCLUSION: The results show the existence of contraction-excitation feedback in a physiologically ejecting whole heart preparation and suggest that raised end diastolic pressure may contribute to arrhythmogenesis in heart failure.
Antiarrhythmic therapy and survival following myocardial infarction.
Arrhythmias remain a major cause of late mortality following myocardial infarction. They arise due to fibrosis within the infarct, which creates the conditions of slow conduction necessary for re-entry. In individual patients who have already manifested a malignant arrhythmia, antiarrhythmic drug therapy, guided by invasive electrophysiological testing, is of proven benefit in prolonging survival. By contrast, when used on a population basis, antiarrhythmic drug therapy has proved singularly ineffective. This is illustrated by the recent Cardiac Arrhythmia Suppression Trial (CAST) study--far from improving survival, antiarrhythmic therapy increased mortality. The use of antiarrhythmic drugs on a population basis is therefore fundamentally flawed. Hemodynamic intervention provides an alternative strategy in arrhythmia prevention. Hemodynamic changes may influence electrophysiological parameters and arrhythmogenesis in a number of ways. First, myocardial stretch may contribute to arrhythmogenesis through contraction-excitation feedback. Second, hemodynamic changes can influence ventricular remodeling following infarction, which may be an important determinant of subsequent arrhythmogenesis. Hemodynamic intervention, therefore, represents a promising new approach to arrhythmia prevention following myocardial infarction.
The effects of palmitate on intracellular potentials recorded from Langendorff-erfused guinea-pig hearts in normoxia and hypoxia, and during perfusion at reduced rate of flow.
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Chick edema factor: removal from soybean oil.
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