Search PubMed⌕ Search

Biomedical subjects

D C Russell

Publications and source records attributed to D C Russell.

At least 37 records · Page 2Linked to original sources
PubMed1984

Relationship of neurosympathetic responsiveness to early ventricular arrhythmias in ischaemic myocardium.

Myocardial catecholamine overflow has been measured in open-chest anaesthetised dogs after graded stimulation of the left ansa subclavia before and during left anterior descending coronary artery occlusion and on reperfusion. Sequential 1 min periods of ansa stimulation over 3 h resulted in reproducible, frequency dependent regional myocardial noradrenaline (NA) overflow without tachyphylaxis. In seven dogs, two successive 10 min periods of LAD occlusion did not modify peak myocardial NA overflow from the predominantly ischaemic (I) or non-ischaemic (NI) areas at either low (1 Hz) or high (10 Hz) frequency ansa stimulation. In a second group of nine dogs, myocardial catecholamine overflow was related to changes in ischaemic area epicardial activation delay during repeated ansa stimulation on four occasions during 75 min of ischaemia. Stimulation at the period of peak spontaneous arrhythmias 5 and 17 min after coronary occlusion resulted in NA overflow from I of 2.8 +/- 1.3 and 3.0 +/- 1.6 pmol X ml-1 respectively and a significant increase in mean activation delay in I of 12 +/- 4 ms at 5 min and 9 +/- 4 ms at 17 min (p less than 0.05). In contrast, stimulation 30 and 60 min after coronary occlusion, when spontaneous arrhythmias are rare, was not associated with NA overflow from ischaemic areas (0.3 +/- 0.3 and 0.9 +/- 0.5 pmol X ml-1 respectively) and resulted in a minor reduction in mean activation delay in ischaemic areas of 2 +/- 3 ms at 30 min and 3 +/- 4 ms at 60 min. NA overflow from non-ischaemic areas and increases in blood pressure and myocardial lactate release were similar during each period of ansa stimulation. Coronary reperfusion induced massive overflow of NA (11.4 +/- 2.8 pmol X ml-1) and reduced extraction of adrenaline (A) from ischaemic areas with a time course similar to early reperfusion arrhythmias. Stimulation-evoked release of NA in ischaemic myocardium is thus maintained during the early period of enhanced vulnerability to arrhythmias and during reperfusion but is inhibited after 30 min. This temporal variability may be a factor in the time course of spontaneous arrhythmias in this model.

Animals↗
PubMed1984

Experimental studies into mechanisms of cardiac arrest.

Experimental studies have revealed that a wide variety of different pathophysiological mechanisms may induce ventricular fibrillation (VF) and cardiac arrest during acute myocardial ischaemia or infarction. Distinct phases of enhanced vulnerability (the amount of current required to stimulate ectopic activity in the heart following application of an extra stimulus) to VF follow coronary occlusion and correspond to 'pre-hospital', 'in-hospital' and 'out-of-hospital' periods of arrhythmogenesis. Electrophysiological evidence suggests very early (phase 1a) VF results from multiple re-entrant excitation within the ischaemic zone. Slowed and fragmented conduction and inhomogeneities in refractoriness rapidly develop which mapping studies show to occur in association with development of spatial inhomogeneities in residual blood flow distribution and metabolism. Onset of VF may be triggered by adrenergic mechanisms or influenced by peripheral metabolic responses. Automatic mechanisms (spontaneous pacemaker activity) may induce later VF or VF on reperfusion or trigger re-entry. Findings indicate no single therapeutic approach to be likely to protect against all forms of cardiac arrest.

Animals↗
PubMed1983

Amiodarone associated alveolitis and polyarthropathy. Treatment by plasma exchange.

In a case of severe alveolitis and polyarthropathy occurring within two to five months of starting amiodarone treatment high plasma concentrations of immune complexes were found, suggesting a drug mediated hypersensitivity reaction. Initial symptomatic response followed high dosage corticosteroid and immunosuppressant treatment, but reduction in the dosage of corticosteroids was achieved only by successive plasma exchange with concomitant reduction in plasma concentrations of both amiodarone and immune complexes.

Amiodarone↗
PubMed1982

Patterns of flow and conduction during early ventricular arrhythmias following coronary arterial occlusion in the dog.

The early ventricular arrhythmias of acute myocardial ischaemia arise against a background of rapid alterations in regional myocardial blood flow and electrophysiological properties. The relation between patterns of flow and epicardial activation has been examined in eight open chest anaesthetised dogs at time of onset of these arrhythmias following a proximal occlusion of the left anterior descending coronary artery. Data were derived from 80 epicardial and endocardial sites within a 4 X 5 cm area of left ventricular free wall and processed utilising a three-dimensional computer plotting program. Mean flow within the ischaemic zone was reduced to 0.27 and 0.24 cm3 x g-1 x min-1 in epicardium and endocardium respectively. Marked epicardial activation delays and fragmentation of conduction were observed confined to areas of flow less than 0.3 cm3 x g-1 x min-1. 74% of endocardial and 71% of epicardial tissue samples within the ischaemic zone derived from this area and analysis of flow distribution between adjacent samples demonstrated spatial heterogeneity of flow. It is suggested that local spatial variability in flow within the central ischaemic region may be a prerequisite for abnormal fractionation of conduction leading to re-entrant excitation at the time of onset of early ventricular arrhythmias.

Animals↗
PubMed1982

Effect of heparin on plasma free fatty acid concentrations after acute myocardial infarction.

Free fatty acid concentrations in plasma measured after in vivo heparinisation are often overestimated because of ex vivo lipolysis of variable degrees. A new method has been developed using immediate extraction of blood which obviates this and shows that the true rise in plasma free fatty acid concentration after heparin in ambulant ward patients and in patients with acute myocardial infarction is less than previously reported. The small rise in plasma free fatty acid concentration after heparin is unlikely to have adverse metabolic effects in most patients during acute myocardial infarction.

Adult↗
PubMed1981

Metabolic aspects of rhythm disturbances.

[Profound alterations in metabolism occur within the first few minutes of myocardial ischaemia which may induce or modulate myocardial electrophysiological abnormalities and arrhythmogenesis, Fatty acid oxidation is inhibited with accumulation of long-chain acyl CoA esters and glycolysis is stimulated but later inhibited. This may be worsened by a peripheral sympathetic response. In particular regional variations in glycolytic ATP productions which can modulate "slow channel" ion flux and hence slow conducting "slow response" potential activity, could influence patterns of slow conduction in ischaemic myocardium of importance in generating early re-entrant arrhythmias. This possibility has been examined in open chest anaesthetised dogs following experimental coronary occlusion by detailed computer aided analysis and construction of three dimensional maps of regional metabolism, blood flow and epicardial activation patterns at the time of early ventricular arrhythmias. Activation patterns were obtained using an electronic multiplexing system, flow using tracer microspheres and metabolic changes by analysis of multiple tissue samples for lactate and indices of glycolytic activity after rapid excision and freezing of the heart. Marked spacial inhomogeneities in flow, lactate and glycolytic activity were associated with delayed and fragmented activation in the central ischaemic region. Within the border region of flow, however, glycolytic activity was enhanced and conduction generally little impaired. It is suggested that transient changes in the homogeneity of myocardial metabolism and flow are critical in determining patterns of conduction and hence arrhythmogenesis. This may provide a basis for understanding anti-arrhythmic effects of metabolic interventions.

Animals↗
PubMed1981

Haemodynamic effects of sulphinpyrazone in experimental myocardial ischaemia.

The effect of sulphinpyrazone (30 mg/kg i.v.) on heart rate, blood pressure and ventricular arrhythmias was studied in open-chested anaesthetized dogs during sequential 10 min occlusions of the left anterior descending coronary artery. An increased duration of occlusion without ventricular fibrillation and reduction in epicardial activation delay in the central ischaemic region were observed after intravenous sulphinpyrazone (n = 7). These effects were associated with a progressive and significant reduction in intrinsic heart rate (up to 15 beats/min) but no change in blood pressure. These findings suggest that heart rate changes alone may account for the observed protective effect of sulphinpyrazone against early ventricular fibrillation during acute experimental myocardial ischaemia.

Animals↗
PubMed1980

Haemodynamic effects of sulphinpyrazone on exercise responses in normal subjects.

The effects of sulphinpyrazone on heart-rate and blood-pressure responses to exercise were assessed in 15 normal volunteers by a randomised double-blind crossover technique. Submaximal exercise tests were performed 1 and 2 hours after either sulphinpyrazone (SPZ) 200 mg orally or placebo. Heart-rate and blood-pressure responses were unchanged at rest and during exercise 1 hour after SPZ but after 2 hours there was a significant fall in the product of heart-rate and blood-pressure during exercise (peak 35.8 +/- 1.5 x 10(-3) mmHg beats/min, placebo: 33.0 +/- 1.3 x 10(-3) sulphinpyrazone, p < 0.005) and for the first 2 minutes of recovery. This was mainly due to a decreased exercise-induced rise in systolic blood-pressure with lesser effects on heart-rate. This haemodynamic effect of SPZ has a potentially protective oxygen-sparing effect on the normal myocardium during exercise and may explain its apparent benefit in reducing sudden cardiac death after myocardial infarction.

Adult↗
PubMed1978

Ventricular refractoriness during acute myocardial ischaemia and its relationship to ventricular fibrillation.

Studies were made in anaesthetised dog of the effects of repeated acute occlusions of a branch of the anterior descending coronary artery on ventricular refractory periods in adjacent ischaemic and non-ischaemic myocardium. Differences occurred in refractoriness between normal and ischaemic areas in the ventricle. This was greatest 2.5 min after occlusion, and on release of occlusion, ventricular refractory periods reverted to normal within 5 min. Spontaneous ventricular fibrillation was directly and significantly related to the degree of dispersion of refractoriness in a given dog immediately preceding release and following release of occlusion. Infusion of isoprenaline caused significant shortening of refactory period and increased dispersion of refractoriness during ischaemia. Studies of dispersion of refractoriness should prove valuable in assessing the efficiency of metabolic or antiarrhythmic protection against ventricular fibrillation.

Animals↗
PubMed1978

Haemodynamic effects on the myocardial blood flow supply/oxygen demand ratio in pacing induced angina pectoris.

Angina pectoris results from an imbalance between oxygen supply and demand in the subendocardium. The haemodynamic effects contributing to this imbalance have been studied in 10 patients with coronary artery disease. Myocardial oxygen demand was estimated from the tension time index (TTI), potential subendocardial flow from a diastolic pressure time index (DPTI), and the oxygen supply/demand ratio from (DPTI/TTI. With progressively increasing pacing rates up until induction of angina, no significant change in TTI was found whereas a significant fall in DPTI and DPTI/TTI occurred (P less than 0.001). During pacing runs with induction of angina DPTI/TTI reached a minimum value 5 s before,and at the onset of angina. No such relationship was seen for TTI or DPTI alone. A significant rise in LVEDP (P less than 0.05) and fall in dP/dt min (P less than 0.01) occurred at angina both contributing to a further reduction in DPTI and DPTI/TTI. Changes in DPTI/TTI may then reflect changes in the myocardial blood flow supply/oxygen demand ratio in the presence of coronary artery disease and haemodynamic changes before and at the induction of angina lead to a further reduction of this ratio.

Angina Pectoris↗
PubMed1977

Praecordial ST segment elevation. New technique for continuous recording and analysis.

The measurement of praecordial ST segment elevation after myocardial infarction is of value in assessing the natural history of ischaemic injury and the effectiveness of intervention. Hand analysis is, however, time consuming and inaccurate. A technique for continuous recording from 35 praecordial leads and subsequent computer analysis is presented, together with illustrative case studies. Changes in body posture and in heart rate are of importance in subsequent data interpretation.

Adult↗