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Biomedical subjects

R M Norris

Publications and source records attributed to R M Norris.

At least 127 records · Page 7Linked to original sources

Effects of verapamil on infarct size following experimental coronary occlusion.

Open-chest anaesthetized dogs were given verapamil after left anterior descending artery occlusion, and ST-segment alterations and haemodynamic variables were monitored. Verapamil produced a highly significant reduction in ST-segment elevation in the epicardial electrocardiogram and prevented the haemodynamic deterioration seen in the control animals in which ST-segment elevation persisted. The apparent protective effect of verapamil in myocardial ischaemia is discussed in relation to its ability to inhibit selectively the transmembrane fluxes of calcium ions in excitable tissues.

Animals↗

The effects of isoprenaline on epicardial ST-segment elevation, lactate production, and myocardial blood flow following coronary artery ligation.

Isoprenaline was infused at low and high rates into anaesthetized dogs after ligation of the left anterior descending coronary artery, the resultant changes in epicardial ST-segment elevation being compared with lactate production and myocardial blood flow in the infarcting myocardium. Although ST elevation was increased at both infusion rates, there was no change in the arterial-local coronary venous difference of lactate concentration nor in myocardial blood flow at the centre of the infarct. The results suggest that the relationship between epicardial ST-segment elevation and other indices of ischaemic myocardial injury is complex and requires further evaluation.

Acute Disease↗

Treatment with digoxin and measurement of serum digoxin levels after myocardial infarction.

Forty-nine patients admitted to a Coronary Care Unit with myocardial infarction complicated by left ventricular failure, were treated with 1.75 mg Lanoxin over 36 hours. Serum digoxin levels were measured by radioimmunoassay at 8, 24, and 48 hours. No difference in serum levels was observed between those patients who received 'old' (reduced bioavailability) and those who received 'new' Lanoxin. Serum levels were significantly higher at 8 and 24 hours in those patients who received their first dose intramuscularly compared with those who received their first dose orally, irrespective of the bioavailability of the oral preparation used. No correlation was observed between serum digoxin levels and serum urea or creatinine during the 48-hour period of study. The incidence of arrhythmias is reported, but no conclusion can be drawn as to whether or not the glycoside contributed to this in any way. The use of digoxin in patients with acute myocardial infarction complicated by left ventricular failure is justifiable in the light of available evidence. However, in view of the possible predisposition of such patients to toxicity, lower serum levels than were achieved in many of our patients seem desirable and a modified dosage schedule is suggested.

Administration, Oral↗

Clinical measurement of myocardial infarct size. Modification of a method for the estimation of total creatine phosphokinase release after myocardial infarction.

A modified method for the measurement of total creatine phosphokinase release from venous blood samples taken four-hourly after myocardial infarction has been used in 43 patients admitted to a Coronary Care Unit. The fractional decay rate (Kd) of enzyme activity has been measured by a standardized method in each patient, and accuracy of the calculation of total enzyme release has been improved by allowance for individual variations in decay rate, and discarding of data from which decay rates cannot be measured within confidence limits of less than plus or minus 15 per cent. Total enzyme release was greater in cases of transmural infarction than in patients with subendocardial infarction, and showed a good positive correlation with clinical indices of the extent of myocardial damage. As noted by previous workers, this method allows for the measurement of the rate as well as the extent of enzyme release, and so should prove useful in the clinical evaluation of therapeutic agents which might accelerate or retard the rate of myocardial necrosis in patients with acute myocardial infarction.

Blood Specimen Collection↗

Changes in myocardial blood flow and S-T segment elevation following coronary artery occlusion in dogs.

The relationship between regional blood flow and epicardial S-T segment elevation was studied in 26 open-chest anesthetized dogs with left anterior coronary artery ligations. Changes in myocardial blood flow, measured with 15 plus or minus 5mu (diameter) microspheres labeled with 141-Ce, 85-Sr, and 169-Yb, were correlated with summated S-T segment elevations 15 minutes, 1 hour, and 2 hours after coronary artery occlusion. In normal areas, myocardial blood flow was 113 plus or minus 5 ml/min 100 g- minus 1 and summated S-T segment elevation was 0.3 plus or minus 0.2 mv. Fifteen minutes after coronary artery occlusion in 26 dogs, S-T segment elevation was 5.7 plus or minus 0.7 mv over the center of the infarct and myocardial blood flow was 10 plus or minus 1 ml/min 100 g- minus 1; over the border zone, myocardial blood flow was 63 plus or minus 4 ml/min 100 g- minus 1 and S-T segment elevation was 3.1 plus or minus 0.1 mv. One third of the areas with a myocardial blood flow of 10 ml/min 100 g- minus 1 or less had no S-T segment elevation. In the center and border zones of the infarct in 9 dogs, myocardial blood flow increased from 11 plus or minus 2 and 67 plus or minus 8 ml/min 100 g- minus 1 15 minutes after occlusion to 20 plus or minus 4 and 84 plus or minus 12 ml/min 100 g- minus 1, respectively, 2 hours after coronary artery occlusion. These increases were not associated with a significant reduction in summated S-T segment elevation. The results do not suggest a simple quantitative relationship between epicardial S-T segment elevation and myocardial blood flow following acute coronary artery occlusion.

Animals↗

Reduction in infarct size following experimental coronary occlusion by administration of verapamil.

The effect of verapamil, a calcium antagonist and antiarrhythmic and anti-anginal actions, were studied on the size of infarct in open-chest anesthetized dogs with left anterior descending coronary artery occlusion. Hemodyamic functions were monitored by standard techniques, and infarct size was assessed by epicardial electrocardiography. Myocardial blood flow was measured by radioactive microspheres, and regional metabolism was studied by measuring lactate concentration in the venous drainage of the ischemic myocardium. Verapamil produced a significant reduction to ST segment elevation in the epicardial electrocardiogram and prevented the hemodynamic deterioration seen in the control animals in which ST segment elevation persisted. The drug had no effect on either total collateral blood flow or on the relative distribution of flow to the inner and outer halves of the ventricular wall. No significant differences were found between the levels of coronary venous lactate in the control animals and those in the verapamil-treated group. The results raise the possibility that the apparent protective effect of verapamil in myocardial ischemia may be due to its electrophysiological action on the cardiac membrane in relation to its calcium-antagonistic properites in excitable tissues.

Animals↗