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J Ross

Publications and source records attributed to J Ross.

At least 829 records · Page 46Linked to original sources
PubMed1972

Coronary artery reperfusion. I. Early effects on local myocardial function and the extent of myocardial necrosis.

The effects of coronary artery reperfusion 3 hr after coronary occlusion on contractile function and the development of myocardial damage at 24 hr was studied experimentally. In 14 control and 6 reperfused dogs, relationships between epicardial ST segment elevation 15 min after coronary occlusion and myocardial creatine phosphokinase activity (CPK) and histologic appearance 24 hr later were examined. The electrocardiograms were recorded from 10 to 15 sites on the left ventricular epicardium and transmural samples for CPK and histology were obtained from the same sites where epicardial electrocardiograms had been recorded. An inverse relation existed between ST segment elevation (mv) 15 min after occlusion and log CPK activity (IU/ mg of protein) 24 hr later, log CPK = - 0.06ST + 1.26. In dogs subjected to coronary artery reperfusion, there was significantly less CPK depression (log CPK = - 0.01ST + 1.31, [P < 0.01]) than that expected from the control group. In the control group 97% of specimens showing ST segment elevations over 2 mv at 15 min showed abnormal histology 24 hr later. In contrast, in the reperfused group 43% of sites exhibiting elevated ST segment at 15 min showed abnormal histology 24 hr later. In six additional dogs it was shown that the paradoxical movement of the left ventricular wall could be reversed within 1 hr of perfusion. Therefore, by enzymatic and histologic criteria, as well as by functional assessment, coronary artery reperfusion 3 hr after occlusion resulted in salvage of myocardial tissue.

Animals↗
PubMed1972

Coronary artery reperfusion. II. Reduction of myocardial infarct size at 1 week after the coronary occlusion.

The question of whether or not the size of an area of myocardial infarction, measured at 1 wk after coronary occlusion, can be influenced by coronary artery reperfusion was examined in dogs. In seven control experiments the anterior descending coronary artery was ligated, while in seven other studies the occlusion was released after 3 hr. In all animals calibrated photographs were used to assess the zone of hypoperfusion and the acutely injured area of epicardial ST segment elevation, as well as the extent of damage at postmortem 1 wk later. In control dogs, the gross infarct size at postmortem averaged 63.8+/-7.3% of that predicted from the acutely injured zone. However, in reperfused hearts the average gross infarct size at 1 wk was only 10.2+/-4.4% of that predicted. Transmural specimens were obtained at autopsy for histology and measurement of myocardial creatine phosphokinase (CPK) activity from sites initially used for epicardial electrocardiography. In control animals, there was a direct relationship between the degree of ST segment elevation and the degree of cell necrosis in transmural histologic sections. ST segment elevation also predicted myocardial CPK (international units per milligram protein): log CPK = - 0.0613 ST + 1.17 (r = 0.66, n = 56 sites). In the reperfused animals, log CPK = - 0.166 ST + 1.36 (r = 0.69, n = 46 sites) showing almost complete preservation of CPK activity at 1 wk, sparing being most prominent in the epicardial zone. Similarly, there was a good correlation between myocardial CPK activity and the histological assessment of cell destruction, the degree of cell damage = - 0.152 CPK + 3.86 (r = 0.86; n = 102 sites). Thus, control dogs showed severe myocardial CPK depletion and histologic evidence of extensive cell destruction, whereas animals subjected to coronary artery reperfusion had little CPK depletion and much less evidence of myocardial cell necrosis 1 wk later.

Animals↗
PubMed1971

Left ventricular performance after acute myocardial infarction.

Current knowledge concerning the major hemodynamic features of acute myocardial infarction has been reviewed and discussed in relation to present concepts of cardiac pathophysiology. The physical examination provides a great deal of information and new, noninvasive methods promise to supplement the bedside appraisal of left ventricular function. Direct hemodynamic methods of serially monitoring patients with acute myocardial infarction are finding increasing application and recently have added considerably to our understanding of this condition. Certain limitations in the use of the central venous pressure, pulmonary arterial pressure, and cardiac output in appraising left ventricular function have become apparent, but together with direct catheterization of the left ventricle such hemodynamic studies have now provided limited correlations between the clinical picture and various hemodynamic patterns. It is becoming increasingly clear that most of these features, including cardiogenic shock, probably reflect varying degrees of left ventricular failure. These initial findings and interpretations will require confirmation, however, and so far insufficient objective data are available concerning the natural history of acute myocardial infarction and its responses to various forms of therapy. The aims of investigations now being carried in specialized Myocardial Infarction Research Units and other cardiovascular research centers, are to gain such further understanding of the pathophysiology of this disease and to aid in its clinical management by developing accurate indirect monitoring techniques as well as new forms of therapy.

Acidosis↗