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J Thorvaldson

Publications and source records attributed to J Thorvaldson.

21 records · Page 2Linked to original sources
PubMed1979

Myocardial ischemia. Relationship between local flow, function and ST-segment elevation.

The significance of reductions in local myocardial flow on mechanical function and intramural electrocardiograms (ECG) was studied in anesthetized open-chest dogs. Local dimensional changes in the anterior wall of the left ventricle were recorded by ultrasonic technique. By platinum electrodes in the same region, both intramural ECG and hydrogen tension were recorded. Local flow was calculated from hydrogen desaturation curves. At approx. 25% flow reduction (constriction of the left anterior descending coronary artery (LAD)) local enddiastolic dilation and reduced systolic shortening appeared. Significant ST-segment elevation first appeared with flow reduction of 50%. After complete LAD-occlusions, enddiastolic dilation appeared within 20 sec, ST-segment elevation 40 sec later. It is concluded that mechanical and electrical events can be dissociated during acute myocardial ischemia: enddiastolic dilation and reduced systolic shortening are more sensitive indicators of moderate reductions in myocardial tissue flow than ST-segment elevation.

Animals↗
PubMed1976

Left ventricular function during acute elevation of aortic blood pressure in dogs.

Cardiac responses to mechanical constriction of the aorta proximal and distal to the arch arteries and to intravenous infusion of angiotensin were examined in open-chest atropinized dogs during continuous recording of left ventricular and aortic dimensions by means of ultrasonic elements. Proximal constriction reduced stroke volume by 18% both before and during isoproterenol infusion without changing left ventricular end-diastolic pressure, dimensions, or contractility, (dP/dt)IP; angiotensin induced less pronounced increments in stroke volume and end-diastolic volume. By combining proximal constriction with saline-dextran infusion, stroke volume and end-diastolic volume increased as during distal constriction. These results indicate that differences in preload account for the differences in stroke volume responses to proximal and distal aortic constriction. We propose that increased preload is caused by redistribution of blood from capacitance vessels rather than retention secondary to cardiac decompensation.

Angiotensin II↗