The APS Journal Legacy Content is the corpus of 100 years of historical scientific research from the American Physiological Society research journals. This package goes back to the first issue of each of the APS journals including the American Journal of Physiology, first published in 1898. The full text scanned images of the printed pages are easily searchable. Downloads quickly in PDF format.

Pairs of ultrasonic dimension gauges and a micromanometer implanted in the subendocardium of the left ventricles of unanesthetized dogs were used to analyze serial changes in hemodynamic status and segmental function for up to 4 weeks after permanent circumflex coronary artery occlusion. Regional function was studied in control segments and in segments identified as marginal (hypokinetic) and ischemic. In three dogs, after transient regional dysfunction, no myocardial infarction developed, whereas in five dogs regional dysfunction at 3 hours after occlusion was followed by the development of persistent dysfunction and infarction. Left ventricular end-diastolic segment length (EDL) changes over time; EDL of the control segments increased progressively, but in marginal segments EDL was 12% below control and in the ischemic segments 30% below control by 4 weeks. Progressive increases in percent active shortening occurred in control segments; but holosystolic bulging was replaced by akinesia in ischemic segments, and persistent reduction in shortening was present in marginal segments at 4 weeks. Correlations were found between percent scar and reductions in percent shortening, EDL, and the ratio of change in diastolic length to change in diastolic pressure. These methods have detected hyperfunction in normal regions and variable segmental loss of contractile function, together with reduction of subendocardial dimensions and changes that may reflect decreased diastolic compliance in ischemic regions. We conclude that this model for the conscious animals may be useful for studying the influence of therapy on the extent of myocardial damage after experimental coronary occlusion.

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SUMMARY. To examine the interaction between normal and nonischemic areas of the left ventricle during acute ischemia, we implanted midwall ultrasonic segment length gauges in the ischemic zone and in nonischemic areas of the canine left ventricle. During acute ischemia, enddiastolic pressure and segment length in the nonischemic areas increased. There was no change from control in the segment length at the time of aortic valve opening and closure. Thus, in nonischemic areas, total segment shortening, as measured by the percent change in segment length from the time of end-diastole to aortic valve closure, increased. This was due to an increase in isovolumic shortening (end-diastole to aortic valve opening) with no change in ejection shortening (aortic valve opening to closure). The progressive increase in isovolumic shortening in nonischemic areas over time was directly paralleled by the progressive development of the isovolumic lengthening or bulge in the ischemic zone. Nonischemic areas, whether adjacent, on the opposite wall, or distant to the ischemic zone, all behaved similarly. Adrenergic blockade did not qualitatively alter these findings. We conclude that acute ischemia induces a mechanical disadvantage which is greater than just the loss of contractile function by the ischemic segment. Despite the apparent hyperfunction of nonischemic areas, the increased total segment shortening is expended in stretching the ischemic zone during isovolumic systole. As a result, there is no significant "compensatory' increase in ejection shortening in nonischemic areas. The results from the present study indicate that augmented total segment shortening in nonischemic areas is due ' to a combination of the Frank-Starling mechanism and regional intraventricular unloading of the nonischemic into the ischemic areas. (Circ Res 56: 351-358, 1985)