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Ann Thorac Surg 1994;57:151-156
© 1994 The Society of Thoracic Surgeons
First Department of Surgery, Osaka University Medical School, Osaka, Japan
Accepted for publication February 25, 1993.
* Address reprint requests to Dr Matsuwaka, First Department of Surgery, Osaka University Medical School, 2-2, Yamadaoka, Suita, 565, Osaka, Japan.
To determine the effect of ischemia and reperfusion on left ventricular systolic function, we studied the ischemia-induced rightward shift of the ventricular pressure-volume relationship. Eight mongrel dogs were intubated, and their hearts were exposed through a thoracotomy. A conductance catheter and micromanometer were used to obtain instantaneous left ventricular pressure-volume data. The dogs were subjected to 20 minutes of normothermic global myocardial ischemia, followed by 80 minutes of reperfusion under total cardiopulmonary bypass. Data were acquired during transient (10- to 12-second) periods of acute volume loading before ischemia and at 20-minute intervals during reperfusion as bypass was continued. The relationship between stroke work and end-diastolic volume (ie, preioad recruitable stroke work [PRSW]) and the end-systolic pressure-volume relationship were highly linear throughout the study (mean r = 0.954 to 0.983 for PRSW; mean r = 0.954 to 0.984 for end-systolic pressure-volume relationship). Ischemia produced changes in the PRSW; (1) the slope decreased significantly at 20 minutes and 40 minutes of reperfusion then returned to preischemic levels at 60 minutes and 80 minutes, and (2) the x-intercept increased significantly up to 60 minutes. The preload recruitable work area (the area under the linear regression line of PRSW) reflected changes in both slope and x-intercept of PRSW and was significantly decreased throughout the 80 minutes of reperfusion despite gradual recovery. The slope and the x-intercept of the endsystolic pressure-volume relationship did not change after ischemia. These results indicate that systolic dysfunction, defined as preload recruitable work area, is related to the rightward shift of the ventricular pressure-volume relationship and that systolic dysfunction may be present, even when the slopes of both PRSW and the end-systolic pressure-volume relationship have recovered.
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