Effects of acute ischemia on the normal and hypertrophied left ventricle

In the last 30 years, myocardial hypertrophy and congestive heart failure have been among the main causes of circulatory disorders in clinical practice. Therefore, a great effort has been payed in the research of the underlying causes of these diseases and in the nature of their structural and functional changes. The majority of this research work done until now has been mainly oriented towards hypertensive hypertrophy (O’Keefe et al, 1978 ; Bache et al., 1981a-b, 1984 ; Marcus et al., 1983 ; Laskey et al, 1983), whereas the volume-overload hypertrophy has not been fully-covered, in particular when accompanied by myocardial infarction.
This work is therefore oriented to study the volume-overload hypertrophy and its repercussion on the circulation. Many scientists (LeWinter et al., 1980; Grossman Et al., 1980; Badke et al., 1981; Fujisawa et al., 1984; Sasayama et al., 1985) reported that in the presence of an increase in diastolic load imposed on the left ventricle, e.g. by an arteriovenous communication, an adequate stroke volume could be preserved by the progressive augmentation of the end-diastolic volume until the maximum length of the myofibrils of 2.2 μ is obtained (Ross et al., 1971). This process of ventricular enlargement is not a simple mechanism; it is mostly achieved by an addition of new sarcomeres in series, together with progressive and moderate muscle hypertrophy. Such changes in ventricular volume not only result in a new pressure-volume relationship but also modify the relations between myocardial cells and coronary perfusion. The viability of the heart is indeed dependent on its supply of oxygen and substrates through a complex network of coronary vessels; this sophisticated system for blood supply can be modified by the process of the hypertrophy. In this respect, many questions are still opens such as : a- does the increase in capillary density equilibrate the increase in muscle mass ? b does the increase in capillary-cell distance influence the myocardial oxygen supply? c- does the increase in left ventricular end-diastolic pressure which accompanies the volume-overload hypertrophy decrease the subendocardial myocardial perfusion?
For these reasons, an important part of this study on a canine model of volume-overload hypertrophy was planned to test the relations between myocardial perfusion and function under resting conditions, during inotropic stimulation as well as during acute ischemia followed by reperfusion