In isolated rabbit hearts, intramyocardial pressure is primarily determined by the stretching of tissues surrounding interstitial spaces rather than left ventricular cavity pressure itself.
OBJECTIVE: Since muscles, vessels and interstitial spaces are in close physical proximity in the heart wall, interstitial (i.e., intramyocardial) pressure (IMP) should be affected by the stresses of the vessels and/or the muscular tissue surrounding the interstitial spaces. Thus, we tested the hypothesis that increasing the stresses (or stiffness) of the surrounding tissues by muscle contraction or stretching--produced externally by stretching the LV cavity or internally by increasing coronary perfusion pressure--has a greater effect than LV cavity pressure per se on IMP. METHODS: In isolated rabbit hearts we measured IMP with small (< 10 microns diam) glass micropipettes while stretching the vessels (by changing coronary perfusion pressure) and the wall (by inflating a balloon in the left ventricle) during the passive state as well as during barium contracture. RESULTS: With LV cavity pressure equal to 0 (balloon open to air) or equal to 30 mmHg, a 20 mmHg increase in perfusion pressure increased IMP by 3.6 and 5 mmHg, respectively, in the passive state and by 7.6 and 7.9 mmHg, respectively, in the contracted state. This 30 mmHg increase in LV pressure produced a significant but small (3-5 mmHg) increase in IMP in the passive state but no effect in the contracture state. CONCLUSIONS: These results can be explained by a unifying concept in which stretching of the tissues surrounding the intestinal spaces--produced externally by increasing ventricular cavity size or internally by pressurizing vessels--but not LV cavity pressure per se is the major determinant of IMP.
Frank C. P. Yin (Thu,) studied this question.
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