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In contrast to a close relation between hydrostatic pressure and EVLW in cardiac tamponade, hydrostatic pressure was not a determinant of pulmonary edema during the reperfusion period after myocardial ischemia.

The importance of the mitral apparatus to the left ventricular function has been suggested in several clinical studies of mitral valve replacement [1][2][3][4][5][6]. These studies showed that mitral valve replacement with chordal transsection depressed postoperative ejection performance compared with mitral valve replacement with chordal preservation. Although the exact mechanism of the global depression of function observed after chordal transsection remains unclear, most evidence pointed to a local depression of function near the papillary muscle. Takayama et al. [7] reported that sectioning of the chordae tendineae led to a systolic bulge in the area of the papillary muscle. However, enhanced circumferential shortening and wall thickening in the myocardium overlying the papillary muscle insertion site were also found after chordal transsection in that study. These results indicated that the depressed ventricular function after chordal transsection was due to heterogeneity of regional wall motion at this site and speculated that regional myocardial fibers at this site were loaded by chordal tension.We hypothesized that circumferential shortening at the papillary muscle insertion site with intact mitral apparatus would be different from that at the free wall in the same axis hoop. This difference might be enhanced with increased left ventricular pressure because of change of afterload. In this present study using ultrasound crystal techniques, we investigated the difference of circumferential shortening between free wall (FREE) and papillary muscle insertion site (PAP). Key words: pressure-length relation, afterload, function of papillary muscle insertion site. Abstract:The importance of the mitral apparatus to the global left ventricular (LV) function has been suggested in several clinical studies. One recent study reported that chordal transsection induced an unloading of myocardium at the papillary muscle insertion site. We hypothesized that the regional response for afterloading at this site with intact mitral apparatus was different from that at the free wall. We investigated the endsystolic pressure-regional segment length relations (ESPLR) in two anterior LV sites, free wall (FREE) and the papillary muscle insertion site (PAP), during an increasing afterload by aortic occlusion in 7 anesthetized open-chest dogs. To measure the regional segment length at FREE and PAP, two sets of the pair of sonomicrometer crystals were implanted in the same midwall depth at the same circumferential hoop by using an echocardiographic guide. ESPLR both at FREE and PAP were always highly linear in a physiological range (r Ն0.9). The slope of this relation at FREE (274Ϯ164 mmHg/mm) was significantly steeper than that at PAP (157Ϯ 118 mmHg/mm) for each dog (pϽ0.05). These data indicate that the regional response for afterloading at PAP loaded by chordal tension is different from that at FREE in the same heart.

Platelet-activating factor (PAF), one of the harmful substances released after coronary reperfusion, has been reported to increase pulmonary vascular permeability and induce pulmonary edema. In this study, we sought to examine the possible role of PAF in the genesis of pulmonary edema after coronary reperfusion. Extravascular lung water (EVLW) was measured by the thermal-dye double indicator dilution method during coronary ligation and after reperfusion in situ in dogs. The proximal left anterior descending coronary artery was occluded for 15 min and reperfused in 5 dogs (group 1), while five other dogs (group 2) were treated with PAF-antagonist (TCV-309, 1 mg/kg) before coronary artery occlusion. EVLW and hemodynamic indices were measured at baseline, 15 min of coronary occlusion, and 15 and 30 min after coronary reperfusion. EVLW increased at 15 min of coronary occlusion in both groups, but there was no significant difference between the two groups (6.4 to 10.3 ml/kg and 5.4 to 7.1 ml/kg in groups 1 and 2, respectively). After coronary reperfusion, EVLW increased further in group 1 (6.4 to 16.5 ml/kg, p < 0.01), but no further increase was observed in group 2 at 30 min after coronary reperfusion. There were no significant differences in hemodynamic indices between the two groups throughout the test. Thus, PAF-antagonist attenuated the increase in EVLW after coronary reperfusion independent of hemodynamic indices, and hence, PAF may play an important role in the genesis of pulmonary edema caused by coronary reperfusion.