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  • Title: Transcapillary exchange of indium 111-labeled anticardiac myosin Fab and thallium 201 in isolated reperfused rabbit hearts.
    Author: Meerdink DJ, Leppo JA.
    Journal: J Nucl Cardiol; 1994; 1(3):236-45. PubMed ID: 9420706.
    Abstract:
    BACKGROUND: The physiologic mechanisms of 111In-labeled anticardiac myosin antibody [111In]-AM) imaging are fairly well established. However, to better understand the transcapillary exchange characteristics of normal and reperfused myocardium, a standard first-pass, indicator-dilution analysis was undertaken in hearts subjected to global no-flow and low-flow ischemia. METHODS AND RESULTS: The first-pass myocardial transport of 201Tl and [111In]-AM was evaluated in an in vitro rabbit model of no-flow ischemia/reperfusion with indicator-dilution analysis during normal and ischemic flows and whole-blood perfusate. The maximum extraction fraction (Emax) of 201Tl was dominated by flow rate as expected and averaged 0.75 (+/- 0.009) and 0.57 (+/- 0.008) during ischemic and normal flows, respectively (p < 0.01). Emax values for [111In]-AM, which were 0.02 or less in all hearts at control, increased to 0.06 or greater at moderate to longer perfusion times after 50 or more minutes of no-flow ischemia. Permeability surface area (in milliliters per minute per gram) tended to decline for 201Tl with longer reperfusion periods in both ischemic and normal flow groups and paralleled the changes observed for Emax for [111In]-AM. CONCLUSIONS: These data demonstrate that the first-pass extraction of [111In]-AM is quite low in this model of acute coronary occlusion and reflow and enhanced only in severe ischemia-reperfusion treatment. Therefore in this model there appears to be no significant [111In]-AM uptake in either normal or mildly ischemic myocardium. Consequently, [111In]-AM uptake into myocardium must depend on tracer recirculation, as well as sarcolemmal cell wall disruption, to achieve specific and sufficient [111In]-AM uptake for localization of clinical imaging.
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