Regional ischemia in hypertrophic Langerdorff-perfused rat hearts

Myocardial hypertrophy decreases the muscle mass-to-vascularization ratio, thereby changing myocardial perfusion. The effect of these changes on myoca rdial oxygenation in hypertrophic Langendorff-perfused rat hearts was measu red using epimyocardial NADH videofluorimetry, whereby ischemic myocardium displays a high fluorescence intensity. Hypertrophic hearts, in contrast to control hearts, developed ischemic areas during oxygen-saturated Langendor ff perfusion. Reoxygenation of control hearts after a hypoxic episode resul ted in a swift decrease of fluorescence in a heterogeneous pattern of small , evenly dispersed, highly fluorescent patches. Identical patterns could be evoked by occluding capillaries with microspheres 5.9 mu m in diameter. Te n seconds after reoxygenation there were no more dysoxic areas, whereas reo xygenation in hypertrophic hearts showed larger ischemic areas that took si gnificantly longer to return to normoxic fluorescence intensities. Hypothes izing that the larger areas originate at a vascular level proximal to the c apillary network, we induced hypoxic patterns by embolizing control hearts with microspheres 9.8 and 15 mu m in diameter. The frequency distribution h istograms of these dysoxic surface areas matched those of hypertrophic hear ts and differed significantly from those of hearts embolized with 5.9-mu m microspheres. These results suggest the existence of areas in hypertrophic Langendorff-perfused hearts with suboptimal vascularization originating at the arteriolar and/or arterial level.