Lanthanum staining of coronary microvascular endothelium: Effects of ischemia reperfusion, propranolol, and atenolol

Cat isolated hearts were perfused via the aorta with normothermic arterial blood from donor cats. After 1 hr of equilibration, dl-propranolol (1.9 mg/kg), atenolol (1.65 mg/kg), or physiological saline solution was infused via the aortic cannula. The hearts were made globally ischemic for 1 hr and reperfused for 1 hr. Hearts given saline but not made ischemic, and hearts from blood-donor cats served as controls. The hearts were flushed with physiological saline for 2 min, then perfused with cacodylate-buffered glutaraldehyde containing 1% LaCl 3. Samples of left ventricle were postfixed in osmium and prepared for electron microscopy. Microvessels in nonischemic tissues had heavy La 3+ staining on luminal surfaces of endothelial cells. Many plasmalemmal vesicles along luminal surfaces of endothelial cells were filled with La 3+. Several vesicles appeared to open onto both surfaces thus forming channels through the endothelium. Lanthanum penetrated into, and occasionally through, interendothelial junctions. Endothelial cells lining vessels in ischemic myocardium were swollen, had pale cytoplasm, and showed little La 3+ on the luminal surfaces. Few plasmalemmal vesicles were present and the mitochondria contained deposits of La 3+. Extravascular spaces were distended but interendothelial junctions seemed to be intact. Lanthanum staining and morphology of endothelial cells in hearts treated with propranolol or atenolol were very similar to nonischemic myocardium. The data suggest that the β-blocking agents, propranolol and atenolol, maintain the integrity of coronary vascular endothelium during ischemia.