But a crisis loomed.
As E-1173 made its return journey, now a tired, deoxygenated blue, it entered the renal circulation. The kidney was a master of . Blood pressure forced plasma through the glomerulus, but E-1173 was too large to pass. It tumbled through the vasa recta, past the loop of Henle, where countercurrent multiplication was busy concentrating urine. Suddenly, the vessel ruptured. A microscopic tear in the arteriole wall.
E-1173, however, was trapped and doomed. A macrophage, the tissue’s resident sentinel, engulfed it in a quiet act of . The heme group was broken down into biliverdin, then bilirubin, which the liver would eventually excrete in bile. The iron atom was carefully saved, bound to transferrin, and shipped back to the bone marrow to build a new red blood cell.
E-1173’s first challenge was to leave the marrow. It squeezed, deforming its flexible membrane (a property called ) through a tiny pore in the sinusoidal wall. It was now adrift in a raging river: the venous bloodstream. The current was driven by the right ventricle of the heart, a four-chambered marvel of hemodynamics . E-1173 was swept through the vena cava, into the right atrium, through the tricuspid valve, and into the right ventricle. With a coordinated electrical impulse from the sinoatrial node—a cardiac action potential —the ventricle contracted. Lub . E-1173 was shot through the pulmonary artery toward the lungs.