The bronchial circulation is poorly accessible and dwarfed in size by the pulmonary vasculature. Studies highlighting the unique attributes of the bronchial endothelium are few in number and represent a contemporary work-in-progress. Despite the current paucity of information regarding bronchial endothelial phenotypes, it has long been recognized that bronchial vessels undergo structural changes in pathological states. Most notable among these changes are dilation, neovascularization, and contribution to bronchial mucosal swelling.

Perhaps the first documentation of disease-associated bronchial neovascularization (hence, bronchial endothelial proliferation) is found in one of Leonardo da Vinci's anatomical drawings (circa 1513 A.D.) (Figure 127.1). Close scrutiny of a tuberculous cavity in a terminal lung unit shows bronchial vessels supplying the walls of the cavity. Whether da Vinci used artistic license in his depiction of the vasculature has been argued over the years (1).

In 1847, Rudolph Virchow demonstrated an association between chronic pulmonary artery obstruction and a proliferative bronchial phenotype (2). He interpreted these studies to suggest pulmonary vascular ischemia leads to compensatory recruitment of systemic bronchial vessels to ischemic regions. Others more recently have speculated that obstruction of even small pulmonary vessels (e.g., within a tuberculous cavity) is sufficient to induce proliferation of bronchial vessels (3).

In his original textbook (1892), Sir William Osler noted that during an asthma attack “the hyperaemia and swelling of the mucosa … explain well the hindrance to inspiration and expiration” (4). Although mechanisms regulating endothelial cell (EC) barrier function were not known at the time, the clinical consequences certainly were.