Airway microvasculature

Nedocromil inhibits the development of early and late bronchoconstriction responses to inhaled antigen. The development of airway hyperresponsiveness to nonspecific bronchoconstrictors was also inhibited in airway microvasculature leakage. Nedocromil is bound to plasma proteins to the extent of 89%, is not metabolized, and is excreted unchanged. 

As discussed in Section 3.3, few histopathological studies of asthma have focused specifically on the microvasculature. Nonetheless, there is evidence that neovascularization is one of the changes in the airways of asthmatics (Kuwano et al., 1991). This observation in potentially important because newly formed blood vessels may be abnormally leaky (Schoefl, 1967) or abnormally responsive to inflammatory mediators (McDonald, 1992). The plasma leakage that occurs in the airway mucosa of asthmatics could result from the heightened response of the mucosal blood vessels to inflammatory mediators. 

Microvasculature [37] peritonitis [38,53] dermal inflammation [28,39,40,53] intestinal inflammation [41,45,54] acute inflammation [42] blood [43] periodontal disease [44,51] airway inflammation [48] glomerulonephritis [35] renal ischemia reperfusion [49,61] bone loss [51] cystic fibrosis [55,56] acute lung injury [57,62] asthma [58] corneal wound heahng [59] vascular inflammation [60] rheumatoid arthritis [63]. 

---