Is profound inhibition of myogenic tone in rat cardiac allografts due to eNOS- and iNOS-based nitric oxide and an intrinsic defect in vascular smooth muscle contraction?
Our data indicate that the profound inhibition of myogenic tone in allograft arteries involves direct vasodilation by eNOS- and iNOS-based NO, as well as an intrinsic defect in vascular smooth muscle contraction. The hemodynamic profile resulting from these changes in allograft resistance vessel function would favor movement of extracellular fluid from the intravascular space into the myocardial interstitium, resulting in edema, increased ventricular stiffness, and poor ventricular performance.
Clinical examination appears undervalued by those assessing injured children and is poorly recorded. Radiography can be used more selectively. Initial assessment using a single lateral projection can be followed in doubtful cases by cross sectional imaging.