Effects of high-dose XXXX on the pulmonary circulation.

@entity1667 @entity1 @entity3952 @entity742 @entity101 @entity548 @entity235 @entity649 @entity4 @entity35 @entity1808 @entity1426 @entity288 @entity519 @entity112 @entity230 @entity551 @entity616 @entity479
A major controversy in the treatment of the @entity649 ( @entity649 ) is the role of @entity230 , which may attenuate permeability as well as pulmonary vascular resistance (PVR). Empirically @entity1667 (MP) in high doses (30 mg/kg) has been "the @entity479 of choice" in clinical practice. By autoradiography MP has been shown to penetrate more easily into lung tissue than other @entity230 tested. MP prevented the late phase increase in lung vascular permeability to endotoxin in @entity742 , whereas the inhibition of the pulmonary @entity101 response was far less pronounced. In @entity1 septic @entity649 MP reduced both PVR and the increased vascular permeability. However, a few @entity1 characterized by more severe @entity649 did not respond to MP. There is some evidence that @entity230 may modulate both pre- and postcapillary vasomotion in the lungs. MP was found to inhibit pulmonary venoconstriction as well as pulmonary erythrocyte sludging in @entity235 @entity548 . @entity3952 induced @entity4 also appears to be attenuated by MP. This effect is partly due to a lowering of hydrostatic pressure in the lung capillaries, because @entity616 the downstream resistance increase. @entity519 pulmonary vasoconstriction has predominantly a precapillary localisation. MP inhibits @entity519 vasoconstriction in a dose-dependent fashion in isolated @entity35 lungs, but does not cause a general dampening of vascular reactivity, as the pulmonary constrictor response to @entity1808 is unchanged. However, MP inhibits @entity112 -induced vasoconstriction in isolated @entity235 lung lobes. The increased vascular resistance in atelectatic lungs is also inhibited by MP. @entity288 may alter the reaction of the pulmonary vasculature to various stimuli or agents by influencing the release of mediators, for instance, the cyclooxygenase and lipoxygenase products of @entity1426 , modulate the action of mediators, reducing the activation of leukocytes and/or platelets, or changing the state of the pulmonary vascular muscle cells. Which mechanisms are active in the various situations are at present objects of pure speculation. However, in most situations with @entity649 a @entity551 and PVR may be regarded as beneficial.
