It is also involved in regulation of cell adhesion, vasoconstriction at sites of vessel-wall injury and stimulation of platelet aggregation.
This suggests that severe muscular hypertrophy without occlusive disease may be sufficient to produce irreversible pulmonary hypertension, possibly due to marked vasoconstriction.
Vasoconstriction follows, in response to factors released by these cells.
This, however, results in generalized vasoconstriction, sludging of blood cells in the microcirculation, and poor perfusion of the tissues.
The vasoconstriction caused by ergometrine involves mainly capacitance vessels, leading to increase in central venous pressure and blood pressure.
Nitric oxide alone, at least in this group of patients, does not unmask all the reversible vasoconstriction.
Evidence from recent clinical trials suggests that concerns about uteroplacental vasoconstriction caused by phenylephrine are unfounded and this is the authors' drug of choice.
First, ongoing perfusion of the placenta may cause continuous stimulation of production of vasoactive substances, which will tend to increase placental vasoconstriction.
