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Department of Pharmacology, Tulane University School of Medicine, New Orleans, Louisiana, 70112; and Nu-Med Inc., Hopkinton, New York 12940
The present study employed a new
right-heart catheterization technique to measure pulmonary arterial
pressure, pulmonary arterial wedge pressure, and pulmonary vascular
resistance in anesthetized intact-chest, spontaneously breathing mice.
Under fluoroscopic guidance, a specially designed catheter was inserted
via the right jugular vein and advanced to the main pulmonary artery.
Cardiac output was determined by the thermodilution technique, and
measured parameters were stable for periods of
3 h. Pressure-flow
curves in vivo were curvilinear, with mean pulmonary arterial pressure increasing more rapidly at low pulmonary blood flows of 5-10
ml/min and less rapidly at higher blood flow rates. The pressure-flow relationship was shifted to the left by the nitric oxide synthase inhibitor nitro-L-arginine methyl ester
(L-NAME) at higher blood flow
levels, whereas the cyclooxygenase inhibitor sodium meclofenamate was
without effect. The increase in pulmonary arterial pressure in response
to acute hypoxia (fractional inspired
O2 10%) was augmented by
L-NAME but unaltered by sodium
meclofenamate. The present results demonstrate that the right-heart
catheterization technique can be used to measure pulmonary vascular
pressures and responses in the mouse. This is, to our knowledge, the
first report of a right-heart catheterization technique to measure
pulmonary vascular pressures and responses in the intact-chest,
spontaneously breathing mouse and should prove useful for the
investigation of pulmonary vascular responses in transgenic mice.
cardiac output; pulmonary vascular bed; mouse; vascular resistance; pressure-flow relationship; acute hypoxia; nitric oxide
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