Submitted on October 14, 2007
Accepted on February 18, 2008
Simultaneous pulmonary trunk and pulmonary arterial wave intensity analysis in fetal lambs: evidence for cyclical, mid-systolic pulmonary vasoconstriction
Joseph J Smolich1*, Jonathan P Mynard2, and Daniel J Penny3
1 Australia & New Zealand Children's Heart Research Centre, Murdoch Children's Research Institute, Flemington Road, Parkville, Victoria, 3052, Australia; Department of Paediatrics, University of Melbourne, Parkville, Victoria, Australia
2 Australia and New Zealand Children's Heart Research Centre, Murdoch Children's Research Institute, Melbourne, Victoria, Australia
3 Australia and New Zealand Children's Heart Research Centre, Murdoch Children's Research Institute, Melbourne, Victoria, Australia; Department of Paediatrics, University of Melbourne, Parkville, Victoria, Australia
* To whom correspondence should be addressed. E-mail: joe.smolich{at}mcri.edu.au.
The physiological basis of a characteristically low blood flow to the fetal lungs is incompletely understood. To determine the potential role of pulmonary vascular interaction in this phenomenon, simultaneous wave intensity analysis (WIA) was performed in the pulmonary trunk (PT) and left pulmonary artery (LPA) of 10 anesthetized late-gestation fetal sheep instrumented with PT and LPA micromanometer catheters to measure pressure (P) and transit-time flow probes to obtain blood velocity (U). Studies were performed at rest and during brief complete occlusion of the ductus arteriosus to augment pulmonary vasoconstriction (n=4) or main pulmonary artery to abolish wave transmission from the lungs (n=3). Wave intensity (dIW) was calculated as the product of the P and U rates of change. Forward and backward components of dIW were determined after calculation of wave speed. PT and LPA WIA displayed an early-systolic forward compression wave (FCWis) increasing P and U, and a late-systolic forward expansion wave decreasing P and U. However, a marked mid-systolic fall in LPA U to near-zero was related to an extremely prominent mid-systolic backward compression wave (BCWms) that arose 
5 cm distal to the LPA, was 3-fold larger than the PT BCWms (P<0.001), of similar size to FCWis at rest (P>0.6), larger than FCWis following ductal occlusion (P<0.05) and abolished after main pulmonary artery occlusion. These findings suggest that the absence of pulmonary arterial mid-systolic forward flow which accompanies a low fetal lung blood flow is due to a BCWms generated in part by cyclical vasoconstriction within the pulmonary microcirculation.
