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Am J Physiol Regul Integr Comp Physiol 294: R1554-R1562, 2008. First published February 20, 2008; doi:10.1152/ajpregu.00743.2007
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DEVELOPMENTAL PHYSIOLOGY AND PREGNANCY

Simultaneous pulmonary trunk and pulmonary arterial wave intensity analysis in fetal lambs: evidence for cyclical, midsystolic pulmonary vasoconstriction

Joseph J. Smolich,1,2 Jonathan P. Mynard,1,2 and Daniel J. Penny1,2,3

1Australia and New Zealand Children's Heart Research Centre, Murdoch Children's Research Institute; and 2Department of Paediatrics, University of Melbourne and 3Department of Cardiology, Royal Children's Hospital, Melbourne, Australia

Submitted 14 October 2007 ; accepted in final form 18 February 2008

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 midsystolic fall in LPA U to near-zero was related to an extremely prominent midsystolic backward compression wave (BCWms) that arose ~5 cm distal to the LPA, was threefold 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 midsystolic 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.

fetal pulmonary vascular interaction; fetal pulmonary blood flow; fetal pulmonary blood pressure



Address for reprint requests and other correspondence: J. J. Smolich, Dept. of Cardiology, Royal Children's Hospital, Flemington Road, Parkville, Victoria, Australia, 3052 (e-mail: joe.smolich{at}mcri.edu.au)







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