Starling resistor vs. distensible vessel models for embolic pulmonary hypertension
Mélot, C.; Delcroix, M.; Closset, J.; Vanderhoeft, P.; Lejeune, P.; Leeman, M.; Naeije, R.
American Journal of Physiology 268(2 Pt 2): H817-H827
1995
ISSN/ISBN: 0002-9513 PMID: 7864209 Document Number: 449560
We investigated whether the Starling resistor model (Mitzner et al. J. Appl. Physiol. 51: 1065-1071, 1981) or a distensible vessel model (Haworth et al. J. Appl. Physiol. 70: 15-26, 1991) best describes pulmonary vascular pressure-flow ( ovrhdot Q) relationships in embolic pulmonary hypertension. Mean pulmonary arterial pressure (P-pa)- ovrhdot Q plots at constant left atrial pressure (P-la) and P-pa-P-la plots at constant ovrhdot Q were investigated in seven dogs before and after 500-mu-m glass bead pulmonary embolism. Embolization to a mean angiographic obstruction of 78% increased the slope and extrapolated pressure intercept (P-i) of P-pa- ovrhdot Q plots and increased the inflection point of P-pa-P-la plots, above which an increase in P-la is transmitted to P-pa in a ratio of apprx 1:1. The Starling resistor and the distensible vessel model provided a reasonably good fit to the P-pa- ovrhdot Q and P-pa-P-la coordinates before and after embolism. However, contrary to the prediction of the Starling resistor model, no correlation was found between the inflection point of P-pa-P-la plots and P-i. We therefore conclude that an increased closing pressure is unlikely to contribute to embolic pulmonary hypertension.