C. Melot et al., STARLING RESISTOR VS, DISTENSIBLE VESSEL MODELS FOR EMBOLIC PULMONARY-HYPERTENSION, American journal of physiology. Heart and circulatory physiology, 37(2), 1995, pp. 817-827
We investigated whether the Starling resistor model (Mitzner et al. J.
Appl. Physiol. 51: 1065-1071, 1981) or a distensible vessel model (Ha
worth et al. J. Appl. Physiol. 70: 15-26, 1998) best describes pulmona
ry vascular pressure-flow (Q) relationships in embolic pulmonary hyper
tension. Mean pulmonary arterial pressure (P-pa)-Q plots at constant l
eft atrial pressure (P-la) and P-pa-P-la plots at constant Q were inve
stigated in seven dogs before and after 500-mu m glass bead pulmonary
embolism. Embolization to a mean angiographic obstruction of 78% incre
ased the slope and extrapolated pressure intercept (P-i) of P-pa-Q plo
ts 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 similar to 1:
1. The Starling resistor and the distensible vessel model provided a r
easonably good fit to the P-pa-Q and P-pa-P-la coordinates before and
after embolism. However, contrary to the prediction of the Starling re
sistor model, no correlation was found between the inflection point of
P-pa-P-la plots and P-i. We therefore conclude that an increased clos
ing pressure is unlikely to contribute to embolic pulmonary hypertensi
on.