Pulmonary artery constriction produces a greater right ventricular dynamic afterload than lung microvascular injury in the open chest dog.

Abstract

SUMMARY. Investigators model noncardiogenic pulmonary hypertension by constricting the pulmonary artery to increase right ventricular afterload. To investigate this model's validity, we compared the right ventricular afterload, quantified as pulmonary input impedance, created by constricting the pulmonary artery and by inducing a pulmonary microvascular injury (with glass beads infused into the pulmonary circulation). The pulmonary injury constriction produced a different right ventricular afterload than the microvascular injury. The constriction increased both the input resistance and the characteristic impedance. Mircrovascular injury increased only input resistance. Physiological levels of lung inflation did not influence pulmonary impedance, but lung hyperinflation increased input resistance both before and while constricting the pulmonary artery or after producing microvascular injury. Total right ventricular power output and stroke work were unchanged during each vascular intervention. Pulmonary artery constriction did not affect power output distribution, whereas microvascular injury decreased oscillatory power and its relative contribution to total power. Lung hyperinflation dramatically reduced right ventricular power and left ventricular stroke work. These effects appeared mediated by right ventricular afterload increase uncompensated for by right ventricular preload increase. These observations help explain the hemodynamic consequences of acute pulmonary hypertension and the effects of lung hyperinflation with positive end-expiratory pressure respiration in such patients. (Circ Res 56: 40-56, 1985)

Pulmonary artery smooth muscle activation attenuates arterial dysfunction during acute pulmonary hypertension

“…Several authors found an increase in Z C during acute PH induced by an abrupt proximal obstruction of the pulmonary arterial tree. This effect mainly results from the reflected waves that come back during systole (before closure of the pulmonary valve) and thus directly oppose blood ejection during ventricular contraction (11,15,16,23,26,39). On the other hand, previous studies of acute PH induced by lung injuries, such as the injection of small (150 -200 m) glass spheres (11,16,23,27), injury with oleic acid (11,29), and during autologous blood clot embolism (23), reported an increase in peripheral resistance, with either stable or decreased Z C .…”

A new experimental model of ARDS and pulmonary hypertension in the dog

“…This is in conlrast 10 Ihc finding of Malik , who did not measure any change in PAP and PVR oncc peak levels had been reached [281. Thc reasons for this discrepancy are not c1ear because the experimental settings have basieally been the same (dogs.…”

“…Thus, the typical elinical symptoms of ARDS [2) were prescnt in our model. The relatively high VofVTof 51% at control see ms 10 be valid: standard techniques have been used for ils detcnnination and similar values have been demonstratcd by others in anesthctized and ventilated dogs as weil as in baboons [11 , 18J. 11 is difficuh to assess to what extent either OA or GB contribuled to the pathological changes in lung funClion. Using l00}.lm GS alone in nonheparinized dogs at a Fi0 2 of 1.0. no diSlurbances of gas exchange have been fou nd in our own pilot experiments.…”

“…The techniques used indude pulmonary microembolization (e.g., g1ass beads (5,22,26,28], fat emboli [4] , oleie acid [3 , 12, 19, 40] , stareh granules [9J, alpha-naphthyl-thiourea (ANTU) [21], blood dots {39] , air [40], barium sulfate [25]) and the intraveflous (thrombin [1 , 27], bacteria [8 , 38], endotoxin [7 , 15], lycopodium spores [13], heroin , alloxan , pyrroles [21]) , intratracheal (ozone [34] , Hel [16] , papain [30]) or intraperitoneal (ammonium sulfate [21]) administration of agents. Most oCten PAH was induced by constriction or OCclflSioli of the pulmonary artery (10,32].…”

“…By developing and characterizing an aeute animal model , we tried tO encompass the clinical features of both ARDS and PAH as closely as possible in order 10 aHow for evaluation of cardiac function under these conditions.…”