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

Abstract

Summary. The aim of (his study was to establish a stable and reproducible model of pulmonary artery hypertension with concomitant A RDS-Iike changes o f lung fun ction and lung morphology. In eight anesthetized and ventilated dogs, 0.01 mVkg oleic acid (OA) was given i. v. fo llowed by repetitive injections of 100 J1m glass beads (OB) ioto the right atrium until a mean pulmonary artery pressure of 35~40 mm Hg was reached. Mean fight ventricular (R VP) and pulmonary artery (PA P) pressures, pulmonary vascular resistance (PVR), lung compliance and resistance, Pa0 2, intrapulmonary shunt and colloidosmotic pressure (COP) were c10sely mo nitored for 150min . PAP, RVP, and PVR considerably inereased subsequent 10 O Al GB injection, and slabilized at a high level within 70min , showing only a minimal decrease (PAP, RVP) ur no change (PVR) during the following 8O min . A signifieant decrease of Pa02 and pulmonary eomplianee as weil as an inerease o f resistance and intrapulmonary shunt were found as early as 30 min after the last embolization and they remained unchanged for 120 min . Reduction of COP suggested transcapiUary leakage of maeromoleeules. Histology revealed an interstitial and intraalveolar edema. We conclude that the eombined injeetion of oleie aeid and glass beads provokes microvascul ar Jung injury and results in stable pulmo nary artery hypertensio n wirh concomitant ARDS-like ehanges of lung funetion. Thus, an aeute mode l is provided in the dog allowing for the study of eardiac funetion in ARDS complicated by pulmo nary artery hypertension.

Flow-controlled expiration: a novel ventilation mode to attenuate experimental porcine lung injury

“…27 It might cause structural disruptions in the hydrophobic lipid bilayer core, and disturb membrane fluidity and lipid-protein interactions. 28 Comparable Pa O 2 /FI O 2 ratios in both groups throughout the observation period are indicative of comparable and sustained lung injury.…”

Acute pulmonary microembolism induces different regional changes in preload and contraction pattern in canine right ventricle

“…Thereafter, embolisation continued and was terminated when mean pulmonary artery pressure had reached a peak level of -40 mm Hg. 19 A third set of measurements was obtained 10 min after the end of acute pulmonary microembolisation (APME2).…”

Overview of the Pathology of Three Widely Used Animal Models of Acute Lung Injury

“…The widely adopted dose of OA falls in the range of 0.06-0.15 ml/kg, which is mixed thoroughly with 15-20 ml of normal saline solution and injected slowly within 20-30 min [6,[26][27][28][29] , targeting a PaO 2 / FIO 2 ratio of 80-120 mm Hg. Sometimes a dose as small as 0.01 ml/kg [30] is used to produce a very slight lung injury or a dose as high as 0.3 ml/kg [31] is applied to achieve a quite severe lung injury. Apart from the normal saline, pure or high concentration of ethanol [32,33] or freshly drawn arterial blood [34][35][36] has been used as the dilution liquid for OA.…”