Comparison of the effects of isoflurane with those of propofol on pulmonary vascular impedance in experimental embolic pulmonary hypertension

Abstract

Inhaled but not i.v. anaesthetics are reported to decrease pulmonary vascular resistance. The aim of this study was to compare the effects of isoflurane with those of propofol on the interaction between right ventricular (RV) function and the pulmonary vascular system in embolic pulmonary hypertension. Nine dogs received in random sequence propofol 18 mg kg-1 h-1 and 1.4% end-tidal isoflurane. Pulmonary haemodynamic state was evaluated by pulmonary arterial pressure/flow (PAP/Q) plots and pulmonary vascular impedance (PVZ) spectra. Right ventricular function was assessed by total hydraulic power (Wtot), ratio of oscillatory power (Wosc) to Wtot, and dP/dtmax. Measurements were obtained, with both anaesthetics, before and after pulmonary embolic hypertension induced by autologous blood clots. Embolism increased PAP, 0 Hz and low frequency input impedance, displaced first minimum of PAP/Q moduli and zero crossing of phase to higher frequencies, decreased characteristic impedance, decreased Wosc/Wtot without affecting Wtot, and increased dP/dtmax. Compared with propofol, isoflurane at baseline did not affect PAP/Q plots, PVZ or hydraulic power data, but decreased dP/dtmax. After embolism, isoflurane shifted PAP/Q plots to lower PAP without affecting PVZ, did not affect hydraulic power data and decreased dP/dtmax. We conclude that in canine embolic pulmonary hypertension, isoflurane compared with propofol impeded RV vascular coupling caused by decreased RV contractility, while after-load remained unchanged despite some decrease in pulmonary vascular tone.

Pulmonary Vascular Resistance and Impedance in Isolated Mouse Lungs: Effects of Pulmonary Emboli

“…The existence of a maximum at 0 Hz followed by a minimum and fluctuations at higher frequencies is the classic pulmonary vascular impedance pattern, and is consistent with many other studies in animals and humans. 8,16,18,20,26,30,32 After embolization, Z 0 increased significantly compared to baseline. This increase represents the increased opposition to mean flow through the pulmonary vascular system due to the microsphere emboli.…”

“…In the healthy lungs of dogs, minipigs, and humans, f min is in the 2-4 Hz range 18,20 whereas after embolization in dogs and minipigs, f min shifts to 5-12 Hz. 7,8,18,22 This increase in f min with embolization is due to a more proximal location of the major reflecting sites in the pulmonary arteries. 7 The increase in calculated index of wave reflection with embolization, which also has been shown to occur in larger animal models, 8,18 is consistent with a more proximal location of the major reflecting sites.…”

“…For example, Z C in dog lungs decreased after pulmonary embolization with 0.5 mm or 100 µm glass beads or autologous blood clots. 8,18,22,26,32 However, in species with higher pulmonary vascular reactivity such as pigs and goats, Z C increased. 18,32 Others have suggested that this species-dependency of Z C is due to passive vessel distension, the capacity for which is species dependent.…”

“…15,20,21 In particular, resistance and impedance have been measured in animal models such as rats, dogs, goats, and pigs. 8,11,18,22,32 To our knowledge, the effects of pulmonary hypertension on pulsatile pressure-flow rate relationships in mice have not been investigated.…”

Physiologic Changes In A Non-Human Primate Model Of HIV-Associated Pulmonary Arterial Hypertension

“…Second, pulmonary pressure measurements were not available in our control animals used for radiologic analyses, so we were unable to perform correlation studies. Third, we saw relatively low pressures in both uninfected and infected cynomolgus and rhesus macaques, which may be an attribute of these species or an effect of the inhaled anesthetic used in the procedure (37,38). In addition, the SHIV 89.6P infection of CMs results in a rapid depletion of peripheral blood CD4…”