Hemodynamic, sympathetic and angiotensin II responses to PEEP ventilation before and during administration of isoflurane.

Abstract

Positive end-expiratory pressure (PEEP) ventilation and isoflurane anesthesia may opposingly affect the sympathetic nervous and renin-angiotensin systems. This study was performed to elucidate the modulatory effects of isoflurane anesthesia on the neurohumoral and cardiovascular responses to PEEP. Renin-angiotensin and sympathetic nervous activity were investigated in mechanically ventilated, normovolemic, chloralose anesthetized pigs before and during administration of 1.4% isoflurane. Arterial angiotensin II (AII) concentrations were measured and systemic, mesenteric, hepatic and renal spillover of norepinephrine (NE-SO) were calculated using isotope dilution. Regional hemodynamic variables were investigated in parallel. PEEP10 alone moderately elevated AII levels (+12.5 +/- 4.9 pg/ml, P < 0.05) and increased systemic (+22 +/- 2.9 pmol.min.100 g-1, P < 0.05) and notably mesenteric (+32 +/- 9.6 pmol.min.100 g-1, P < 0.05) NE-SO. Blood flow decreased in all vascular beds studied. Except for in the liver, isoflurane generally reduced NE-SO compared to baseline but did not change AII concentrations. Strikingly, the sympathoexcitatory response to PEEP10 was inhibited, whereas AII increased markedly (+284 +/- 64 pg/ml, P < 0.05) during PEEP10 and isoflurane. Renal blood flow was significantly more reduced during PEEP10 and isoflurane compared to PEEP10 alone, whereas the magnitude of reductions were similar in the other vascular beds. The data suggest that renin-angiotensin activation is important to attenuate the impact of PEEP ventilation on cardiovascular performance during administration of the sympathodepressant isoflurane. Interference with the renin-angiotensin system may cause cardiovascular decompensation in isoflurane anesthetized patients subjected to PEEP-ventilation.