TY - JOUR
T1 - Anesthesia alters pulmonary vasoregulation by angiotensin II and captopril
AU - Nyhan, D. P.
AU - Chen, B. B.
AU - Fehr, D. M.
AU - Rock, P.
AU - Murray, P. A.
PY - 1992
Y1 - 1992
N2 - We investigated the effects of an intravenous (pentobarbital sodium) and inhalational (halothane) general anesthetic on the pulmonary vascular responses to angiotensin II and angiotensin-converting enzyme inhibition (CEI). Multipoint pulmonary vascular pressure-flow (P/Q̇) plots were generated in conscious pentobarbital- (30 mg/kg iv) and halothane- anesthetized (~1.2% end-tidal) dogs in the intact (no drug) condition, during angiotensin II administration (60 ng · kg-1 · min-1 iv), and during CEI (captopril 1 mg/kg plus 1 mg · kg-1 · h-1 iv). In conscious dogs, angiotensin II increased (P < 0.001) the pulmonary vascular pressure gradient [pulmonary arterial pressure - pulmonary arterial wedge pressure (PAP-PAWP)] over the empirically measured range of Q̇; i.e., angiotensin II caused pulmonary vasoconstriction. Pulmonary vasoconstriction (P < 0.01) in response to angiotensin II was also observed during pentobarbital sodium anesthesia. In contrast, angiotensin II had no effect on the P/Q̇ relationship during halothane anesthesia. In conscious dogs, CEI decreased (P < 0.001) PAP-PAWP over the empirically measured range of Q̇; i.e., CEI caused pulmonary vasodilation. However, CEI caused pulmonary vasoconstriction (P < 0.02) during pentobarbital sodium and had no effect on the P/Q̇ relationship during halothane. Thus, compared with the conscious state, the pulmonary vasoconstrictor response to angiotensin II is unchanged or abolished, and the pulmonary vasodilator response to CEI is reversed to vasoconstriction or abolished during pentobarbital sodium and halothane anesthesia, respectively.
AB - We investigated the effects of an intravenous (pentobarbital sodium) and inhalational (halothane) general anesthetic on the pulmonary vascular responses to angiotensin II and angiotensin-converting enzyme inhibition (CEI). Multipoint pulmonary vascular pressure-flow (P/Q̇) plots were generated in conscious pentobarbital- (30 mg/kg iv) and halothane- anesthetized (~1.2% end-tidal) dogs in the intact (no drug) condition, during angiotensin II administration (60 ng · kg-1 · min-1 iv), and during CEI (captopril 1 mg/kg plus 1 mg · kg-1 · h-1 iv). In conscious dogs, angiotensin II increased (P < 0.001) the pulmonary vascular pressure gradient [pulmonary arterial pressure - pulmonary arterial wedge pressure (PAP-PAWP)] over the empirically measured range of Q̇; i.e., angiotensin II caused pulmonary vasoconstriction. Pulmonary vasoconstriction (P < 0.01) in response to angiotensin II was also observed during pentobarbital sodium anesthesia. In contrast, angiotensin II had no effect on the P/Q̇ relationship during halothane anesthesia. In conscious dogs, CEI decreased (P < 0.001) PAP-PAWP over the empirically measured range of Q̇; i.e., CEI caused pulmonary vasodilation. However, CEI caused pulmonary vasoconstriction (P < 0.02) during pentobarbital sodium and had no effect on the P/Q̇ relationship during halothane. Thus, compared with the conscious state, the pulmonary vasoconstrictor response to angiotensin II is unchanged or abolished, and the pulmonary vasodilator response to CEI is reversed to vasoconstriction or abolished during pentobarbital sodium and halothane anesthesia, respectively.
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U2 - 10.1152/jappl.1992.72.2.636
DO - 10.1152/jappl.1992.72.2.636
M3 - Article
C2 - 1559942
AN - SCOPUS:0026548842
VL - 72
SP - 636
EP - 642
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
SN - 8750-7587
IS - 2
ER -