Failure of enflurane in altering renal responses to acute intracranial pressure increases

The effects of acute increases of intracranial pressure (ICP) on renal function before and during enflurane and enflurane-N ₂O anesthesia were determined in 12 mongrel dogs. Prior to anesthesia, acute elevations of 10 and 20 torr in ICP significantly increased urine osmolarity (U(OSM)), mean arterial blood pressure (MAP), and renal vascular resistance (RVR); significantly decreased urine volume (U(VOL)), paraaminohippurate clearance (C(PAH)), and free water clearance (C(H2O)); and had no effect on inuline clearance (C(IN)) or plasma levels of antidiuretic hormone (ADH). Thirty minutes of enflurane (2.2 percent end-tidal concentration) in 70 percent nitrogen and O ₂ in the presence of normal ICP caused significant increases in U(OSM) while MAP, C(PAH), U(VOL), C(H2O), C(IN), and osmolar clearance C(OSM) were significantly decreased and ADH was unchanged. Substituting 70 percent N ₂O for nitrogen had no significant effect on any variable measured. Increasing ICP 10 torr during enflurane-N ₂O anesthesia caused significant increases (compared to enflurane-N ₂O values in the presence of normal ICP) in U(OSM), RVR, and C(OSM), as well as significant decrease in U(VOL), C(H2O), and C(PAH), but had no effect on ADH, C(IN), or MAP. Enflurane and N ₂O anesthesia moderates the elevation of MAP in response to an acute increase in ICP but fails to alter the renal response to increased ICP.