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-N2O anesthesia were determined in 12 mongrel dogs. Prior to anesthesia, acute elevations of 10 and 20 torr in ICP significantly increased urine osmolarity (Uosm), mean arterial blood pressure (MAP), and renal vascular resistance (RVR); significantly decreased urine volume (U vol), para-aminohippurate clearance (Cpah), and free water clearance (C/20); and had no effect on inuline clearance (Cin) or plasma levels of antidiuretic hormone (ADH). Thirty minutes of enflurane (2.2 percent end-tidal concentration) in 70 percent nitrogen and O2 in the presence of normal ICP caused significant increases in Uosm while MAP, CPAH, UVOL CH20, CIN, and osmolar clearance (CosM) were significantly decreased and ADH was unchanged. Substituting 70 percent N2O 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-N2O values in the presence of normal ICP) in UosM, RVR, and CosM, as well as significant decreases in UVOL, CH2O, AND CPAH, but had no effect on ADH, CIN, or MAP. Enflurane and N2O anesthesia moderates the elevation MAP in response to an acute increase in ICP but fails to alter the renal response to increased ICP.