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

G. E. Hill, T. H. Stanley, M. R. Hodges, C. R. Sentker, D. Philbin

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)200-205
Number of pages6
JournalAnesthesia and Analgesia
Volume57
Issue number2
StatePublished - 1978

Fingerprint

Enflurane
Intracranial Hypertension
Arterial Pressure
Intracranial Pressure
Kidney
Osmolar Concentration
Urine
Anesthesia
Vasopressins
Vascular Resistance
Nitrogen
Dogs
Water

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Hill, G. E., Stanley, T. H., Hodges, M. R., Sentker, C. R., & Philbin, D. (1978). Failure of enflurane in altering renal responses to acute intracranial pressure increases. Anesthesia and Analgesia, 57(2), 200-205.

Failure of enflurane in altering renal responses to acute intracranial pressure increases. / Hill, G. E.; Stanley, T. H.; Hodges, M. R.; Sentker, C. R.; Philbin, D.

In: Anesthesia and Analgesia, Vol. 57, No. 2, 1978, p. 200-205.

Research output: Contribution to journalArticle

Hill, GE, Stanley, TH, Hodges, MR, Sentker, CR & Philbin, D 1978, 'Failure of enflurane in altering renal responses to acute intracranial pressure increases', Anesthesia and Analgesia, vol. 57, no. 2, pp. 200-205.
Hill, G. E. ; Stanley, T. H. ; Hodges, M. R. ; Sentker, C. R. ; Philbin, D. / Failure of enflurane in altering renal responses to acute intracranial pressure increases. In: Anesthesia and Analgesia. 1978 ; Vol. 57, No. 2. pp. 200-205.
@article{ded9cb2acdf648618018aa37da1aee4e,
title = "Failure of enflurane in altering renal responses to acute intracranial pressure increases",
abstract = "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.",
author = "Hill, {G. E.} and Stanley, {T. H.} and Hodges, {M. R.} and Sentker, {C. R.} and D. Philbin",
year = "1978",
language = "English (US)",
volume = "57",
pages = "200--205",
journal = "Anesthesia and Analgesia",
issn = "0003-2999",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - Failure of enflurane in altering renal responses to acute intracranial pressure increases

AU - Hill, G. E.

AU - Stanley, T. H.

AU - Hodges, M. R.

AU - Sentker, C. R.

AU - Philbin, D.

PY - 1978

Y1 - 1978

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0018137301&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018137301&partnerID=8YFLogxK

M3 - Article

C2 - 565158

AN - SCOPUS:0018137301

VL - 57

SP - 200

EP - 205

JO - Anesthesia and Analgesia

JF - Anesthesia and Analgesia

SN - 0003-2999

IS - 2

ER -