title: Hypothermia does not alter somatosensory evoked potential amplitude and global cerebral oxygen extraction during marked sodium nitroprusside-induced arterial hypotension.
abstract: BACKGROUND
  To prevent neurologic damage, monitoring cerebral function by somatosensory evoked potentials is used in selected settings. Excision of intraocular melanoma provides a unique opportunity to assess independently during anesthesia the effects on median nerve somatosensory evoked potentials (MN-SSEPs) and cerebral oxygen extraction of sodium nitroprusside-evoked arterial hypotension with and without hypothermia.
  
  
  METHODS
  Median nerve somatosensory evoked potentials, arterial pressure, jugular venous bulb oxygen saturation (Sjo(2)) and lactate concentration, and arterial-jugular bulb oxygen content difference were assessed during propofol-remifentanil anesthesia under sodium nitroprusside-evoked arterial hypotension (mean arterial pressure, 40 mmHg) with and without surface hypothermia (32 degrees C) in 11 otherwise healthy patients undergoing resection of choroidal melanoma.
  
  
  RESULTS
  Hypothermia alone did not affect peak-to-peak amplitude of N20/P25 but prolonged cortical latency of N20 (22.6 +/- 2.2 vs. 25.9 +/- 2.5 ms, P < 0.05), cervical latency of N13 (14.3 +/- 1.2 vs. 15.7 +/- 1.6 ms, P < 0.05), and central conduction time (8.3 +/- 1.4 vs. 10.2 +/- 1.6 ms, P < 0.05). Evoked arterial hypotension did not depress MN-SSEP N20/P25 amplitude either with or without hypothermia (-0.31 vs. -0.28 microV, P > 0.05) or alter latency (0.08 vs. 0.1 ms, P > 0.05). Furthermore, hypotension with or without hypothermia did not change Sjo(2), arterial-jugular bulb oxygen content difference, or lactate concentration.
  
  
  CONCLUSIONS
  Thus, hypothermia to 32 degrees C does not alter MN-SSEP amplitude and global cerebral oxygen extraction during marked sodium nitroprusside-induced arterial hypotension with a mean arterial pressure of 40 mmHg but prolongs MN-SSEP latencies during propofol-remifentanil anesthesia in individuals without cerebrovascular disease.
authors.affiliation: Klinik für Anästhesiologie und Intensivmedizin, Universitätsklinikum Essen, Hufelandstrasse 55, D-45122 Essen, Germany. eva.kottenberg@uni-essen.de
authors.forename: Eva
authors.initials: E
authors.lastname: Kottenberg-Assenmacher
authors.forename: Wolf
authors.initials: W
authors.lastname: Armbruster
authors.forename: Norbert
authors.initials: N
authors.lastname: Bornfeld
authors.forename: Jürgen
authors.initials: J
authors.lastname: Peters
mesh_terms: D000328:Adult; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001831:Body Temperature / Q000187:drug effects; D001921:Brain / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D004947:Esophagus; D005073:Evoked Potentials, Somatosensory / Q000502:physiology*; D005260:Female; D006801:Humans; D007022:Hypotension / Q000139:chemically induced*; D007036:Hypothermia, Induced; D008297:Male; D008875:Middle Aged; D009599:Nitroprusside / Q000494:pharmacology*; D010101:Oxygen Consumption / Q000187:drug effects; D011930:Reaction Time / Q000187:drug effects; D012016:Reference Values; D013997:Time Factors
chemical_list: D009599:Nitroprusside