This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by McPherson, R. W. Articles by Traystman, R. J. Search for Related Content PubMed PubMed Citation Articles by McPherson, R. W. Articles by Traystman, R. J.

Stroke, Vol 17, 30-36, Copyright © 1986 by American Heart Association

ARTICLES

Relationship of somatosensory evoked potentials and cerebral oxygen consumption during hypoxic hypoxia in dogs

RW McPherson, S Zeger and RJ Traystman

The effects of hypoxic hypoxia on cerebral hemodynamics and somatosensory evoked potential (SEP) were studied in 10 pentobarbital anestheteized dogs. Cerebral blood flow (CBF) was measured using the venous outflow technique and cerebral oxygen consumption (CMRO2) was calculated from the arterio-cerebro-venous oxygen difference times CBF. SEP was evaluated by percutaneous stimulation of an upper extremity nerve and was recorded over the contralateral somatosensory cortex. The latencies of the initial negative wave (N1), second positive wave (P2) and the amplitude of the primary complex (P1N1) were measured. Animals were breathed sequentially with oxygen concentrations of 21, 10, 6, 5, and 4.5% for five minutes each. Animals were returned to room air breathing when the amplitude of the SEP decreased to less than 20% of control and were observed for 30 minutes following reoxygenation. Severe hypoxia (4.5% O2) increased CBF to 200% of control, decreased CMRO2 to 45% of control, decreased amplitude and increased latency of SEP. Following reoxygenation, as CMRO2 increased toward control, latency of SEP decreased and amplitude increased and CBF returned to baseline within 30 min. During hypoxia and reoxygenation, the latencies of N1 and P2 and the amplitude of P1N1 were correlated with CMRO2 in individual animals. We conclude that changes in SEP amplitude and latency reflect changes in CMRO2 despite high CBF during rapidly progressive hypoxic hypoxia and following reoxygenation.

This article has been cited by other articles:

				C. Limperopoulos, A. Majnemer, B. Rosenblatt, M. Shevell, C. Rohlicek, and C. Tchervenkov Multixnodality Evoked Potential Findings in Infants With Congenital Heart Defects J Child Neurol, November 1, 1999; 14(11): 702 - 707. [Abstract] [PDF]

				R. B. Mink and A. J. Dutka Hyperbaric Oxygen After Global Cerebral Ischemia in Rabbits Reduces Brain Vascular Permeability and Blood Flow Stroke, December 1, 1995; 26(12): 2307 - 2312. [Abstract] [Full Text]

				H. Tanaka, T. Kazui, H. Sato, N. Inoue, O. Yamada, and S. Komatsu Experimental Study on the Optimum Flow Rate and Pressure for Selective Cerebral Perfusion Ann. Thorac. Surg., March 1, 1995; 59(3): 651 - 657. [Abstract] [Full Text]