Effects of hemorrhagic hypotension on the cerebral circulation. II. Electrocortical function.

Abstract

SEVERE HYPOTENSION produces a loss of cerebral function, the extent and reversibility of which depends on the degree and duration of the period of hypotension. Recent studies have described the changes in cerebral function over periods of sustained hypotensionThe present study forms part of a systemic investigation which attempts to correlate the changes in cerebral blood flow during graded hemorrhagic hypotension with the subsequent alteration in cerebral functional activity and the development of hypoxic brain damage.This communication reports the changes observed in cerebral functional activity during hypotension and relates these changes to the arterial pressure and to the corresponding alterations in the cerebral circulation. The detailed accounts of the impairment of the cerebral circulation and development of brain damage due to hypotension are given in the accompanying papers. 5 ' 6 It has been suggested 7 that the somatosensory evoked response is a more accurate guide than the EEG to brain damage during hypotension. Therefore, both these parameters were measured in this study. Methods General DescriptionThe effect of graded hemorrhagic hypotension on electrocortical activity was determined in 2 parallel studies in a total of 12 cats, of either sex, weighing between 1.6 and 4.8 kg. Anesthesia and general Reprints: Dr. David I. Graham, the University of Glasgow, Wellcome Surgical Institute, Garscube Estate, Bearsden Road, Bearsden, Glasgow, G61 1QH, Scotland. preparation of the animals were identical to those described previously. Measurement of Somatosensory Evoked ResponseSix cats were used to study the effects of hypotension on the somatosensory evoked response. The cats were placed in a head-holder and the scalp was incised along the midline and reflected. A small craniotomy (approximately 1.5 X 1.0 cm) was made over the sensory cortex, using a saline-cooled dental drill, and a reference silver-electrode was implanted in the neck muscle. A supramaximal stimulus (0.5-2V, 0.2 msec, 1 Hz) was applied via a DISA type 14 E12 time base unit to the contralateral superficial radial nerve. Bipolar silver ball-tipped recording electrodes were then positioned (1 cm apart) on the surface of the dura to obtain maximal potential. Signals from the recording electrodes were amplified with a band width of 2-500 Hz and the average of 16 evoked potentials recorded with a DISA type 14 GO1 digital averager from which the measurements were taken and of which a photographic record was kept.The somatosensory evoked response was recorded for a control period of 30 min and then the animal was subjected to stepwise hypotension induced by controlled hemorrhage.5 Mean arterial pressure was decreased by approximately 10 mm Hg at each step and allowed to stabilize for approximately 10 min at each new level before the potentials were recorded. The effect of this hypotension on the evoked response was assessed in terms of the average peak-to-peak amplitude of the positive/negative sequence of the primary evoked response; 8 and t...

Lidocaine accelerates neuroelectrical recovery after incomplete global ischemia in rabbits.

“…23 Rather, they favor the hypothesis that various neuronal groups differ in their sensitivity to ischemia or hypoxia. 24 Our results showed a faster recovery of the EEG compared with the somatosensory-evoked potentials; these findings confirm the experience of other authors 12 …”

“…To evaluate these contradictory findings, we tested the effect of lidocaine by using a moderate level of blood flow reduction defined by changes in the electroencephalogram (EEG) comparable with those studied by Gregory et al 12 and Graham et al, 13 who reported no neuropathologic alterations after 20 minutes of incomplete global ischemia. We tested a low dose of the drug, expecting some central nervous system beneficial action because lidocaine has a significant effect at low concentrations in other excitable tissue; one of these effects is the suppression of cardiac arrhythmias.…”

Effects of hemorrhagic hypotension on the cerebral circulation. I. Cerebral blood flow and pial arteriolar caliber.

“…Such mechanisms and relationships have not previously been described systematically. In the accompanying communications, the vascular mechanisms will be related to changes in electrocortical function, 2 and to the development of neuropathological changes in the cerebral parenchyma. …”

Relative Cerebral Ischemia in SHR Due to Hypotensive Hemorrhage: Cerebral Function, Blood Flow and Extracellular Levels of Lactate and Purine Catabolites

“…Branston and co-workers used a combination of middle cerebral artery occlusion and hypotension, while we only use general hypotension. On the other hand, Gregory et al (1979) also used only hypotension and found a threshold for transmission failure at a slightly higher flow than Branston and co-workers, i. e. , when CBF had decreased to about 50% of control.…”