Anesthetic modulation of cerebral hemodynamic and evoked responses to transient middle cerebral artery occlusion in cats.

Abstract

We measured cerebral blood flow and somatosensory evoked potentials during transient focal cerebral ischemia in cats to compare the effects of four commonly used anesthetic regimens: ketamine/fentanyl/N 2 O (fentanyl), pentobarbital, ketamine/o^chloralose (cv-chloralose), and ketamine/halothane/N 2 O (halothane). Six cats in each group were subjected to 60 minutes of left middle cerebral artery occlusion followed by 120 minutes of reperfusion. Although the amplitude of the initial somatosensory evoked potential wave complex was highest in the tt-chloralose group (58.6±16.5 /iX) and smallest in the halothane group (27J±5.7 fiV), amplitude fell by 75% in all groups upon occlusion. Baseline cerebral blood flow varied substantially between groups (e.g., in the right intersylvian gyrus: fentanyl, 96 ±12; pentobarbital, 30±5; o-chloralose, 24±3; and halothane, 76±11 ml/min/100 g). Occlusion decreased cerebral blood flow to subcortical (e.g., left caudate) structures in all groups (fentanyl, 29±11%; pentobabital, 45±12%; o-chloralose, 27±13%; and halothane, 18±5% of baseline). Postischemic hyperemia occurred in the cortical regions of cats anesthetized with pentobarbital or «-chloralose that had reduced cerebral blood flows during occlusion but not in cats anesthetized with fentanyl (cerebral blood flow during occlusion not different from that of cats anesthetized with pentobarbital or <v-chloralose) or halothane. After 120 minutes of reperfusion, cerebral blood flow had returned to baseline values in all groups. Recovery of cerebral blood flow and somatosensory evoked potential amplitude at that time did not differ among groups. We conclude that anesthetics alter baseline cerebral blood flow and baseline somatosensory evoked potentials as well as the cerebral blood flow pattern during reperfusion after middle cerebral artery occlusion independent of insult severity. (Stroke 1990^21:795-800) A lthough the model of focal cerebral ischemia produced by middle cerebral artery (MCA) >. occlusion has been used by many laboratories, 1 -5 cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRO 2 ), and histologic patterns have been difficult to compare among laboratories. This difficulty results in part from not knowing whether differences in results can be attributed to differences in anesthetics, species, or models.Anesthetics (e.g., pentobarbital, ketamine/achloralose, and ketamine/halothane/r^O), Received April 26, 1989; accepted January 11, 1990. evoked potentials. For example, pentobarbital decreases CBF, CMRO 2 , 7 and the amplitude of somatosensory evoked potentials.8 Ketamine increases CBF, has variable effects on CMRO2, 9 and increases the amplitude of somatosensory evoked potentials.10 The effect of a-chloralose upon CMRO2, CBF, and baseline electrophysiologic parameters has not been well studied. Halothane increases CBF, decreases CMRO2, 11 decreases the amplitude, and increases the latency of somatosensory evoked potentials.12 N 2 O increases CMRO 2 13 and C B F 4 and decreases the amplitude of soma...

The Cerebrovascular Response to Ketamine

“…Eight animal studies demonstrated no effect of ketamine on CBF, 24,28,29,32,33,36,37,45 as measured with 14 C-iodoantipyrine autoradiography, 24 SPECT, 28 diffuse correlation spectroscopy, 29 PET, 32 microspheres, 33,36,37 and the Takasato perfusion technique. 45 …”

“…Within the 38 animal studies identified, 18-55 the majority of cases measured CBF response to ketamine, and to other anesthetic agents, utilizing imaging [18][19][20][21][22][23][24][25][26][27][28][29]32,33,[35][36][37][38][41][42][43][44][45][46][47][48][49][50]52,55 : 131 Xe CT, PET, SPECT, indocyanine green (ICG) angiography, and magnetic resonance imaging (MRI). Less commonly utilized methods included radioactive microsphere-based CBF determination, ultrasound-based flow probes, 14 C-iodoantipyrine autoradiography, diffuse correlation spectroscopy, and direct measurements through sinus cannulation among others.…”

“…In 22 of the studies, 21,[24][25][26]29,33,[35][36][37][38][39][40][41][42][43][44][45][46][47][48][49]55 there was coadministration of another intravenous (IV) or inhalational anesthetic agent during ketamine administration and assessment of cerebrovascular response.…”

Rapid monitoring of changes in water diffusion coefficients during reversible ischemia in cat and rat brain

“…SEP were recorded over the cerebral cortex in a modified method as previously described (16). Briefly, stimulating and ground needle electrodes were placed percutaneously into the volar surface of the foreleg in a location that caused a distal twitch.…”

Tirilazad treatment does not decrease early brain injury after transient focal ischemia in cats.

“…However, we have previously measured CBF as early as 15 minutes of reperfusion and demonstrated postischemic hyperemia after transient focal ischemia in cats anesthetized with pentobarbital or a-chloralose but not with halothane or fentanyl. 37 By chance hemoglobin concentration was lower in control cats compared with the other two groups at baseline conditions (Table 1). Because moderate he-modilution can attenuate infarct volume, 38 it is possible that infarct volume in the control group was lower than normal because of hemodilution and thereby masked a beneficial effect of tirilazad.…”