The Effect of Ketamine on Regional Cerebral Blood Flow in Man

Hougaard, Kjeid; Hansen, Aksel; Brodersen, P

doi:10.1097/00000542-197412000-00006

Cited by 55 publications

(19 citation statements)

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“…Ketamine has been reported to cause from a 50% decrease to an 80% increase in global CBF [Dawson et al, 1971;Fukuda et al, 1983;Kreuscher and Grote, 1967] or no effect [Schwedler et al, 1982]. In humans, studies of global changes in CBF with ketamine are also inconsistent: Hougaard et al [1974] reported no effect on global CBF; Takeshita et al [1972] reported an increase in CBF, whereas Herrschaft and Schmidt [1973] reported that ketamine decreased CBF. Takeshita suggested that the increases in global cerebral perfusion were in part secondary to hypercapnia in anesthetized patients, although some animal studies have reported increased CBF with ketamine in normocapnic preparations [Artru, 1990].…”

Section: Introductionmentioning

confidence: 99%

Ketamine and fMRI BOLD signal: Distinguishing between effects mediated by change in blood flow versus change in cognitive state

Abel¹,

Allin²,

Kucharska-Pietura

et al. 2002

Human Brain Mapping

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No human fMRI studies have examined ketamine effects on the BOLD signal change associated with cognitive task performance. We wished to distinguish between effects on 1) cerebral blood flow, with resultant change in BOLD signal; and 2) cognition and neural mechanisms underlying BOLD signal change associated with task performance. Eight right-handed men (mean age 28.75 years) received ketamine or saline i.v. in a randomized, double-blind manner (bolus 0.23 mg/kg; 0.5 mg/kg over 45 min to a maximum 1 hr). Subjects viewed 10 alternating 30-sec blocks of faces with neutral expressions and a fixation cross and discriminated gender of faces. Gradient echo echoplanar images were acquired on a GE Signa 1.5 T Neurovascular system. One hundred T2-weighted images depicting BOLD contrast were acquired over 5 min (for each task) at each of 14 near-axial noncontiguous 7-mm thick planes. Ketamine significantly increased dissociative phenomena and negative symptoms, but did not affect performance of the gender discrimination task. Significant BOLD signal change was demonstrated predominantly in occipitotemporal cortex with both ketamine and placebo. Only two clusters in middle occipital gyrus (BA 18) and precentral gyrus (BA 4) showed significantly decreased BOLD signal change during ketamine compared to placebo. BOLD signal change was not significantly greater in any region during ketamine. Our findings demonstrate subtle rather than major differences between the effects of ketamine and placebo upon the BOLD signal change during perception of face-non face contrast. We suggest that they represent task-dependent effects of the drug/placebo, rather than task-independent effects of the drug per se, and indicate that the effects of ketamine on cerebral blood flow are predominantly focal and task-dependent, rather than global and task-independent.

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Section: Introductionmentioning

confidence: 99%

Ketamine and fMRI BOLD signal: Distinguishing between effects mediated by change in blood flow versus change in cognitive state

Abel¹,

Allin²,

Kucharska-Pietura

et al. 2002

Human Brain Mapping

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“…In such tiny babies, the diameter of the ACA cannot be measured with precision. As the conditions of our study were that of a steady state, and no changes were registered in HR, CO and gas pressures, we speculate that MAV stability is related to unchanged cerebral blood flow, although sev eral studies done using invasive methods [21][22][23] in rabbits or man, and specifically dedi cated to the study of ketamine effects, showed that this drug enhanced cerebral blood flow. There is a direct relationship between arterial velocities and intracranial pressure varia tions.…”

Section: Discussion Resultsmentioning

confidence: 70%

Doppler Ultrasound Assessment of the Effects of Ketamine on Neonatal Cerebral Circulation

Bétrémieux¹,

Carré²,

Pladys³

et al. 1993

Dev Pharmacol Ther

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The effects of a single dose of 5 mg-kg-(1) of ketamine administered intravenously to 10 critically ill preterm infants prior to epicutaneo-caval catheterization were analyzed using pulsedwave Doppler ultrasound. The infants weighed between 670 and 1,885 g and their gestational ages ranged from 26 to 33 weeks. Arterial pressure (MAP), cardiac output (CO), transcutaneous oxygen pressure (TCPO(2)), transcutaneous carbon dioxide pressure (TCPCO(2)), end-diastolic velocity (EDV), peak systolic velocity (PSV), mean arterial velocity (MAV) of the cerebral anterior artery as well as Pourcelot’s resistance index (PRI) were measured before and after injection of the drug. We observed a significant decrease in arterial pressure at 2 min after injection while heart rate and CO did not vary significantly. TCPO(2) and TCPCO(2), also remained unchanged throughout the period of measurement. EDV, PSV, and MAV did not vary significantly nor did PRI. As this drug provides major comfort to the baby during painful procedures and considerably facilitates difficult thin vessel catherization, we believe that it may be used in such conditions.

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“…22 It would seem unlikely that the vasodilatory properties of Ketamine may have augmented the above mechanism as the agent was administered more than 4 hrs before flow measurements were initiated. 23 As in all animal and human studies, species and model differences warrant caution in interpretation of results.…”

Section: Discussionmentioning

confidence: 99%

Effects of nimodipine on acute focal cerebral ischemia.

Barnett¹,

Bose

Little

et al. 1986

Stroke

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SUMMARY Nimodipine is a calcium slow channel blocker with several pharmacologlc properties suggesting the potential to favorably modify outcome in focal cerebral ischemia. Thirty adult cats underwent unilateral middle cerebral artery (MCA) occlusion for 4 hours. Seventeen cats were treated with an ipsilateral intracarotid infusion of nimodipine (1 /xg kg" 1 min ~') beginning 15 minutes before MCA ocdusion and continuing throughout the occlusion period. Eight nimodipine treated cats maintaining MAP > 90 mmHg were assigned to a Higher Pressure Nimodipine (HPN) group. The remaining nine treated cats with MAP < 90 mmHg were assigned to the Lower Pressure Nimodipine (LPN) group. Thirteen cats were untreated, receiving an isovolumetric amount of vehicle through the ipsilateral carotid artery. Local cerebral blood flow (1CBF) was continuously monitored using thermal diffusion probes. The brains, assessed for colloidal carbon perfusion, fluorescein and Evans blue staining, electroencephalographic activity (EEG), and histological changes, revealed no significant differences by any of these methods between the HPN and control animals with the exceptions of: 1) HPN treated cats exhibited a preservation of EEG activity at 15 minutes post-occlusion compared to the untreated cats, and 2) Post-iscbemic surface colloidal carbon perfusion was better preserved in the treated cats than hi the untreated cats. Mild hypotension, as demonstrated by the LPN group, negated these two positive effects. Prior to MCA occlusion, 1CBF was bilaterally significantly increased after nimodipine infusion in the HPN group as compared to vehicle infusion. Intra-arterially infused nimodipine did not reduce infarct size.

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The Effect of Ketamine on Regional Cerebral Blood Flow in Man

Cited by 55 publications

References 0 publications

Ketamine and fMRI BOLD signal: Distinguishing between effects mediated by change in blood flow versus change in cognitive state

Ketamine and fMRI BOLD signal: Distinguishing between effects mediated by change in blood flow versus change in cognitive state

Doppler Ultrasound Assessment of the Effects of Ketamine on Neonatal Cerebral Circulation

Effects of nimodipine on acute focal cerebral ischemia.

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