Enhanced disruption of the blood brain barrier by intracarotid mannitol injection during transient cerebral hypoperfusion in rabbits.

Fairly large volumes of intracarotid mannitol (20% to 25%) are required to disrupt the blood brain barrier (BBB), that is, 200 to 300 mL/30 s in humans or 10 mL/40 s in rabbits. During transient cerebral hypoperfusion blood flow to the rabbit brain is decreased to 0.2 to 0.

Transient cerebral hypoperfusion enhances intraarterial carmustine deposition into brain tissue.

We hypothesized that bolus injections of lipid soluble chemotherapeutic drugs during transient cerebral hypoperfusion could significantly boost regional drug delivery. In the first two groups of New Zealand White rabbits we measured brain tissue carmustine concentrations after intravenous infusion, intraarterial infusion with normal perfusion, and after intraarterial injections during transient cerebral hypoperfusion. In the third group of animals we assessed the safety of the technique by assessing electroencephalographic changes for 6 h after flow arrest carmustine administration and subsequent histological examination.

Augmentation of cerebral blood flow and reversal of endothelin-1-induced vasospasm: a comparison of intracarotid nicardipine and verapamil.

Objective: Local intra-arterial infusions of verapamil and nicardipine have been used to treat human cerebral vasospasm. Only a few reports of early clinical experience with these medications are currently available, and limited data are available regarding their cerebral physiological activity. We assessed the efficacy of intracarotid administration of verapamil and nicardipine on augmenting cerebral blood flow of New Zealand White rabbits and compared the ability of these drugs with reverse topical endothelin (ET)-1-triggered vasospasm.

Bolus configuration affects dose requirements of intracarotid propofol for electroencephalographic silence.

We hypothesized that an intracarotid bolus injection of propofol to produce electroencephalographic (EEG) silence would require a smaller dose of the drug compared with the continuous infusion of the drug. Furthermore, the bolus propofol dose will be a function of the bolus characteristics in each bolus (mass/volume). We compared the dose requirements of intracarotid propofol needed to maintain EEG silence when delivered as bolus injections to continuous infusions in rabbits.

Comparison of intracarotid anesthetics for EEG silence.

The goal of this study was to compare systemic and cerebrovascular effects of three anesthetic drugs (etomidate, thiopental, and propofol) when delivered by intracarotid and intravenous routes in doses that produce electrocerebral silence (electroencephalography [EEG]). EEG activity, mean arterial pressure (MAP), and laser Doppler flow as a proxy of cerebral blood flow (CBF) of 24 anesthetized New Zealand white rabbits were continuously recorded. Data were compared at three timepoints: baseline, during EEG silence, and after recovery of EEG activity.

Cerebral blood flow affects dose requirements of intracarotid propofol for electrocerebral silence.

Background: The authors hypothesized that cerebral blood flow (CBF) changes will affect the dose of intracarotid propofol required to produce electrocerebral silence.

Methods: The authors tested their hypothesis on New Zealand White rabbits. The first group of 9 animals received intracarotid propofol during (1) normoventilation, (2) hyperventilation, and (3) hypoventilation.

Reducing cerebral blood flow increases the duration of electroencephalographic silence by intracarotid thiopental.

The effects of IV anesthetics are enhanced by increased cerebral blood flow (CBF) because of a greater delivery of drugs to the brain. In contrast, mathematical simulations suggest that a decrease in CBF, by increasing regional drug uptake and decreasing drug washout, enhances the efficacy of intraarterial drugs. We hypothesized that administrating intracarotid anesthetics during cerebral hypoperfusion will significantly prolong the duration of electroencephalographic (EEG) silence.