Related Experiment Videos
Reduction of infarct volume by halothane: effect on cerebral blood flow or perifocal spreading depression-like
Insights
Halothane anesthesia reduced spreading depression (SD) and infarct volume in experimental focal ischemia. This anesthetic shows protective effects in brain ischemia models, potentially via cerebrovascular and electrophysiologic mechanisms.
Area of Science:
- Neuroscience
- Anesthesiology
- Cerebrovascular Research
Background:
- Spreading depression (SD) is a wave of neuronal depolarization linked to brain injury.
- Halothane is known to inhibit potassium-evoked SD.
- The effects of halothane on SD during focal ischemia are not well understood.
Purpose of the Study:
- To investigate the effects of halothane on SD induction, cerebral blood flow (CBF), and infarct evolution in a feline model of focal cerebral ischemia.
- To compare halothane anesthesia with alpha-chloralose anesthesia in this model.
Main Methods:
- Focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) in cats for 16 hours.
- Anesthesia was administered using either halothane (0.75%) or alpha-chloralose (60 mg/kg).
- Cortical direct current potential and CBF were measured using electrodes in different cortical gyri.
Main Results:
- Under alpha-chloralose, MCAO caused severe ischemia and immediate terminal depolarization in most areas.
- Halothane anesthesia resulted in less severe ischemia in some regions and prevented terminal depolarization in most cases.
- Halothane significantly reduced the number of transient depolarizations and infarct volume, particularly in the suprasylvian gyrus.
Conclusions:
- Halothane exhibits protective properties in experimental focal brain ischemia.
- These protective effects may be attributed to both cerebrovascular and electrophysiologic influences of halothane.
- Halothane may be a beneficial anesthetic choice for studies involving experimental brain ischemia.
Abstract:
Halothane is a strong inhibitor of potassium evoked spreading depression (SD) in cats. In the current study, we investigate halothane effects on induction of perifocal SD-like depolarizations, CBF, and infarct evolution in focal ischemia. Calomel and platinum electrodes measured cortical direct current potential and CBF in ectosylvian, suprasylvian, and marginal gyri. Left middle cerebral artery occlusion (MCAO) induced permanent focal ischemia for 16 hours in artificially ventilated cats (30% oxygen, 70% nitrous oxide) under halothane (0.75%, n = 8) or alpha-chloralose anesthesia (60 mg/kg intravenously, n = 7). Under alpha-chloralose, MCAO induced severe ischemia in ectosylvian and suprasylvian gyri(mean CBF < 10 mL/100 g/min), and direct current potentials turned immediately into terminal depolarization. In marginal gyri, CBF reduction was mild (more than 20 mL/100 g/min), and in six of seven animals, frequent SD-like depolarizations turned into terminal depolarization at a later stage of the experiments. Under halothane, MCAO induced severe ischemia (less than 10 mL/100 g/min) and immediate terminal depolarization only in ectosylvian gyrus. In suprasylvian gyrus, residual CBF remained significantly higher (more than 10 mL/100 g/min) than under alpha-chloralose, whereas in marginal gyri, CBF did not differ between groups. Compared with chloralose, the number of transient depolarizations was significantly reduced in marginal gyrus, and in suprasylvian gyrus transient but significantly longer depolarizations than in marginal gyrus were recorded. Except for one animal, transient depolarizations did not turn into terminal depolarization under halothane, and infarct volume reduction was particularly seen in suprasylvian gyrus. We conclude that halothane, the most commonly used anesthetic in studies of experimental brain ischemia, has protective properties, which may depend on both cerebrovascular and electrophysiologic influences.