Pig Sedation and Anesthesia for Medical Research

Costea, Ruxandra; Ene, Ioana; Pavel, Ruxandra

doi:10.3390/ani13243807

Cited by 1 publication

(1 citation statement)

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“…The half-life for ketamine varies between 1 and 4 h, depending on the species. The ketamine dosage given in the initial sedation was approximately ten times below the recommended dosage for maintaining anesthesia (see, e.g., [44,45]) and below the rates that have been shown to have an inhibiting effect on spreading depolarizations [43,46]. We therefore judge that the ketamine dosage applied in the present work was so low that it had no inhibiting effect on the cortical signals.…”

Section: Cortical Response Rapidly Decreased Following Et-1 Applicationmentioning

confidence: 82%

Porcine Model of Cerebral Ischemic Stroke Utilizing Intracortical Recordings for the Continuous Monitoring of the Ischemic Area

Nielsen,

Dancause,

Janjua

et al. 2024

Sensors

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Purpose: Our aim was to use intracortical recording to enable the tracking of ischemic infarct development over the first few critical hours of ischemia with a high time resolution in pigs. We employed electrophysiological measurements to obtain quick feedback on neural function, which might be useful for screening, e.g., for the optimal dosage and timing of agents prior to further pre-clinical evaluation. Methods: Micro-electrode arrays containing 16 (animal 1) or 32 electrodes (animal 2–7) were implanted in the primary somatosensory cortex of seven female pigs, and continuous electrical stimulation was applied at 0.2 Hz to a cuff electrode implanted on the ulnar nerve. Ischemic stroke was induced after 30 min of baseline recording by injection of endothelin-1 onto the cortex adjacent to the micro-electrode array. Evoked responses were extracted over a moving window of 180 s and averaged across channels as a measure of cortical excitability. Results: Across the animals, the cortical excitability was significantly reduced in all seven 30 min segments following endothelin-1 injection, as compared to the 30 min preceding this intervention. This difference was not explained by changes in the anesthesia, ventilation, end-tidal CO2, mean blood pressure, heart rate, blood oxygenation, or core temperature, which all remained stable throughout the experiment. Conclusions: The animal model may assist in maturing neuroprotective approaches by testing them in an accessible model of resemblance to human neural and cardiovascular physiology and body size. This would constitute an intermediate step for translating positive results from rodent studies into human application, by more efficiently enabling effective optimization prior to chronic pre-clinical studies in large animals.

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