Early cardiovascular and respiratory changes after etorphine immobilization and naltrexone reversal in sheep
Anna Binetti1, Hathaipat Rattanathanya2, Friederike Pohlin2
1Anaesthesiology and Intensive Care, Clinical Centre for Small Animals, Clinical Department for Small Animals and Horses, University of Veterinary Medicine Vienna, Vienna, Austria.
Introduction:
The immediate cardiorespiratory responses to etorphine immobilization and reversal with naltrexone in wildlife are underexplored.
Objective:
To evaluate the early cardiorespiratory changes after etorphine immobilization and reversal with naltrexone in sheep, as a model for wild ungulates.
Methods:
Six sheep instrumented with electrical impedance tomography (EIT) belt, arterial and pulmonary arterial catheters were immobilized with intramuscular etorphine (0.05 mg kg-1) and reversed with intravenous naltrexone (1 mg kg-1) 26 min later. Mean pulmonary arterial pressure (MPAP) and EIT derived variables (minute tidal impedance variation-TIVMIN; tidal impedance variation-TIV; respiratory rate-RR; end-expiratory lung impedance-EELI) were recorded continuously from 5 min before to 10 min after each drug. Arterial blood gasses were drawn at baseline and 5 min after each drug. Statistical analysis was performed in R to determine the timing of significant deviations from baseline, defined as the mean of the 5 min preceding drug administration, and compared with each minute thereafter. Post-administration values were expressed as ratios to baseline and analyzed using two-sided one-sample t-tests with False Discovery Rate (FDR) correction at 10% for multiple comparisons; FDR-adjusted p-values (q-values) < 0.10 were considered significant.
Results:
Three minutes after etorphine, MPAP increased (q = 0.08, median 42%), accompanied by a decrease in TIVMIN (q = 0.09, median 40.9%) due to decrease in TIV and RR. Arterial blood gasses confirmed hypoxemia (PaO₂ median [range]: 57.1 [26.9-93.6] mmHg) and hypercapnia (PaCO₂ 49.45 [40-61.3] mmHg). Conversely, regional ventilation distribution and EELI remained unchanged. One minute after naltrexone, median RR (q = 0.04) and TIVMIN (q = 0.05) increased by 119.3 and 223.6% from baseline respectively, followed by increase in TIV from minute 4 (q = 0.06, median 50.8%). Arterial blood gasses improved marginally (PaO₂ 63.5 [48.6-115.7] mmHg; PaCO₂ 46 [41.5-52.4] mmHg) while MPAP did not return toward baseline.
Conclusion:
Etorphine immobilization caused early pulmonary hypertension followed by progressive hypoventilation without ventilation redistribution. Naltrexone rapidly restored ventilation, whereas pulmonary vascular effects persisted.
