Frontiers in veterinary science · 2026
Early cardiovascular and respiratory changes after etorphine immobilization and naltrexone reversal in sheep.
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Binetti Anna, Rattanathanya Hathaipat, Pohlin Friederike, Auer Ulrike, Schramel J Peter, Dolezal Marlies, Kalogeropoulu Szilvia, Gösele Cosima L, Stahl Lisa, Ebenhofer Lisa J, Braun Christina, Stalder Gabrielle, Mosing Martina
Аннотация
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.
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.