Respiratory depression is a common side effect when
opioids are used to immobilize wildlife. Serotonergic
ligands have the potential to reverse
opioid-induced
respiratory depression. We examined whether any of three serotonergic
ligands could reverse this depression in
etorphine-immobilized (0.07 mg/kg) impala (Aepyceros melampus). The study took place in September-December 2007. Impala received
intravenous injections of
metoclopramide (10 mg/kg, n=6),
buspirone (0.05 mg/kg, n=8),
pimozide (1 mg/kg, n=8),
doxapram (1 mg/kg, n=6), and control solutions on separate occasions. During the immobilization, partial pressures of
oxygen (PaO(2), mmHg) and
carbon dioxide (PaCO(2), mmHg), respiratory rate (breaths/min), ventilation (l/min), peripheral O(2) saturation (%), tidal volume (l), and respiratory exchange ratio were measured before and after injection of the experimental drugs.
Etorphine immobilization caused
respiratory depression and
hypoxia (mean+/-SD, PaCO(2)=51+/-2 mmHg, PaO(2)=40+/-3 mmHg).
Metoclopramide and
buspirone, but not
pimozide, attenuated the hypoxic effects of
etorphine; 3 min after injection,
metoclopramide increased the PaO(2) by 7.5+/-6.3 mmHg and
buspirone by 6+/-6.6 mmHg (F=3.9, P=0.02). These effects were similar to those of
doxapram (8+/-7 mmHg, F=3.9; P>0.05). Neither
metoclopramide nor
buspirone significantly increased ventilation, but they increased PaO(2) by significantly improving the alveolar-arterial
oxygen partial pressure gradient (A-a gradient, F=1.4, P<0.05), indicating improved
oxygen diffusion.
Metoclopramide and
buspirone transiently improved blood oxygenation of
opioid-immobilized impala, probably by improving ventilation-perfusion ratios, without reversing catatonic immobilization.