When wild animals are captured they often develop capture-related side-effects that
may result in morbidity and mortality. During chemical capture of wild ungulates,
capture-induced hyperthermia and opioid-induced respiratory depression occur
commonly. Little is known about the mechanisms of capture-induced hyperthermia,
and the effects of opioid drugs on respiratory function still need to be clarified. Also,
current methods of reversing opioid-induced respiratory depression are inadequate. I
therefore investigated the mechanisms and patterns of capture-induced hyperthermia,
by continuously measuring body temperatures of impala during different capture
procedures. I also investigated the effects of opioid drugs on respiratory function and
pulmonary performance by examining the changes of cardiorespiratory variables
before and during opioid immobilization of goats and impala. Concurrently, I
investigated whether serotonergic ligands could be used to reverse the opioid-induced
respiratory depression that occurred in these animals.
I found stress to be the major factor associated with capture-induced hyperthermia,
with exercise playing a minor role. I also found that environmental thermal conditions
and the pharmacological effects of the capture drugs played no role in inducing
capture-induced hyperthermia. I found that the opioid drug etorphine, which is
commonly used to chemically capture wild animals, not only causes depression in
respiratory rhythm and ventilation, but also a decrease in alveolar-arterial oxygen
exchange. I demonstrated that serotonergic ligands with agonist effects at 5-HT1A and
5-HT4 receptors partially reversed opioid-induced respiratory depression and hypoxia,
predominantly by improving alveolar-arterial oxygen exchange, presumably by increasing pulmonary perfusion and improving ventilation perfusion ratios, but also,
in some cases, by improving ventilation.
I advise that to limit the morbidity and mortality associated with capture-induced
hyperthermia, procedures that cause the least stress should be used and animals should
be exposed to stressors for the shortest time possible. The use of anxiolytic drugs to
reduce stress may also be considered. If animals are captured by chemical
immobilization with opioid drugs their respiratory function should be monitored
closely. Counting breaths does not adequately monitor respiratory function and
methods to assess carbon dioxide and oxygen levels in arterial blood should be used.
If respiratory depression occurs, efforts to reverse this depression should not focus
only on improving ventilation but also should aim at improving gas exchange in the
lungs. Serotonergic ligands with agonist effects at 5-HT1A and 5-HT4 receptors could
be used to achieve these aims. Although some of these ligands can cause arousal in
immobilized animals, if they are administered with the opioid they enhance the
induction of catatonic-immobilization, and their use in a dart may not only improve
knock down times, thereby minimising stress and capture-induced hyperthermia, but
they may also prevent opioid-induced respiratory depression
