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Hypoxia during immobilization, not a simple cause https://vimeo.com/216824933 Leith Meyer Associate Professor Pharmacology, Department of Paraclinical Sciences, Faculty of Veterinary Science, Onderstepoort, University of Pretoria and Honorary Research Fellow, Brain Function Research Group, School of Physiology, Faculty of Medicine, University of the Witwatersrand. Leith.meyer@up.ac.za Introduction Arguably, hypoxia is the leading cause of morbidity and mortality during chemical immobilization of wildlife. This hypoxia is thought to be primarily associated with drug-induced respiratory depression and mainly occurs when potent opioids are used. That opioids cause respiratory depression is a well-known phenomenon. However, the assumption that this depression is the primary cause of hypoxia during chemical immobilization may not be entirely correct. Opioids do depress the respiratory system by affecting neuronal function in the central and peripheral nervous systems. Neuronal depression in the brainstem respiratory centres results in a decrease in respiratory rate and rhythm, and reduced chemoreceptor response to hypercapnia. Peripheral neuron depression in the aortic and carotid bodies also depresses chemoreceptor responses to hypoxia, hypercapnia and acidaemia. These neuronal effects result in hypoventilation with uncompensated hypercapnia, acidaemia and hypoxia. These effects are described as classical opioid-induced respiratory depression. This depression does cause significant hypoxia, but it doesn’t completely account for the hypoxia that occurs during chemical immobilization. Opioids also compromise the respiratory system through a number of other mechanisms. Included in these mechanisms are an increase in airway resistance, a decrease in chest and abdominal wall compliance, pulmonary hypertension and hyper- metabolism. This presentation will focus on these mechanisms and discuss the significance of other capture related effects and drugs which may also compromise respiration and exacerbate hypoxia, hypercapnia and acidaemia. Background Opioids cause respiratory depression when they are used during general anaesthesia and analgesia, both in man and other animals. This respiratory depression may cause hypoxic damage to vital organs and leads to an increase in morbidity and mortality. Opioid drugs cause respiratory depression mainly through their activation of opioid receptors that occur in respiratory neurones (McCrimmon & Alheid 2003; Shook et al. 1990). Different opioid drugs do not cause equivalent respiratory depressive effects as their effects on respiratory function are dependent on which opioid receptors they activate. The activation of mu(µ)-opioid receptors, in particular µ2 receptors, causes respiratory depression (Haji et al. 2000; Shook et al. 1990). There is also evidence that activation of both delta (δ)- and kappa (κ)-opioid receptors also causes some degree of respiratory depression (Ballanyi et al. 1997; Bowdle 1988; Lonergan et al. 2003; Takeda et al. 2001), but the main depressant effects of opioids appear to result from the activation of μ2-opioid receptors (Haji et al. 2000). The activation of opioid receptors results in a number of effects that cause respiratory depression. The neurones in the pre-Bötzinger complex appear to be the most sensitive to μ-opioid agonists and therefore the most important of these effects is a disturbance in respiratory rhythm (Lalley 2003; Pattinson 2008). Opioids also disturb respiratory rhythm by activating respiratory neurones in the pons and also reduce the ability of the ventral respiratory group neurones to react to the chemoreceptor response to hypercapnia and hypoxia (Lalley 2008; McCrimmon & Alheid 2003; Pattinson 2008; Santiago & Edelman 1985; Shook et al. 1990). Opioids also depress the neurones that regulate tidal volumes, and thus may decrease the depth of breathing (Lalley 2003; Lalley 2008). They 2017 MAY 21