Anesthesiology
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Comparative Study
A peripheral adrenoceptor-mediated sympathetic mechanism can transform stress-induced analgesia into hyperalgesia.
Stress has paradoxical effects on pain, causing stress-induced analgesia but also exacerbating pain via poorly understood mechanisms. Adrenergic neurotransmission is integral in pathways that regulate the response to both pain and stress. Hyperalgesia is often associated with enhanced adrenergic sensitivity of primary afferents, but sympathetic nervous system outflow has not been demonstrated to exacerbate pain perception after stress. ⋯ Sympathetic postganglionic nerves can enhance pain sensation via a peripheral α-1-adrenoceptor mechanism when sympathetic outflow is disinhibited. The net effect of stress on pain sensation reflects a balance between descending spinal inhibition and sympathetic outflow that can shift toward pain facilitation when central and peripheral α-2-adrenoceptor inhibitory mechanisms are attenuated.
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Anecdotal reports suggest that carnitine deficiency increases susceptibility to bupivacaine-induced cardiotoxicity. Bupivacaine inhibits lipid-based respiration in myocardial mitochondria via inhibition of acylcarnitine exchange in rats. The authors hypothesized that carnitine deficiency increases susceptibility to bupivacaine-induced asystole in rats and that acute repletion with L-carnitine reverses this effect. ⋯ Carnitine deficiency increased sensitivity to bupivacaine-induced asystole, an effect that was reversed completely by L-carnitine repletion. This study suggests that carnitine deficiency may predispose to bupivacaine-induced cardiotoxicity. L-carnitine may have a protective role against bupivacaine cardiotoxicity.
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Editorial Comment
Perioperative hyperoxia: the debate is only getting started.