Chronic pain induces anxiety with concomitant changes in opioidergic function in the amygdala.

Clinically, it has been reported that chronic pain induces depression, anxiety, and reduced quality of life. The endogenous opioid system has been implicated in nociception, anxiety, and stress. The present study was undertaken to investigate whether chronic pain could induce anxiogenic effects and changes in the opioidergic function in the amygdala in mice. We found that either injection of complete Freund's adjuvant (CFA) or neuropathic pain induced by sciatic nerve ligation produced a significant anxiogenic effect at 4 weeks after the injection or surgery. Under these conditions, the selective mu-opioid receptor agonist [D-Ala2,N-MePhe4,Gly5-ol]-enkephalin (DAMGO)- and the selective delta-opioid receptor agonist (+)-4-[(alphaR)-alpha-((2S,5R)-4-allyl-2,5-dimethyl-1-piperazinyl)-3-methoxybenzyl]-N,N-diethylbenzamide (SNC80)-stimulated [35S]GTPgammaS binding in membranes of the amygdala was significantly suppressed by CFA injection or nerve ligation. CFA injection was associated with a significant increase in the kappa-opioid receptor agonist 2-(3,4-dichlorophenyl)-N-methyl-N-[(1S)-1-phenyl-2-(1-pyrrolidinyl)ethyl]acetamide hydrochloride (ICI199,441)-stimulated [35S]GTPgammaS binding in membranes of the amygdala. The intracerebroventricular administration and microinjection of a selective mu-opioid receptor antagonist, a selective delta-opioid receptor antagonist, and the endogenous kappa-opioid receptor ligand dynorphin A caused a significant anxiogenic effect in mice. We also found that thermal hyperalgesia induced by sciatic nerve ligation was reversed at 8 weeks after surgery. In the light-dark test, the time spent in the lit compartment was not changed at 8 weeks after surgery. Collectively, the present data constitute the first evidence that chronic pain has an anxiogenic effect in mice. This phenomenon may be associated with changes in opioidergic function in the amygdala.

[Anesthetic management of a patient with dilated cardiomyopathy for left ventricular pacing lead insertion under video-assisted thoracic surgery].

A 54-year-old man with dilated cardiomyopathy treated with diuretics, alpha-beta blockers, antiarrhythmics for the previous 5 years, had the indication for biventricular pacing and was scheduled for placing of pacing leads in his left ventricular wall under video-assisted thoracic surgery. Preoperative tests revealed first degree A-V block with left bundle branch block and left ventricular dilation with an ejection fraction of 0.11 on echocardiography. Anesthesia was induced with ketamine and midazolam. Endotracheal intubation was facilitated by administration of vecuronium. Anesthesia was maintained with oxygen-sevoflurane and fentanyl. One lung ventilation was carried out during surgery and the arterial oxygen saturation was kept satisfactory with the intermittent insuffilation of oxygen to the non ventilated lung. The procedure was completed uneventfully while ventricular tachycardia was observed. Biventricular pacing increased the ejection fraction from 0.11 to 0.27. We conclude that any special monitoring such as TEE would be helpful to evaluate the cardiac function during the operation.