The purpose of this study is to investigate the hypothesis that epidural analgesia combined with fentanyl suppresses endocrine responses and prevents renal impairment during thoracotomy. Thirty patients undergoing elective lung lobectomy via thoracotomy were randomly divided into three groups according to the anesthetic method. The patients of group GA received only general anesthesia. Those in group CGE received general anesthesia and epidural analgesia with 1% mepivacaine. Those in group F received general anesthesia, epidural analgesia with 1% mepivacaine, and fentanyl given both intravenously and to the epidural space. Plasma cortisol and aldosterone were measured as indicators of the endocrine response. Urinary output of N-acetyl-beta-D-glucosaminidase(NAG) was also measured as an indicator of renal tubular damage. In group F, NAG and cortisol releases were suppressed. NAG increased by 191% and by 119%, and cortisol increased by 247% and by 167% in group GA and CGE, respectively(p<0.05). In group F, the aldosterone release was attenuated down to 48% over the pre-operative values, while it increased markedly by 358% and by 264%, in group GA and CGE, respectively. These results suggest that fentanyl in addition to epidural analgesia attenuates the endocrine responses and the renal tubular damage during thoracotomy.

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The aim of this study is to evaluate the relationship between the increase in the expression of Na⁺/Ca²⁺ exchanger(NCX) and the increased vulnerability to ischemia/reperfusion in the remodeled hearts. The coronary artery of male adult rats was ligated. One week later, the hearts were removed and perfused with Krebs-Henseleit buffer(KHB) solution. Control hearts were perfused with KHB solution for 2 hours. Ischemic hearts were first perfused with KHB solution for 30 minutes, and then the perfusion was perfectly terminated and the hearts were immersed in saline for 30 min. The hearts were perfused again with KHB solution for 1 hour. Western blotting revealed that the expression of cardiac NCX in the remodeled hearts was significantly increased as compared with that in the non-remodeled hearts. Both the secondary ischemia-induced increases in the caspase-3 cleavage and the calpain activity were more intensively detected in the remodeled hearts than those in the non-remodeled hearts. These results suggest that the expression of cardiac NCX is increased in association with cardiac remodeling, and that the secondary ischemia might result in the marked increase in the concentration of intracellular Ca²⁺ via reversed NCX, leading to the increase in apoptotic cardiomyocytes in the remodeled hearts.

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This is a report of a 47-yo female patient who had been suffering from obstructive sleep apnea(OSAS) concomitant with frequent ventricular premature complexes(VPCs) during sleeping which might lead to sudden death. Standard polysomnography(PSG) revealed her OSAS with apnea-hypopnea index(AHI) of 14.7, the longest apnea time(LAT) of 83.5 sec, nadir SpO₂ of 81%, and snoring index(SI) of 295.1. Frequent VPCs(total of 763 times) were also observed during the PSG. Oral appliance(ORAP) therapy was applied to her OSAS because she could not tolerate nasal continuous positive airway pressure previously applied elsewhere. The PSG under ORAP therapy showed the improvements of OSAS(AHI of 0.6, LAT of 22.3sec, nadir SpO₂ of 93%, SI of 0.1) as well as the disappearance of frequent VPCs.

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A 51 year-old man was admitted for displacement of the discending aorta for traumatic aortic injury. After induction of anesthesia, we inserted a transesophageal echocardiography probe and found dissection of the discending aorta, dilatation of the proximal part of the left subclavian artery and exfoliation of inner and mediam membrane of the left subclavian artery.

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A 64 year-old patient with compromised severe right-coronary artery disease underwent cholecystectomy under total intravenous anesthesia(TIVA) using propofol-fentanyl-vecuronium. Third degree A-V block occurred during surgery; however after administration of atropine, normal sinus rhythm was restored. Since TIVA using propofol and fentanyl tends to cause bradycardia, we should be particularly aware of the possibility of A-V block in patients with compromised severe right-coronary artery disease.

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