hile coronary perforation is an uncommon complication following percutaneous coronary intervention (PCI), [1][2][3][4][5][6][7][8] it is one that may lead to cardiac tamponade, 6-9 emergency coronary artery bypass surgery (CABG), or pseudoaneurysm formation, 10 with the potential for late coronary rupture. New coronary devices that resect (eg, directional or transluminal extraction atherectomy), ablate (eg, rotational atherectomy or excimer laser angioplasty), or score (eg, the cutting balloon) atherosclerotic plaque may increase the risk of coronary perforation, and a number of angiographic risk factors for its occurrence have been described previously. [11][12][13][14] The use of newer higher-weight and hydrophilic coronary guidewires may also increase the risk of coronary perforation, particularly during the treatment of chronic coronary occlusions. Clinical algorithms for the treatment of coronary perforation based on angiographic and clinical criteria have been Circulation Journal Vol.66, April 2002 less well studied. Moreover, descriptions of the long-term sequelae after coronary perforation, and delineation of the potential risk for late pseudoaneurysm formation and coronary rupture, have been lacking.The present study examines the frequency of coronary perforation during PCI, evaluates the management strategies used to treat the perforation, and describes the long-term prognosis in patients who have developed coronary perforation during PCI. To address these issues, we reviewed our experience with coronary perforation in a consecutive series of 7,443 patients undergoing PCI at a single, highvolume clinical center. Methods Patient PopulationBetween January 1992 and December 1996, 7,443 coronary interventional procedures were performed in the Cardiac Catheterization Laboratory at National Toyohashi Higashi Hospital. These procedures included conventional balloon angioplasty (n=4,895; 65.8%), cutting balloon angioplasty (n=1,274; 17.1%), coronary artery stenting (n=810; 10.9%), directional coronary atherectomy (DCA) (n=440; 5.9%), and transluminal extraction catheter atherectomy (n=24, 0.32%). Coronary perforation is a rare but serious complication that occurs during percutaneous coronary intervention (PCI). This study examines the frequency of coronary perforation during PCI, evaluates the management strategies used to treat perforations, and describes the long-term prognosis of patients who have developed coronary perforation during PCI. Coronary perforations were found in 69 (0.93%) of 7,443 consecutive PCI procedures, occurring more often after use of a new device (0.86%) than after use of balloon angioplasty (0.41%) (p<0.05).Coronary perforation was attributable solely to the coronary guidewire in 27 (0.36%) cases. Coronary perforations were divided into 2 types: (1) Those with epicardial staining without a jet of contrast extravasation (type I, n=51), and (2) those with a jet of contrast extravasation (type II, n=18). Patients with type I and type II perforations were managed by observation only (3...

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Measurements of electrical resistivity ͑͒, dc magnetization ͑M͒, and specific heat ͑C͒ have been performed on layered oxide Li x CoO 2 ͑0.25Յ x Յ 0.99͒ using single-crystal specimens. The versus temperature ͑T͒ curve for x = 0.90 and 0.99 is found to be insulating but a metallic behavior is observed for 0.25Յ x Յ 0.71. At T S ϳ 155 K, a sharp anomaly is observed in the -T, M-T, and C / T-T curves for x = 0.66 with thermal hysteresis, indicating the first-order character of the transition. The transition at T S ϳ 155 K is observed for the wide range of x = 0.46-0.71. It is found that the M-T curve measured after rapid cool becomes different from that after slow cool below T F , which is ϳ130 K for x = 0.46-0.71. T F is found to agree with the temperature at which the motional narrowing in the 7 Li NMR linewidth is observed, indicating that the Li ions stop diffusing and order at the regular site below T F . The ordering of Li ions below T F ϳ 130 K is likely to be triggered and stabilized by the charge ordering in CoO 2 layers below T S .

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Urinary exosomes are small vesicles secreted into urine from all renal epithelial cell types and known to contain proteins that are involved in renal secretion and reabsorption. Among these proteins, urinary exosomal aquaporin-2 (AQP2) has been suggested to be useful for diagnosis of renal disease. However, the mechanisms underlying the excretion of urinary exosomal AQP2 are largely unknown. In this study, we examined the mechanisms of urinary exosomal AQP2 excretion in vivo, using diuretics including furosemide (FS), an inhibitor of the sodium-potassium-chloride symporter; acetazolamide (ACTZ), an inhibitor of carbonic anhydrase; OPC-31260 (OPC), a vasopressin type 2 receptor antagonist; and NaHCO3, a urinary alkalizing agent. Samples of urine from rats were collected for 2 h just after treatment with each diuretic, and urinary exosomes were isolated by ultracentrifugation. Urinary exosomal AQP2 excretion was dramatically increased by treatment with FS accompanied by urine acidification or with ACTZ accompanied by urine alkalization. Immunohistochemistry showed that apical localization of AQP2 was clearly evident and the plasma vasopressin level was increased after each treatment. Although treatment with OPC alone had no significant effect, coadministration of OPC completely inhibited the FS-induced and partially reduced the ACTZ-induced responses, respectively. Treatment with NaHCO3 increased the excretion of urinary exosomal AQP2 accompanied by urine alkalization. This increased response was partially inhibited by coadministration of OPC. These data suggest that an increased plasma level of vasopressin promoted the excretion of urinary exosomal AQP2 and that urine alkalinization also increased it independently of vasopressin.