Ji Yeon Sim

Intraoperative Renal Regional Oxygen Desaturation Can Be a Predictor for Acute Kidney Injury after Cardiac Surgery

OBJECTIVE To evaluate the usefulness of renal regional oxygen saturation (renal rSO2) in predicting the risk of acute kidney injury (AKI) after cardiac surgery. DESIGN A prospective observational study. SETTING Tertiary care university hospital. PARTICIPANTS One hundred patients undergoing cardiac surgery. INTERVENTIONS Renal rSO2 was monitored continuously by near-infrared spectroscopy (NIRS) throughout the anesthetic period. MEASUREMENTS AND MAIN RESULTS Postoperative AKI was defined using the Risk, Injury, Failure, Loss, and End-stage (RIFLE) criteria. Of 95 patients who were included in the final analysis, 34 patients developed AKI after surgery. Recorded renal rSO2 data were used to calculate the total duration of the time when renal rSO2 was below the threshold values of 70%, 65%, 60%, 55%, and 50%. The total periods when the renal rSO2 level was below each of the threshold values were significantly longer in patients with AKI than in those without AKI (p = 0.001 or p<0.001). Receiver operating characteristic (ROC) curve analysis was used to evaluate the predictive power of renal rSO2 for AKI. The ROC curve analysis showed that renal rSO2 could predict the risk of AKI with statistical significance and that a renal rSO2<55% had the best performance (area under the curve-ROC, 0.777; 95% CI, 0.669-0.885; p<0.001). Multivariate logistic regression analysis revealed that AKI significantly correlated with the duration of renal rSO2<55% (p = 0.002) and logistic EuroSCORE (p = 0.007). CONCLUSIONS Intraoperative renal regional oxygen desaturation can be a good predictor of AKI in adult patients undergoing cardiac surgery.

Conduction block by clonidine is not mediated by α2-adrenergic receptors in rat sciatic nerve fibers☆

Background and Objectives Clonidine, an α 2-adrenergic agonist, has been shown to prolong local anesthesia. It appears that clonidine by itself produces conduction block by acting on peripheral nerves. However, whether clonidine-induced conduction block is mediated through α 2-adrenergic receptors remains unclear. The purpose of this study was to see if clonidine’s nerve-blocking action was through α 2-adrenergic receptors by examining clonidine’s action in the presence of α 2-adrenergic antagonists. Methods The compound action potentials (CAPs) evoked by electrical stimuli were recorded from the isolated rat sciatic nerve in a recording chamber. Conduction block was examined by analyzing CAPs with regard to peak amplitude and time-to-peak in the presence of clonidine alone or clonidine plus α 2-adrenergic antagonist yohimbine or idazoxan. Results Both clonidine and yohimbine produced concentration-dependent, reversible, conduction block. Based on concentration-response relationships, the 50% of effective concentration (EC50) were estimated to be 1.61 ± 0.51 mmol/L (mean ± SD) for clonidine and 51.4 ± 27.2 μmol/L for yohimbine. A mixture of equal volumes of 2.07 mmol/L clonidine and 55.6 μmol/L yohimbine produced conduction block to a level close to the mean value between conduction blocks induced by 2.07 mmol/L clonidine alone and 55.6 μmol/L yohimbine alone. Addition of idazoxan, a more specific α 2-adrenergic antagonist than yohimbine, to clonidine was without effect on clonidine-induced conduction block. Conclusions The results indicated that the mixture of clonidine and yohimbine, in which either drug inhibited impulse conduction, produced conduction block in an additive manner, and that clonidine-induced conduction block was not reversed by coapplication with a specific α 2-adrenergic antagonist idazoxan. These data suggest that clonidine’s effects likely depend on mechanisms not mediated by α 2-adrenergic receptors.

The effects of gabapentin pretreatment on brain injury induced by focal cerebral ischemia/reperfusion in the rat

Background Experimental studies have shown that gabapentin can reduce neuronal injury in the setting of cerebral ischemia, but the mechanisms have not yet been clearly determined. This study was conducted to determine whether gabapentin pretreatment altered expression levels of heat shock protein 70 and reduced acute phase neuronal injury in rats subjected to transient focal cerebral ischemia/reperfusion. Methods Forty male Sprague-Dawley rats (260-300 g) were randomly assigned to one of four groups (saline-treated, or 0.1, 0.5, or 5 mg/kg gabapentin group). In all animals, focal cerebral ischemia was induced by intraluminal middle cerebral artery occlusion for 1 hour. The animals of the gabapentin groups were pretreated with a single intravenous administration of gabapentin 20 minutes before ischemic insults. The infarct volume, brain edema and motor behavior deficits were analyzed 24 hours after ischemic insult. Caspase-3-reactive cells and cells showing Hsp70 activity were counted in the caudoputamen and fronto-parietal cortex. Results The infarction ratio was significantly decreased in the 5 mg/kg gabapentin group (P < 0.05) and brain edema ratios were significantly reduced in the 0.1 mg/kg, 0.5 mg/kg, and 5 mg/kg gabapentin groups 24 hours after ischemia/reperfusion injury (P < 0.05). There were more Hsp70-reactive cells in the 5 mg/kg gabapentin group than in the saline group in both the caudoputamen and fronto-parietal cortex (P < 0.05). Conclusions These results indicate that gabapentin may have a neuroprotective effect and can reduce early neuronal injury caused by focal cerebral ischemia/reperfusion; this may be mediated by expression of Hsp70. However, gabapentin pretreatment did not prevent caspase-dependent apoptosis.

Temporary bilateral sensorineural hearing loss following cardiopulmonary bypass -A case report-

Sudden sensorineural hearing loss has been reported to occur following anesthesia and various non-otologic surgeries, mostly after procedures involving cardiopulmonary bypass. Unilateral sensorineural hearing loss resulting from microembolism is an infrequent complication of cardiopulmonary bypass surgery that has long been acknowledged. Moreover, there are few reports on the occurrence of bilateral sensorineural hearing loss without other neurologic deficits and its etiology has also not been determined. We describe here a rare case of bilateral hearing loss without other neurologic deficits in an otherwise healthy 27-year-old woman who underwent cardiopulmonary bypass surgery for repair of severe mitral valve stenosis. The patient suffered from profound sensorineural hearing loss in both ears that was recognized immediately upon extubation, and audiometry tests confirmed the diagnosis. Without any treatment, her hearing recovered almost completely by the time of her discharge one week after surgery.

Anesthetic considerations of percutaneous transcatheter aortic valve implantation: first attempt in Korea -A report of 2 cases-

Conventional aortic valve replacement for severe aortic stenosis is associated with a high operative mortality in the elderly patients with significant comorbidities, including severe respiratory dysfunction, renal insufficiency, and compromised cardiac function. Human transcatheter aortic valve implantation was first reported in 2002 and has become a valid alternative in selected high-risk patients in Europe and North America. This article describes the first attempt of transfemoral transcatheter aortic valve implantation in Korea. The procedure was applied in two consecutive patients with severe aortic stenosis. Despite several intra-operative complications during procedure, the post-operative outcomes were good for both patients. At post-operative 30 days there was satisfactory prosthetic valve function and hemodynamic stability.

Growth suppression of four cancer cells by hyperbaric nitrous oxide and methotrexate

Background Nitrous oxide concentration is easily controlled by respiratory ventilation. It suppresses bone marrow via the inhibition of thymidylate synthesis. The aim of this work was to determine the optimal pressure and exposure duration of nitrous oxide, as well as methotrexate concentration that maximizes the suppression of 4 cancer cells: CCRF-CEM, K562, A549 and MDA-MB-231. Methods Each cancer cell was cultured in a hyperbaric chamber at 1, 2 and 3 atmosphere of 74% nitrous oxide for 24, 48, and 72 hours at 0, 0.3, 0.7, 1, 2, 5 and 10 µM methotrexate (MTX), respectively. The results were expressed in the ratio of the number of cancer cells cultured under specific conditions (S cells) to that under normal conditions (N cells). Results The S/N ratio of CCRF-CEM cells was 87.4% in 24-hour culture, 95.0% in 48-hour culture and 115.9% in 72-hour culture (P < 0.05). The S/N ratio of K562 cells was 103.6% at 1 atm, 102.4% at 2 atm and 115.6% at 3 atm (P < 0.05). The S/N ratio of A549 cells was 94.3% at 1 atm, 94.1% at 2 atm, 99.3% at 3 atm, 96.2% in 24-hour culture, 99.2% in 48-hour culture and 99.3% in 72-hour culture (P > 0.05). However, the S/N ratio of MDA-MB 231 cells was 66.9% in 24-hour culture, 83.1% in 48 hour culture and 87.8% in 72-hour culture (P < 0.05). Conclusions Only the growth of the MDA-MB-231 cells was significantly reduced after a longer exposure time to nitrous oxide, but those of the other cells were not.