Kyung Yeon Yoo

Acute Respiratory Distress Syndrome Associated With Pulmonary Cement Embolism Following Percutaneous Vertebroplasty With Polymethylmethacrylate

Study Design. A case of acute respiratory distress syndrome following percutaneous vertebroplasty is described. Objective. To alert clinicians to the potential occurrence of acute respiratory distress syndrome following use of polymethylmethacrylate bone cement. Summary of Background Data. Noncardiogenic pulmonary edema has not been reported following intravertebral injection of polymethylmethacrylate. Methods. A 68-year-old woman underwent percutaneous vertebroplasty for a painful L5 compression fracture under local anesthesia. A contralateral transpedicular approach was made to inject polymethylmethacrylate. Results. On the third postoperative day, she developed arthralgia, myalgia, fever, and frequent coughing. Chest radiography revealed bilateral, multifocal, patchy consolidations, suggestive of acute respiratory distress syndrome, and a 5-cm-long tubular radiopacity in the right pulmonary artery. She died 20 days after the vertebroplasty. Conclusion. This case illustrates that clinicians must be aware of the potential occurrence of acute respiratory distress syndrome in patients who received percutaneous vertebroplasty.

The effects of volatile anesthetics on spontaneous contractility of isolated human pregnant uterine muscle : A comparison among sevoflurane, desflurane, isoflurane, and halothane

We examined the effects of equianesthetic concentrations of sevoflurane, desflurane, isoflurane, and halothane on the spontaneous contractility of isolated human pregnant uterine muscles. We also determined if their action was related to potassium channels. Uterine specimens were obtained from normal full-term pregnant women undergoing elective lower-segment cesarean delivery. Longitudinal muscle strips were mounted vertically in tissue chambers. Their isometric tension was recorded while they were exposed to 0.5–3 minimum alveolar concentration (MAC) of volatile anesthetics in the absence and presence of the high conductance calcium-activated potassium channel blocker, tetraethylammonium, or the adenosine triphosphate-sensitive potassium channel (KATP)-blocker, glibenclamide. The anesthetics examined produced a dose-dependent depression of contractility. The inhibitory potency of sevoflurane and desflurane was comparable to, whereas that of isoflurane was smaller than, that of halothane: concentrations causing 50% inhibition of the contractile amplitude (ED50) were 1.72, 1.44, 2.35, and 1.66 MAC (P < 0.05), respectively. Tetraethylammonium and glibenclamide did not affect the uterine response to the anesthetics, except for glibenclamide, which attenuated the response to isoflurane. These results indicate that the volatile anesthetics have inhibitory effects on the contractility of the human uterus. The inhibitory effect of isoflurane may in part be mediated through activation of KATP channels.

Cerebral Oxygen Saturation Measured by Near-infrared Spectroscopy and Jugular Venous Bulb Oxygen Saturation during Arthroscopic Shoulder Surgery in Beach Chair Position under Sevoflurane-Nitrous Oxide or Propofol-Remifentanil Anesthesia

Background: We examined the effects of different anesthetics on cerebral oxygenation and systemic hemodynamics in patients undergoing surgery in beach chair position (BCP). Jugular venous bulb oxygen saturation (SjvO2) and regional cerebral tissue oxygen saturation (SctO2) were determined while patients were placed from the supine to BCP. Whether SctO2 and SjvO2 are interchangeable in assessing the cerebral oxygenation was also examined. Methods: Forty patients undergoing shoulder surgery in BCP were randomly assigned to receive sevoflurane-nitrous oxide (S/N) or propofol-remifentanil (P/R) anesthesia. Four patients taking angiotensin II receptor antagonists were excluded post hoc. Mean arterial pressure and heart rate, as well as SjvO2 and SctO2, were measured before (postinduction baseline in supine position) and after BCP. Results: Mean arterial pressure decreased by BCP in both groups. It was, however, significantly higher in S/N (n = 19) than in P/R group (n = 17) at 7 to 8 min after the positioning. SjvO2 also significantly decreased after BCP in both groups, the magnitude of which was lower in S/N than in P/R group (11 ± 10% vs. 23 ± 9%, P = 0.0006). The incidences of SjvO2 <50% and mean arterial pressure less than 50 mmHg were lower in S/N group, but SctO2and the incidence of cerebral desaturation (more than 20% decrease from baseline) did not significantly differ between the groups. SctO2 and SjvO2 were only weakly correlated (&bgr; = 0.218, r2 = 0.133). Bland-Altman analysis showed a mean difference of −7.2% with 95% limit of agreement between −38.2% and 23.8%. Conclusions: The margin of safety against impaired cerebral oxygenation is greater and SjvO2 is more preserved with S/N than with P/R anesthesia. SctO2 may not be reliable in detecting a low SjvO2 during the surgery in BCP.

In vivo bioluminescence imaging of cord blood derived mesenchymal stem cell transplantation into rat myocardium

ObjectiveThe conventional method for the analysis of myocardial cell transplantation depends on postmortem histology. Here, we have sought to demonstrate the feasibility of a longitudinal monitoring of transplanted cell survival in living animals, accomplished with optical imaging techniques and pharmacological interventions.MethodsHuman cord blood (50 ml) was donated with parental consent. After getting cord blood derived mesenchymal stem cells (CBMSCs), cells were transfected (MOI = 100) overnight with adenovirus encoding firefly luciferase gene (Ad-CMV-Fluc). Our experimental Sprague-Dawley rats (n = 12) were given intramyocardial injections containing 1 × 106 CBMSCs, which had been made to express the firefly luciferase (Fluc) reporter gene. Optical bioluminescence imaging was then conducted using a cooled charged-coupled device (CCD) camera (Xenogen), beginning on the day after the transplantation (day 1). Groups of mice were intraperitoneally injected with cyclosporine (5 mg/kg) or tacrolimus (1 mg/kg), in an attempt to determine the degree to which cell survival had been prolonged, and these values were then compared with the cell survival values of the negative control group. The presence of transplanted CBMSCs on in vivo images confirmed by in situ hybridization for human specific Alu in the myocardium.ResultsCardiac bioluminescence signals were determined to be present for 6 days after transplantation: day 1 (97000 ± 9100 × 105 p/s/cm2/sr), day 3 (9600 ±1110 p/s/cm2/sr), and day 5 (3200 ± 550 p/s/cm2/sr). The six mice that received either cyclosporine or tacrolimus displayed cardiac bioluminescence signals for a period of 8 days after transplantation. We observed significant differences between the treated group and the non-treated group, beginning on day 3 (tacrolimus; 26500 ± 4340 p/s/cm2/sr, cyclosporine; 27200 ± 3340 p/s/cm2/sr, non-treated; 9630 ± 1180 p/s/cm2/sr, p < 0.01), and persisting until day 7 (tacrolimus; 12500 ± 2946 p/s/cm2/sr, cyclosporine; 7310 ±1258 p/s/cm2/sr, non-treated; 2460 ± 160 p/s/cm2/sr, p < 0.01). The human-derived CBMSCs were detected in the myocardium 3 days after transplantation by in situ hybridization.ConclusionsThe locations, magnitude, and survival duration of the CBMSCs were noninvasively monitored with a bioluminescence optical imaging system. We determined that optical molecular imaging expedites the fast throughput screening of pharmaceutical agents, allowing for the noninvasive tracking of cell survival within animals. In rat cardiac CBMSC transplant models, transient immunosuppressive treatment with tacrolimus or cyclosporine was shown to improve donor cell survival.

Effects of remifentanil on cardiovascular and bispectral index responses to endotracheal intubation in severe pre-eclamptic patients undergoing Caesarean delivery under general anaesthesia

BACKGROUND We examined the effects of remifentanil on cardiovascular and bispectral index (BIS) responses to tracheal intubation and neonatal outcomes in pre-eclamptic patients undergoing Caesarean delivery under general anaesthesia. METHODS Forty-two women with severe pre-eclampsia were randomly assigned to receive either remifentanil 1 microg kg(-1) (n=21) or saline (n=21) over 30 s before induction of anaesthesia using thiopentone 4 mg kg(-1) and suxamethonium 1.5 mg kg(-1). Mean arterial pressure (MAP), heart rate (HR) and BIS values as well as plasma catecholamine concentrations were measured. Neonatal effects were assessed using Apgar scores and umbilical cord blood gas analysis. RESULTS Induction with thiopentone caused a reduction in MAP and BIS in both remifentanil and control groups. Following the tracheal intubation MAP and HR increased in both groups, the magnitude of which was lower in the remifentanil group. BIS values also increased, of which magnitude did not differ between the groups. Norepinephrine concentrations increased significantly following the intubation in the control, while remained unaltered in the remifentanil group. The neonatal Apgar scores at 1 min were significantly lower in the remifentanil group than in the control. However, Apgar scores at 5 min, and umbilical artery and vein blood gas values were similar between the groups. CONCLUSIONS These results suggest that a single bolus of 1 microg kg(-1) remifentanil effectively attenuates haemodynamic but not BIS responses to tracheal intubation in pre-eclamptic patients undergoing Caesarean delivery under general anaesthesia. However, its use was associated with maternal hypotension and neonatal respiratory depression requiring resuscitation.

Curcumin protects against regional myocardial ischemia/reperfusion injury through activation of RISK/GSK-3β and inhibition of p38 MAPK and JNK.

Background: Curcumin, the active ingredient of turmeric (Curcuma longa), is known to have anti-inflammatory and antioxidative properties. The present study was aimed to determine the effect of curcumin in regional myocardial ischemia/reperfusion (I/R) injury and its underlying mechanisms involving the role of prosurvival kinases and apoptotic kinases. Methods: Sprague-Dawley rats (n = 109) subjected to a 30-minute left anterior descending coronary artery (LAD) occlusion followed by reperfusion were assigned to receive saline (control), curcumin (100 mg/kg), wortmannin (inhibitor of phosphatidylinositol-3-OH kinase [PI3K]-Akt), wortmannin + curcumin, U0126 (inhibitor of extracellular signal-regulated kinase [ERK1/2]), U0126 + curcumin, SB216763 (inhibitor of glycogen synthase kinase [GSK-3β]), and SB216763 + curcumin 20 minutes before LAD occlusion. Infarct size was measured after 2 hours of reperfusion by triphenyl tetrazolium chloride staining. The phosphorylation of Akt, ERK1/2, GSK-3β, p38, and c-Jun N-terminal kinases (JNK) was determined by immunoblotting after 10 minutes of reperfusion. Results: Curcumin significantly reduced the infarct size compared with the control (33.1% ± 6.2% vs 50.1% ± 3.9%; P < .05). Wortmannin or U0126 alone did not affect the infarct size but abolished the curcumin-induced cardioprotective effect. Curcumin significantly enhanced the phosphorylation of Akt, ERK1/2, and GSK-3β, while it reduced that of p38 and JNK. Wortmannin or U0126 abolished enhanced phosphorylation of GSK-3β induced by curcumin. SB216763 alone or combined with curcumin reduced the infarct size and enhanced phosphorylation of GSK-3β compared with the control. Conclusions: Preconditioning by curcumin effectively protects against regional myocardial I/R injury through the activation of prosurvival kinases involving PI3K-Akt, ERK1/2, and GSK-3β, and attenuation of p38 and JNK.

Dose-related attenuation of cardiovascular responses to tracheal intubation by intravenous remifentanil bolus in severe pre-eclamptic patients undergoing Caesarean delivery

BACKGROUND The optimal dose of remifentanil to attenuate the cardiovascular responses to tracheal intubation in pre-eclamptic patients undergoing Caesarean delivery under general anaesthesia has not been established. We compared the effects of two low doses of remifentanil on the cardiovascular responses to tracheal intubation and neonatal outcomes. METHODS Forty-eight women with severe pre-eclampsia were randomly assigned to receive either remifentanil 0.5 µg kg⁻¹ (R0.5 group, n=24) or 1 µg kg⁻¹ (R1.0 group, n=24) over 30 s before induction of anaesthesia using thiopental 5 mg kg⁻¹ and succinylcholine 1.5 mg kg⁻¹. Systolic arterial pressure (SAP), heart rate (HR), and plasma catecholamine concentrations were measured. Neonatal effects were assessed using Apgar scores and umbilical cord blood gas analysis. RESULTS SAP was decreased by induction of anaesthesia and increased by tracheal intubation in both groups. The peak SAP after intubation was greater in the R0.5 group than in the R1.0 group, whereas it did not exceed baseline values in either group. HR increased significantly above baseline in both groups with no significant differences between the groups. Three subjects in the R1.0 group received ephedrine due to hypotension (SAP < 90 mm Hg). Norepinephrine concentrations remained unaltered after intubation and increased significantly at delivery with no significant differences between the groups. Neonatal Apgar scores and umbilical arterial and venous pH and blood gas values were comparable between the groups. CONCLUSIONS Both doses of remifentanil effectively attenuated haemodynamic responses to tracheal intubation with transient neonatal respiratory depression in pre-eclamptic patients undergoing Caesarean delivery under general anaesthesia. The 1.0 µg kg⁻¹ dose was associated with hypotension in three of 24 subjects.

A dose–response study of remifentanil for attenuation of the hypertensive response to laryngoscopy and tracheal intubation in severely preeclamptic women undergoing caesarean delivery under general anaesthesia

BACKGROUND Remifentanil is known to attenuate the cardiovascular responses to tracheal intubation. We determined effective doses (ED(50)/ED(95)) of remifentanil to prevent the pressor response to tracheal intubation in patients with severe preeclampsia. METHODS Seventy-five women with severe preeclampsia were randomly allocated to one of five remifentanil dose groups (0.25, 0.50, 0.75, 1.0, or 1.25 μg/kg) given before induction of anaesthesia using thiopental 5 mg/kg and suxamethonium 1.5 mg/kg. Systolic arterial pressure, heart rate and plasma catecholamine concentrations were measured. Neonatal effects were assessed by Apgar scores and umbilical cord blood gas analysis. A dose was considered effective when systolic arterial pressure did not exceed 160 mmHg for more than 1 min following tracheal intubation. RESULTS Baseline systolic blood pressure and heart rate did not differ among the groups. The intubation-induced increases of heart rate and blood pressure were attenuated in a dose-dependent manner by remifentanil. ED(50) and ED(95) were 0.59 (95% CI 0.47-0.70) μg/kg and 1.34 (1.04-2.19)μg/kg, respectively. Norepinephrine concentrations remained unaltered following intubation but increased significantly at delivery, with no differences between the groups. Apgar scores and umbilical arterial and venous pH and blood gas values were comparable among the groups. Two women each in the 1.0 and 1.25 μg/kg groups received ephedrine for hypotension defined as systolic arterial pressure <90 mmHg. CONCLUSIONS The ED(95) of remifentanil for attenuating the hypertensive response to tracheal intubation during induction of anaesthesia in severely preeclamptic patients undergoing caesarean delivery under general anaesthesia was 1.34 μg/kg.

Urinary Trypsin Inhibitors Afford Cardioprotective Effects through Activation of PI3K-Akt and ERK Signal Transduction and Inhibition of p38 MAPK and JNK

Background: We determined the effect of urinary trypsin inhibitors (UTI) in regional myocardial ischemia/reperfusion (I/R) injury and its underlying mechanisms involving the role of prosurvival kinases such as phosphatidylinositol-3-OH kinases (PI3K)-Akt and extracellular signal-regulated kinases (ERK 1/2) and apoptotic kinases such as p38 and JNK. Methods: The rats were anesthetized and subjected to an I/R insult consisting of 30-min left anterior descending coronary artery (LAD) occlusion followed by reperfusion. Infarct size was measured after 120 min of reperfusion. UTI was given alone or along with wortmannin (inhibitor of PI3K) or PD098059 (inhibitor of ERK1/2) before LAD occlusion. The phosphorylation of Akt, ERK1/2, p38 and JNK was determined by immunoblotting after 5 min of reperfusion. UTI was administered 10 min before LAD occlusion, and wortmannin and PD098059 were administered 20 min before LAD occlusion. Results: UTI significantly reduced the infarct size compared with the control. Wortmannin or PD098059 alone did not affect the infarct size, but they abolished the UTI-induced cardioprotective effect. UTI significantly reduced the phosphorylation of p38 and JNK, while it enhanced that of Akt and ERK1/2. Conclusions: UTI has a protective effect against regional myocardial I/R injury through activation of survival kinases PI3K-Akt and ERK1/2 and attenuation of p38 and JNK.

Neuroprotective effects of remifentanil against transient focal cerebral ischemia in rats.

Background: Opioid agonists have been implicated in neuroprotection from hypoxic injury through regulating mitogen-activated protein kinases and cytokines. We determined the effects of remifentanil in focal brain ischemia and reperfusion (I/R) injury. Mechanisms linked to mitogen-activated protein kinases, including extracellular signaling-regulated kinase (ERK) 1/2, p38 kinases, and c-Jun N-terminal kinase (JNK), and various cytokines were also examined. Methods: Male Sprague-Dawley rats were subjected to an I/R insult consisting of 90 minutes’ middle cerebral artery occlusion (MCAO) followed by reperfusion under general anesthesia. Neurological deficit scores and infarct volume were determined after 24 hours of reperfusion. Remifentanil (5 &mgr;g/kg/min) was given alone or combined with naltrindole (&dgr;-opioid receptor antagonist; 1 mg/kg), D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2 (&mgr;-opioid receptor antagonist; 1 mg/kg), or 5′-guanidinonaltrindole (&kgr;-opioid receptor antagonist; 1 mg/kg). Opioid antagonists were administered 20 minutes before MCAO. Remifentanil infusion was started 10 minutes before MCAO and continued throughout. The control group was without drugs. The expression levels of ERK1/2, p38, and JNK, and also those of tumor necrosis factor-&agr; (TNF-&agr;) and interleukin-6, were determined after 1, 3, and 24 hours of reperfusion. Results: Remifentanil significantly improved the functional outcome and reduced the infarct volumes (69.0±24.3 mm3 vs. 108.9±24.8 mm3), which were not affected by D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2 or 5′-guanidinonaltrindole, but were abolished by naltrindole. The I/R insult enhanced the phosphorylation of ERK 1/2 and the expression of TNF-&agr;, which were significantly reduced by remifentanil. Neither the phosphorylation of p38 and JNK nor the production of interleukin-6 was altered throughout the experiment. Conclusions: Remifentanil may be neuroprotective against focal I/R injury, possibly through the activation of &dgr;-opioid receptors and attenuation of ERK 1/2 activity and TNF-&agr; production, in the rat brain.