[A Case of Cardiac Arrest Caused by Coronary Spasm Related to Induction of General Anesthesia before Carotid Endarterectomy].

Coronary vasospasm(CV)can cause severe arrhythmia and myocardial infarction(MI). Intraoperative CV is not limited to cardiac surgery alone. We report the case of a patient who experienced cardiac arrest after the induction of general anesthesia, but did not demonstrate any abnormalities on preoperative examination. The patient was a 60-year-old man with no history of ischemic heart disease, with NASCET 80% asymptomatic left internal carotid stenosis(ICS). We decided to perform carotid endarterectomy(CEA). Preoperative stress myocardial scintigraphy did not reveal decreased local uptake. General anesthesia was rapidly induced with propofol and remifentanil, and maintained with sevoflurane. Shortly before the start of CEA, systolic blood pressure dropped to 80 mmHg. Electrocardiography indicated decreased ST, followed by an increase, after which complete atrioventricular block occurred. Cardiopulmonary resuscitation was initiated immediately as the patient's pulse was not palpable;heart beat resumed quickly. CEA was canceled. CV was suspected by the test of nitrate administration to coronary artery performed afterwards. A temporary pacemaker was inserted and carotid artery stenting was performed under local anesthesia. Hence, no pacemaker was used intraoperatively and no abnormality was observed on electrocardiography. In the present case, CV in the coronary artery caused complete atrioventricular block, leading to cardiac arrest after inducing general anesthesia. For ICS treatment performed under general anesthesia, care must be taken regarding the possibility of the occurrence of CV.

Estrogen-mediated renoprotection following cardiac arrest and cardiopulmonary resuscitation is robust to GPR30 gene deletion.

INTRODUCTION: Acute kidney injury is a serious,sexually dimorphic perioperative complication, primarily attributed to hypoperfusion. We previously found that estradiol is renoprotective after cardiac arrest and cardiopulmonary resuscitation in ovariectomized female mice. Additionally, we found that neither estrogen receptor alpha nor beta mediated this effect. We hypothesized that the G protein estrogen receptor (GPR30) mediates the renoprotective effect of estrogen. METHODS: Ovariectomized female and gonadally intact male wild-type and GPR30 gene-deleted mice were treated with either vehicle or 17ß-estradiol for 7 days, then subjected to cardiac arrest and cardiopulmonary resuscitation. Twenty four hours later, serum creatinine and urea nitrogen were measured, and histologic renal injury was evaluated by unbiased stereology. RESULTS: In both males and females, GPR30 gene deletion was associated with reduced serum creatinine regardless of treatment. Estrogen treatment of GPR30 gene-deleted males and females was associated with increased preprocedural weight. In ovariectomized female mice, estrogen treatment did not alter resuscitation, but was renoprotective regardless of GPR30 gene deletion. In males, estrogen reduced the time-to-resuscitate and epinephrine required. In wild-type male mice, serum creatinine was reduced, but neither serum urea nitrogen nor histologic outcomes were affected by estrogen treatment. In GPR30 gene-deleted males, estrogen did not alter renal outcomes. Similarly, renal injury was not affected by G1 therapy of ovariectomized female wild-type mice. CONCLUSION: Treatment with 17ß-estradiol is renoprotective after whole-body ischemia-reperfusion in ovariectomized female mice irrespective of GPR30 gene deletion. Treatment with the GPR30 agonist G1 did not alter renal outcome in females. We conclude GPR30 does not mediate the renoprotective effect of estrogen in ovariectomized female mice. In males, estrogen therapy was not renoprotective. Estrogen treatment of GPR30 gene-deleted mice was associated with increased preprocedural weight in both sexes. Of significance to further investigation, GPR30 gene deletion was associated with reduced serum creatinine, regardless of treatment.

[Case report of re-expansion pulmonary edema in a patient with anorexia nervosa after removal of a huge ovarian tumor].

We described a case of 19-year-old female who developed re-expansion pulmonary edema (RPE) after removal of a huge ovarian tumor. Altered lung volume after the surgery was observed by chest X-ray. Preoperatively, the lung was highly compressed by the tumor. Patient was intubated under general anesthesia and was ventilated by pressure controlled mode with only 5 cmH2O of positive end-expiratory pressure (PEEP). P/F ratio was changed from 163 to 444 after removal of the tumor. At the end of the surgery, P/F ratio decreased to 263 with yellow frothy sputum in the endotracheal tube and we diagnosed re-expansion pulmonary edema based on appearing yellow frothy sputum and chest X-ray. No recruitment procedure was carried out through the course except positive pressure ventilation with 5 cmH2O of PEEP in the intensive care unit after surgery. Twelve hours after the surgery, we could not confirm the recovery of lung volume on chest X-ray; however the patient was extubated because of P/F ratio increasing to 507. After 8 days of the surgery, the chest X-ray showed recovery of the lung volume to almost normal size. In this case, the compressed lung needed almost 1 week to recover the lung volume. This change in chest X-ray might indicate inadequate recovery of lung volume by recruitment maneuver and this should be avoided in order not to allow development of unfavorable clinical course of RPE.

[Prominent elevation of liver enzymes after Fontan operation].

It is known that acute liver dysfunction is one of the complications after Fontan operation. We tend to overlook it because their laboratory abnormalities are typically mild and hepatic dysfunction is an uncommon complication in children after cardiac surgery. However, this complication is likely to be an important indicator of poor prognosis. We report a patient who showed a prominent elevation of liver enzymes after Fontan operation. A year and 5 month old boy was scheduled for Fontan operation due to hypoplastic left heart syndrome. We used arterial pressure, central venous pressure and rSO2 probes (INVOS 5100, Somanetics Corp., USA) attaching on his head, abdomen and leg for circulatory management. The operation was performed with the heart beating. The blood removal tubes were inserted to the superior vena cava and inferior vena cava and the blood sending tube was inserted to the innominate artery when Norwood stage 1 was performed. After making an extracardiac conduit and a fenestration, we tried to take off the oxygenator with dopamine 5 microg x kg(-1) x min(-1), dobutamine 3 microg x kg(-1) x min(-1), isosorbide 2.5 microg x kg(-1) x min(-1). The central venous pressure was increased to 22-25 mmHg and systematic arterial pressure was unstable around 50 mmHg. We suggested the surgeons to expand the fenestration because the low flow through it was found on TEE examination, and introduced 15 ppm of nitric monoxide (NO) to decrease pulmonary vascular resistance and to control the central venous pressure at the same time. rSO2 was decreased to 50 temporarily when the oxygenator was taken off, however it was returned to 70 just after expanding the fenestration. On the first postoperative day, the patient showed marked elevations in GOT 17,305 U x l(-1), GPT 8,110 U x l(-1), gradually peaking out to GOT 105 U x l(-1), GPT 1,348 U x l(-1) by the seventh postoperative day. Hepatic dysfunction is related mainly to hemodynamic disturbances and is also related to the abdominal rSO2 and the high central venous pressure.

Inhibition of soluble epoxide hydrolase after cardiac arrest/cardiopulmonary resuscitation induces a neuroprotective phenotype in activated microglia and improves neuronal survival.

Cardiac arrest (CA) causes hippocampal neuronal death that frequently leads to severe loss of memory function in survivors. No specific treatment is available to reduce neuronal death and improve functional outcome. The brain's inflammatory response to ischemia can exacerbate injury and provides a potential treatment target. We hypothesized that microglia are activated by CA and contribute to neuronal loss. We used a mouse model to determine whether pharmacologic inhibition of the proinflammatory microglial enzyme soluble epoxide hydrolase (sEH) after CA alters microglial activation and neuronal death. The sEH inhibitor 4-phenylchalcone oxide (4-PCO) was administered after successful cardiopulmonary resuscitation (CPR). The 4-PCO treatment significantly reduced neuronal death and improved memory function after CA/CPR. We found early activation of microglia and increased expression of inflammatory tumor necrosis factor (TNF)-α and interleukin (IL)-1ß in the hippocampus after CA/CPR, which was unchanged after 4-PCO treatment, while expression of antiinflammatory IL-10 increased significantly. We conclude that sEH inhibition after CA/CPR can alter the transcription profile in activated microglia to selectively induce antiinflammatory and neuroprotective IL-10 and reduce subsequent neuronal death. Switching microglial gene expression toward a neuroprotective phenotype is a promising new therapeutic approach for ischemic brain injury.

SK2 channels are neuroprotective for ischemia-induced neuronal cell death.

In mouse hippocampal CA1 pyramidal neurons, the activity of synaptic small-conductance Ca(2+)-activated K(+) channels type 2 (SK2 channels) provides a negative feedback on N-methyl-D-aspartate receptors (NMDARs), reestablishing Mg(2+) block that reduces Ca(2+) influx. The well-established role of NMDARs in ischemia-induced excitotoxicity led us to test the neuroprotective effect of modulating SK2 channel activity following cerebral ischemia induced by cardiac arrest and cardiopulmonary resuscitation (CA/CPR). Administration of the SK channel positive modulator, 1-ethyl-benzimidazolinone (1-EBIO), significantly reduced CA1 neuron cell death and improved CA/CPR-induced cognitive outcome. Electrophysiological recordings showed that CA/CPR-induced ischemia caused delayed and sustained reduction of synaptic SK channel activity, and immunoelectron microscopy showed that this is associated with internalization of synaptic SK2 channels, which was prevented by 1-EBIO treatment. These results suggest that increasing SK2 channel activity, or preventing ischemia-induced loss of synaptic SK2 channels, are promising and novel approaches to neuroprotection following cerebral ischemia.

Estrogen is renoprotective via a nonreceptor-dependent mechanism after cardiac arrest in vivo.

BACKGROUND: Severe ischemia induces renal injury less frequently in women than men. In this study, cardiac arrest and cardiopulmonary resuscitation were used to assess whether estradiol is renoprotective via an estrogen receptor (ER)-dependent mechanism. MATERIALS AND METHODS: Male and female C57BL/6 and ER gene-deleted mice underwent 10 min of cardiac arrest followed by cardiopulmonary resuscitation. Serum chemistries and renal stereology were measured 24 h after arrest. RESULTS: Estrogen did not affect mean arterial pressure, regional renal cortical blood flow, and arterial blood gases. Hence, female kidneys were protected (mean +/- SEM: blood urea nitrogen, 65+/- 21 vs.149+/- 27 mg/dl, P = 0.04; creatinine, 0.14 +/- 0.05 vs. 0.73 +/- 0.16 mg/dl, P = 0.01; volume of necrotic tubules, 7 +/- 1% vs. 10 +/- 0%, P = 0.04). Estrogen also reduced renal injury. In intact females (n = 5), ovariectomized/vehicle-treated (n = 8), and ovariectomized/estrogen-treated (n = 8) animals, blood urea nitrogen was 65 +/- 21, 166 +/- 28, and 50 +/- 14 mg/dl (P = 0.002); creatinine was 0.14 +/- 0.05, 0.74 +/- 0.26, and 0.23 +/- 0.27 mg/dl (P = 0.014); necrotic tubules were 2.5 +/- 0.25%, 12.0 +/- 1.9%, and 5.0 +/- 1.6% (P = 0.004), respectively. In ER-[alpha] and ER-[beta] gene-deleted mice and controls estradiol-reduced functional injury (blood urea nitrogen: estradiol 117 +/- 71, vehicle 167 +/- 56, P = 0.007; creatinine: estradiol 0.5 +/- 0.5, vehicle 1.0 +/- 0.4, P = 0.013), but the effect of estradiol was not different between ER-[alpha] or ER-[beta] gene-deleted mice. Adding ICI 182,780 to estradiol did not alter injury. CONCLUSIONS: In women, kidneys were protected from cardiac arrest through estrogen. Estradiol-mediated renoprotection was not affected by ER deletion or blockade. Estradiol is renoprotective after cardiac arrest. The results indicate that estradiol renoprotection is ER-[alpha] and ER-[beta] independent.

Recombinant T cell receptor ligand treats experimental stroke.

BACKGROUND AND PURPOSE: Experimental stroke induces a biphasic effect on the immune response that involves early activation of peripheral leukocytes followed by severe immunodepression and atrophy of the spleen and thymus. In tandem, the developing infarct is exacerbated by influx of numerous inflammatory cell types, including T and B lymphocytes. These features of stroke prompted our use of recombinant T cell receptor ligands (RTL), partial major histocompatibility complex Class II molecules covalently bound to myelin peptides. We tested the hypothesis that RTL would improve ischemic outcome in the brain without exacerbating defects in the peripheral immune system function. METHODS: Four daily doses of RTL were administered subcutaneously to C57BL/6 mice after middle cerebral artery occlusion, and lesion size and cellular composition were assessed in the brain and cell numbers were assessed in the spleen and thymus. RESULTS: Treatment with RTL551 (I-A(b) molecule linked to MOG-35-55 peptide) reduced cortical and total stroke lesion size by approximately 50%, inhibited the accumulation of inflammatory cells, particularly macrophages/activated microglial cells and dendritic cells, and mitigated splenic atrophy. Treatment with RTL1000 (HLA-DR2 moiety linked to human MOG-35-55 peptide) similarly reduced the stroke lesion size in HLA-DR2 transgenic mice. In contrast, control RTL with a nonneuroantigen peptide or a mismatched major histocompatibility complex Class II moiety had no effect on stroke lesion size. CONCLUSIONS: These data are the first to demonstrate successful treatment of experimental stroke using a neuroantigen-specific immunomodulatory agent administered after ischemia, suggesting therapeutic potential in human stroke.

[Comparison of propofol LCT and propofol MCT/LCT regarding the injection pain at different sites and the memory].

BACKGROUND: Incidence and intensity of pain on intravenous injection of propofol LCT were compared with those of propofol MCT/LCT. METHODS: Eighty adult patients scheduled to receive general anesthesia were divided into two groups, propofol LCT (Group L, AstraZeneca) and propofol MCT/LCT (Group M, Maruishi Pharmaceutical). The peripheral vein was inserted with an 18 gauge intravenous catheter at the dorsal hand, the wrist, or the anterior brachial region. Propofol 2.0 mg x kg(-1) was injected at the speed of 5 mg x sec(-1). Noninvasive arterial blood pressure, heart rate, a BIS value and a degree of pain were measured. We used chi2 analysis and Wilcoxon t-test for statistical evaluation. RESULTS: There was a significantly larger incidence of injection pain in the Group L than the Group M (70% vs. 30%). The pain at the brachial region was significantly less as compared with the wrist or the dorsal hand in both groups. The ratio of patients having the memory of pain on the next day to those complaing the injection pain was 50% in the Group L and 36% in the Group M. There were no significant differences between the two groups in changes in BIS values and doses of propofol necessary for the loss of consciousness. CONCLUSIONS: The results suggest that propofol MCT/LCT elicits less pain on injection than propofol LCT. The injection pain is less at the brachial region than the wrist or the hand. Amnesia of pain may be obtained both with propofol MCT/ LCT and propofol LCT.