Disseminated histiocytic sarcoma in a degu (Octodon degus).

A 7-year-and-8-month-old, male degu (Octodon degus) with anorexia, depression, and labored breathing was found to have a thoracic effusion and enlargement of the right testis on radiographic examination. Despite treatment, the animal died. At necropsy, hepatomegaly, splenomegaly, and multifocal nodules on the intestinal serosa and mesentery were observed. Histologically, the foci were densely cellular invasive neoplasms composed of sheets of round to polygonal cells, with occasional multinucleated giant cells. Immunohistochemically, the neoplastic cells were immunopositive for ionized calcium-binding adapter molecule 1, human leukocyte antigen-DR, and CD204. These findings were consistent with disseminated histiocytic sarcoma.

Age and period of ventilator use are related to walking independence at the time of discharge in patients with severe COVID-19 pneumonia: a single-center retrospective observational study.

[Purpose] This study aimed to identify the factors and cutoffs associated with walking independence in patients with severe COVID-19 pneumonia. [Participants and Methods] In total, 112 patients with COVID-19 pneumonia (98 males and 14 females) who were hospitalized between March 2020 and August 2021 and underwent physiotherapy during mechanical ventilation were included in the study. Attributes, respiratory function, physical function, and bed-withdrawal status were compared between two groups of patients, who were classified according to their ability to walk independently at discharge. The independent variables were reduced to four components by principal component analysis. Logistic regression analysis was performed with walking independence at discharge as the dependent variable. Receiver operating characteristic curves for the extracted factors were drawn, and cutoff values were calculated. [Results] At discharge, 76 patients were able to walk independently, while 36 were not. The logistic regression analysis was adjusted according to age and mechanical ventilation time. Cutoffs were an age of 56 years and a ventilation period of 7.5 days. [Conclusion] In cases of patients with severe COVID-19 pneumonia who required ventilators, age and mechanical ventilation time were associated with ambulatory independence at discharge, indicating the importance of reducing the ventilation period by providing respiratory physiotherapy, including expectoration, positioning, and weaning.

Activities of the Japan Council for Implementation of the Maternal Emergency Life Support System reduced direct causes of maternal deaths in Japan.

Here, we aimed to provide an overview of Japan Council for the Implementation of the Maternal Emergency Life-Saving System (J-CIMELS) and its simulation program, which has reduced maternal mortality due to direct causes in Japan. The Japan Association of Obstetricians and Gynecologists (JAOG), Japan Association of Obstetricians and Gynecologists, and Maternal Death Exploratory Committee (JMDEC) launched the Maternal Death Reporting Project in 2010. The project analyzed obstetricians' tendency to delay their initial response to sudden maternal deterioration. Obstetricians can predict small changes before deterioration by monitoring vital signs. In 2015, the J-CIMELS was established to provide practical education. J-CIMELS developed a simulation program (J-MELS; Japan Maternal Emergency Life Support) to ensure that the obstetricians acquire the latest knowledge of emergency physicians, anesthesiologists, and other general practitioners and apply it in clinical situations. In the last 7 years, the J-MELS basic course has been conducted 1000 times with a total attendance of 19 890 people. As a result, the incidence of obstetric hemorrhage progressively decreased from 29% in 2010 to 7% in 2020. We believe that the activities of J-CIMELS are improving obstetric care providers' medical practices in Japan.

Maternal cardiopulmonary resuscitation.

The perinatal resuscitation history in Japan is short, with the earliest efforts in the field of neonatology. In contrast, the standardization and dissemination of maternal resuscitation is lagging. With the establishment of the Maternal Death Reporting Project and the Maternal Death Case Review and Evaluation Committee in 2010, with the aim of reducing maternal deaths, the true situation of maternal deaths came to light. Subsequently, in 2015, the Japan Council for the Dissemination of Maternal Emergency Life Support Systems (J-CIMELS) was established to educate and disseminate simulations in maternal emergency care; training sessions on maternal resuscitation are now conducted in all prefectures. Since the launch of the project and council, the maternal mortality rate in Japan (especially due to obstetric critical hemorrhage) has gradually decreased. This has been probably achieved due to the tireless efforts of medical personnel involved in perinatal care, as well as the various activities conducted so far. However, there are no standardized guidelines for maternal resuscitation yet. Therefore, a committee was set up within the Japan Resuscitation Council to develop a maternal resuscitation protocol, and the Guidelines for Maternal Resuscitation 2020 was created in 2021. These guidelines are expected to make the use of high-quality resuscitation methods more widespread than ever before. This presentation will provide an overview of the Guidelines for Maternal Resuscitation 2020.

First case of hemochromatosis in a sugar glider (Petaurus breviceps).

A 14-year-old, male sugar glider presented with lethargy, anorexia, diarrhea, and paralysis of the hind limbs, and ultrasonography showed possible liver dysfunction. Some medications were administered, but the animal died 10 months after the first presentation, and a necropsy was performed. Histopathologically, hepatocellular degeneration and necrosis, severe deposition of hemosiderin in Kupffer cells and hepatocytes, bridging fibrosis, and regenerative nodules were observed in the liver. Variably amounts of hemosiderin deposition was observed in the heart, lungs, spleen, and kidney. These findings led to the diagnosis of hemochromatosis. No sugar glider cases with hemochromatosis have been reported. The pathological characteristics of hemochromatosis in this species were documented for the first time. The pathogenesis of hemochromatosis in animals remains unclear, but it has been suggested that some commercially available food for sugar gliders containing excessive amounts of iron and vitamin C may induce the disease.

Effect of maternal positioning during cardiopulmonary resuscitation: a systematic review and meta-analyses.

BACKGROUND: Although rare, cardiac arrest during pregnancy is the leading cause of maternal death. Recently, its incidence has been increasing worldwide because more pregnant women have risk factors. The provision of early, high-quality cardiopulmonary resuscitation (CPR) plays a major role in the increased likelihood of survival; therefore, it is important for clinicians to know how to manage it. Due to the aortocaval compression caused by the gravid uterus, clinical guidelines often emphasise the importance of maternal positioning during CPR, but there has been little evidence regarding which position is most effective. METHODS: We searched the Cochrane Central Register of Controlled Trials, MEDLINE, Embase, and OpenGrey (updated on April 3, 2021). We included clinical trials and observational studies with reported outcomes related to successful resuscitations. RESULTS: We included eight studies from the 1,490 screened. The eight studies were simulation-based, crossover trials that examine the quality of chest compressions. No data were available about the survival rates of mothers or foetuses/neonates. The meta-analyses showed that resuscitation of pregnant women in the 27°-30° left-lateral tilt position resulted in lower quality chest compressions. The difference is an 19% and 9% reduction in correct compression depth rate and correct hand position rate, respectively, compared with resuscitations in the supine position. Inexperienced clinicians find it difficult to perform chest compressions in the left-lateral tilt position. CONCLUSIONS: Given that manual left uterine displacement allows the patient to remain supine, the resuscitation of women in the supine position using manual left uterine displacement should continue to be supported. Further research is needed to fill knowledge gaps regarding the effects of maternal positioning on clinical outcomes, such as survival rates following maternal cardiac arrest.

ß-Endorphin Mediates the Development and Instability of Atherosclerotic Plaques.

ß-Endorphin, an endogenous opioid peptide, and its µ-opioid receptor are expressed in brain, liver, and peripheral tissues. ß-Endorphin induces endothelial dysfunction and is related to insulin resistance. We clarified the effects of ß-endorphin on atherosclerosis. We assessed the effects of ß-endorphin on the inflammatory response and monocyte adhesion in human umbilical vein endothelial cells (HUVECs), foam cell formation, and the inflammatory phenotype in THP-1 monocyte-derived macrophages, and migration and proliferation of human aortic smooth muscle cells (HASMCs) in vitro. We also assessed the effects of ß-endorphin on aortic lesions in Apoe -/- mice in vivo. The µ-opioid receptor (OPRM1) was expressed in THP-1 monocytes, macrophages, HASMCs, HUVECs, and human aortic endothelial cells. ß-Endorphin significantly increased THP-1 monocyte adhesion to HUVECs and induced upregulation of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin via nuclear factor-κB (NF-κB) and p38 phosphorylation in HUVECs. ß-Endorphin significantly increased HUVEC proliferation and enhanced oxidized low-density lipoprotein-induced foam cell formation in macrophages. ß-Endorphin also significantly shifted the macrophage phenotype to proinflammatory M1 rather than anti-inflammatory M2 via NF-κB phosphorylation during monocyte-macrophage differentiation and increased migration and apoptosis in association with c-jun-N-terminal kinase, p38, and NF-κB phosphorylation in HASMCs. Chronic ß-endorphin infusion into Apoe -/- mice significantly aggravated the development of aortic atherosclerotic lesions, with an increase in vascular inflammation and the intraplaque macrophage/smooth muscle cell ratio, an index of plaque instability. Our study provides the first evidence that ß-endorphin contributes to the acceleration of the progression and instability of atheromatous plaques. Thus, µ-opioid receptor antagonists may be useful for the prevention and treatment of atherosclerosis.

Dissection of the Vertebral Artery Fenestration Limb Presenting with Occlusion After Rupture.

BACKGROUND: Dissection of a vertebral artery (VA) fenestration is extremely rare. We herein present the first case of a patient who presented with the dissection of a VA fenestration limb accompanied by occlusion after rupture, who was treated with internal trapping of the dissected limb and the parent artery proximal to the fenestration. CASE DESCRIPTION: A 55-year-old man presented with sudden headache and altered consciousness. Computed tomography at admission showed subarachnoid hemorrhage. Angiography showed occlusion of the inner limb of the vertebrobasilar junction fenestration, and the occluded ends had a tapered shape, suggesting the occlusion of the dissection of the inner limb after rupture. Angiography immediately before embolization revealed inner limb recanalization with an irregular string sign; thus only the inner limb was embolized. Angiography after embolization showed near-complete suppression of the blood flow in the inner limb; however, a slight antegrade flow through the coil mass was observed in the late phase. The procedure was finished with the expectation of complete occlusion over time with natural heparin reversal. Angiography 8 days after embolization revealed a significant increase in antegrade blood flow through the coil mass within the inner limb. Therefore additional embolization of the parent artery proximal to the fenestration was performed, which achieved complete occlusion. CONCLUSIONS: The embolization length was limited and the antegrade blood flow through the other limb remained during internal trapping for the dissected VA fenestration limb; therefore careful observation of the blood flow to the dissected segment after embolization is necessary.

Lipocalin-2 exerts pro-atherosclerotic effects as evidenced by in vitro and in vivo experiments.

Lipocalin-2 (LCN2), a multiple bioactive hormone particularly expressed in adipose tissue, neutrophils, and macrophages, is known to exhibit anti-microbial effect, increase inflammatory cytokine levels, and maintain glucose homeostasis. Serum LCN2 level is positively correlated with the severity of coronary artery disease. However, it still remains unknown whether LCN2 affects atherogenesis. We assessed the effects of LCN2 on the inflammatory response and monocyte adhesion in human umbilical vein endothelial cells (HUVECs), inflammatory phenotype and foam cell formation in THP1 monocyte-derived macrophages, and migration and proliferation of human aortic smooth muscle cells (HASMCs) in vitro and aortic lesions in Apoe-/- mice in vivo. LCN2 and its receptor, low-density lipoprotein (LDL)-related protein-2, were expressed in THP1 monocytes, macrophages, HASMCs, and HUVECs. LCN2 significantly enhanced THP1 monocyte adhesion to HUVECs accompanied with upregulation of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin associated with nuclear factor-κB (NF-κB) upregulation in HUVECs. LCN2 significantly increased HUVEC proliferation and oxidized LDL-induced foam cell formation in THP1 monocyte-derived macrophages. LCN2 significantly increased the inflammatory M1 phenotype associated with NF-κB upregulation during differentiation of THP1 monocytes into macrophages. In HASMCs, LCN2 significantly promoted the migration and collagen-1 expression without inducing proliferation, which are associated with increased protein expression of phosphoinositide 3-kinase and phosphorylation of Akt, extracellular signal-regulated kinase, c-jun-N-terminal kinase, and NF-κB. Chronic LCN2 infusion into Apoe-/- mice significantly accelerated the development of aortic atherosclerotic lesions, with increased intraplaque monocyte/macrophage infiltration and pentraxin-3 and collagen-1 expressions. Our results suggested that LCN2 accelerates the development of atherosclerosis. Thus, LCN2 could serve as a novel therapeutic target for atherosclerotic diseases.

A Patient with a Large Basilar Artery Aneurysm in Whom Coil Embolization Was Performed by Protruding an LVIS into the Aneurysmal Neck in a Barrel-like Shape and Preserving a Branch Vessel.

Objective: We report a case of a low-profile visualized intraluminal support device (LVIS) being deployed and protruded into an aneurysmal neck in a barrel-like shape to perform dense coil embolization while preserving the branch vessel from the aneurysmal dome in order to prevent aneurysmal enlargement. Case Presentation: A 74-year-old woman had a recurrent large cerebral aneurysm at the bifurcation of the basilar artery and the left superior cerebellar artery (SCA). Therefore, an LVIS was deployed from the left posterior cerebral artery to the basilar artery and protruded into the aneurysmal neck in a barrel-like shape to increase its metal coverage ratio. As the barrel-shaped protruding LVIS served as a scaffold to support the coils, dense coil embolization was performed while preserving the SCA branching from the aneurysmal dome. Images obtained at 6 months and 1 year after the embolization confirmed preservation of the SCA and prevention of aneurysmal enlargement. Conclusion: Protruding the LVIS into an aneurysmal neck in a barrel-like shape is a technique that may help preserve the branch vessel and facilitate dense coil embolization.

Chemerin-9, a potent agonist of chemerin receptor (ChemR23), prevents atherogenesis.

Plasma levels of chemerin, an adipocytokine produced from the adipose tissues and liver, are associated with metabolic syndrome and coronary artery disease (CAD). Chemerin and its analog, chemerin-9, are known to bind to their receptor, ChemR23. However, whether chemerin and chemerin-9 affect atherogenesis remains to be elucidated. We investigated the expression of chemerin and ChemR23 in human coronary arteries and cultured human vascular cells. The effects of chemerin and chemerin-9 on atheroprone phenomena were assessed in human THP1 monocytes, human umbilical vein endothelial cells (HUVECs), and human aortic smooth muscle cells (HASMCs) and aortic lesions in Apoe-/- mice. In patients with CAD, a small amount of ChemR23, but not chemerin, was expressed within atheromatous plaques in coronary arteries. Chemerin and ChemR23 were expressed at high levels in THP1 monocytes, THP1-derived macrophages, and HUVECs; however, their expression in HASMCs was weak. Chemerin and chemerin-9 significantly suppressed the tumor necrosis factor-α (TNF-α)-induced mRNA expression of adhesion and pro-inflammatory molecules in HUVECs. Chemerin and chemerin-9 significantly attenuated the TNF-α-induced adhesion of THP1 monocytes to HUVECs and macrophage inflammatory phenotype. Chemerin and chemerin-9 suppressed oxidized low-density lipoprotein (oxLDL)-induced macrophage foam cell formation associated with down-regulation of CD36 and up-regulation of ATP-binding cassette transporter A1 (ABCA1). In HASMCs, chemerin and chemerin-9 significantly suppressed migration and proliferation without inducing apoptosis. In the Apoe-/- mice, a 4-week infusion of chemerin-9 significantly decreased the areas of aortic atherosclerotic lesions by reducing intraplaque macrophage and SMC contents. Our results indicate that chemerin-9 prevents atherosclerosis. Therefore, the development of chemerin analogs/ChemR23 agonists may serve as a novel therapeutic target for atherosclerotic diseases.

Anti-Atherogenic Effects of Vaspin on Human Aortic Smooth Muscle Cell/Macrophage Responses and Hyperlipidemic Mouse Plaque Phenotype.

Vaspin (visceral adipose tissue-derived serine protease inhibitor) was recently identified as a novel adipocytokine with insulin-sensitizing effects. Serum vaspin levels are reported either increased or decreased in patients with coronary artery disease. Our translational research was performed to evaluate the expression of vaspin in human coronary atherosclerotic lesions, and its effects on atherogenic responses in human macrophages and human aortic smooth muscle cells (HASMC), as well as aortic atherosclerotic lesion development in spontaneously hyperlipidemic Apoe−/− mice, an animal model of atherosclerosis. Vaspin was expressed at high levels in macrophages/vascular smooth muscle cells (VSMCs) within human coronary atheromatous plaques. Vaspin significantly suppressed inflammatory phenotypes with nuclear factor κB down-regulation in human macrophages. Vaspin significantly suppressed oxidized low-density lipoprotein-induced foam cell formation with CD36 and acyl-coenzyme A: cholesterol acyltransferase-1 down-regulation and ATP-binding cassette transporters A1 and G1, and scavenger receptor class B type 1 up-regulation in human macrophages. Vaspin significantly suppressed angiotensin II-induced migration and proliferation with ERK1/2 and JNK down-regulation, and increased collagen production with phosphoinositide 3-kinase and Akt up-regulation in HASMCs. Chronic infusion of vaspin into Apoe−/− mice significantly suppressed the development of aortic atherosclerotic lesions, with significant reductions of intraplaque inflammation and the macrophage/VSMC ratio, a marker of plaque instability. Our study indicates that vaspin prevents atherosclerotic plaque formation and instability, and may serve as a novel therapeutic target in atherosclerotic cardiovascular diseases.

Adropin Contributes to Anti-Atherosclerosis by Suppressing Monocyte-Endothelial Cell Adhesion and Smooth Muscle Cell Proliferation.

Adropin, a peptide hormone expressed in liver and brain, is known to improve insulin resistance and endothelial dysfunction. Serum levels of adropin are negatively associated with the severity of coronary artery disease. However, it remains unknown whether adropin could modulate atherogenesis. We assessed the effects of adropin on inflammatory molecule expression and human THP1 monocyte adhesion in human umbilical vein endothelial cells (HUVECs), foam cell formation in THP1 monocyte-derived macrophages, and the migration and proliferation of human aortic smooth muscle cells (HASMCs) in vitro and atherogenesis in Apoe-/- mice in vivo. Adropin was expressed in THP1 monocytes, their derived macrophages, HASMCs, and HUVECs. Adropin suppressed tumor necrosis factor α-induced THP1 monocyte adhesion to HUVECs, which was associated with vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 downregulation in HUVECs. Adropin shifted the phenotype to anti-inflammatory M2 rather than pro-inflammatory M1 via peroxisome proliferator-activated receptor γ upregulation during monocyte differentiation into macrophages. Adropin had no significant effects on oxidized low-density lipoprotein-induced foam cell formation in macrophages. In HASMCs, adropin suppressed the migration and proliferation without inducing apoptosis via ERK1/2 and Bax downregulation and phosphoinositide 3-kinase/Akt/Bcl2 upregulation. Chronic administration of adropin to Apoe-/- mice attenuated the development of atherosclerotic lesions in the aorta, with reduced the intra-plaque monocyte/macrophage infiltration and smooth muscle cell content. Thus, adropin could serve as a novel therapeutic target in atherosclerosis and related diseases.

Neopterin Counters Vascular Inflammation and Atherosclerosis.

BACKGROUND: Neopterin, a metabolite of GTP, is produced by activated macrophages and is abundantly expressed within atherosclerotic lesions in human aorta and carotid and coronary arteries. We aimed to clarify the influence of neopterin on both vascular inflammation and atherosclerosis, as neither effect had been fully assessed. METHODS AND RESULTS: We investigated neopterin expression in coronary artery lesions and plasma from patients with coronary artery disease. We assessed the atheroprotective effects of neopterin in vitro using human aortic endothelial cells, human monocyte-derived macrophages, and human aortic smooth muscle cells. In vivo experiments included a study of aortic lesions in apolipoprotein E-deficient mice. Neopterin expression in coronary artery lesions and plasma was markedly increased in patients with versus without coronary artery disease. In human aortic endothelial cells, neopterin reduced proliferation and TNF-α (tumor necrosis factor α)-induced upregulation of MCP-1 (monocyte chemotactic protein 1), ICAM-1 (intercellular adhesion molecule 1), and VCAM-1 (vascular cell adhesion molecule 1). Neopterin attenuated TNF-α-induced monocyte adhesion to human aortic endothelial cells and the inflammatory macrophage phenotype via NF-κB (nuclear factor-κB) downregulation. Neopterin suppressed oxidized low-density lipoprotein-induced foam cell formation associated with CD36 downregulation and upregulation of ATP-binding cassette transporters A1 and G1 in human monocyte-derived macrophages. In human aortic smooth muscle cells, neopterin suppressed angiotensin II-induced migration and proliferation via c-Src/Raf-1/ERK1/2 downregulation without inducing apoptosis. Exogenous neopterin administration and endogenous neopterin attenuation with its neutralizing antibody for 4 weeks retarded and promoted, respectively, the development of aortic atherosclerotic lesions in apolipoprotein E-deficient mice. CONCLUSIONS: Our results indicate that neopterin prevents both vascular inflammation and atherosclerosis and may be induced to counteract the progression of atherosclerotic lesions. Consequently, neopterin could be of use as a novel therapeutic target for atherosclerotic cardiovascular diseases.

A systematic review of massive transfusion protocol in obstetrics.

Post-partum obstetric haemorrhage is a leading cause of mortality among Japanese women, generally treated with haemostatic measures followed by supplementary transfusion. Commonly used in the setting of severe trauma, massive transfusion protocols (MTPs), preparations of red blood cell concentrate (RBC) and fresh frozen plasma (FFP) with additional supplements, have proved effective in decreasing patient mortality following major obstetric bleeding events. Although promising, the optimal configuration of RBC and FFP utilized for obstetric bleeding needs to be verified. Here, we conducted a systematic literature review to define the optimal ratio of RBC to FFP for transfusion therapy during instances of obstetric bleeding. Our analysis extracted four retrospective, observational studies, all demonstrating that an FFP/RBC ratio of ≥1 was associated with improved patient outcomes following obstetric haemorrhage. We therefore conclude that, from the standpoint of haemostatic resuscitation, an FFP/RBC ratio of ≥1 is a necessary condition for optimal clinical management during MTP administration in the field of obstetrics. Hence, we further propose an optimized MTP strategy to be utilized in the setting of severe obstetric bleeding.

Potent Vasoconstrictor Kisspeptin-10 Induces Atherosclerotic Plaque Progression and Instability: Reversal by its Receptor GPR54 Antagonist.

BACKGROUND: Kisspeptin-10 (KP-10), a potent vasoconstrictor and inhibitor of angiogenesis, and its receptor, GPR54, have currently received much attention in relation to pre-eclampsia. However, it still remains unknown whether KP-10 could affect atherogenesis. METHODS AND RESULTS: We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo. KP-10 significantly increased the adhesion of human monocytes to human umbilical vein endothelial cells, which was significantly inhibited by pretreatment with P234, a GPR54 antagonist. KP-10 stimulated mRNA expression of tumor necrosis factor-α, interleukin-6, monocyte chemotactic protein-1, intercellular adhesion molecule-1, vascular adhesion molecule-1, and E-selectin in human umbilical vein endothelial cells. KP-10 significantly enhanced oxidized low-density lipoprotein-induced foam cell formation associated with upregulation of CD36 and acyl-CoA:cholesterol acyltransferase-1 in human monocyte-derived macrophages. In human aortic smooth muscle cells, KP-10 significantly suppressed angiotensin II-induced migration and proliferation, but enhanced apoptosis and activities of matrix metalloproteinase (MMP)-2 and MMP-9 by upregulation of extracellular signal-regulated kinase 1 and 2, p38, Bcl-2-associated X protein, and caspase-3. Four-week-infusion of KP-10 into ApoE-/- mice significantly accelerated the development of aortic atherosclerotic lesions with increased monocyte/macrophage infiltration and vascular inflammation as well as decreased intraplaque vascular smooth muscle cells contents. Proatherosclerotic effects of endogenous and exogenous KP-10 were completely canceled by P234 infusion in ApoE-/- mice. CONCLUSIONS: Our results suggest that KP-10 may contribute to accelerate the progression and instability of atheromatous plaques, leading to plaque rupture. The GPR54 antagonist may be useful for prevention and treatment of atherosclerosis. Thus, the KP-10/GPR54 system may serve as a novel therapeutic target for atherosclerotic diseases.

[Use of flurbiprofen before emergence from anesthesia relieves pain during immediate postoperative period after laparoscopic inguinal hernia repair].

BACKGROUND: Reduced postoperative pain is considered one of the benefits of laparoscopic inguinal hernia repair (LHR). We investigated the need for intravenous flurbiprofen axetil (FA) before emergence from anesthesia in patients who had undergone LHR. METHODS: Forty adult patients who were prepared for LHR were randomly divided into the FA group (FA 1 mg x kg(-1) administered at the end of surgery, n = 20) and the control group (no FA administration, n = 20). Postoperative pain was evaluated by the Prince Henry Pain Score (PHPS) as well as by the frequency of on-demand use of nonsteroidal antiinflammatory drugs (NSAIDs). RESULTS: The PHPS on arrival at the ward was significantly lower in the FA group than the control group. Additionally, none of the patients of the FA group required NSAIDs in the first two hours of postoperative period, compared with 6 patients (30%) of the control group. However, at 4 hours postoperatively, none of the patients of both groups suffered pain at rest and the PHPS was similar in the two groups. CONCLUSIONS: Although postoperative pain after LHR is mild and disappears rapidly, FA administration before emergence from anesthesia is necessary for management of pain during the immediate postoperative period.

[Intraoperative asystole in a patient with concealed sick sinus syndrome: a case report].

We report a patient with concealed sick sinus syndrome who developed intraoperative bradycardia and asystole. An 81-year-old man was scheduled to undergo total gastrectomy under general and epidural anesthesia. There was no history of syncope, and preoperative 12-lead ECG showed normal sinus rhythm. Anesthesia was induced with propofol and remifentanil, maintained with sevoflurane, remifentanil and thoracic epidural infusion of lidocaine, fentanyl and levobupivacaine. Bradycardia was detected on ECG 110 minutes after the start of surgery. Intravenous atropine (0.5 mg, repeated up to a total dose of 1.5 mg) was ineffective in restoring a normal heart rhythm. Ten minutes later, the ECG changed to asystole lasting for about 15 seconds. Regular chest compression and intravenous administration of dopamine (5 microg x kg(-1) x min(-1)) resulted in successful recovery of sinus rhythm. Postoperative ECG showed sinus rhythm. The final diagnosis by a cardiologist was concealed sick sinus syndrome. Many anesthetic agents have some effects on the cardiac conduction system. Remifentanil may have played a role in the development of asystole in this patient. The existence of concealed sick sinus syndrome should be kept in mind even in patients who show no clinical abnormalities on preoperative assessment.

Breathing movements of the chest and upper abdomen in mechanically ventilated paralyzed patients.

AIM: Assessment of breathing on clinical examination requires visualization of "chest" wall movement. However, in mechanically ventilated paralyzed patients, chest expansion is smaller than that of the abdomen. The aim of this study was to determine chest and upper abdominal movements in mechanically ventilated patients under general anesthesia. METHODS: The subjects were 68 patients scheduled for general anesthesia. Chest and upper abdominal wall movements were measured using laser light at tidal volumes (VT) of 6, 10, and 15 mL/kg. The subjects were divided into the Lean group [body mass index (BMI) < 18.5 kg/m2], Normal group (BMI 18.5-24.9 kg/m2), and Obese group (BMI ≥ 25 kg/m2), and the relationships between chest and upper abdominal wall excursions and BMI at each VT were investigated. RESULTS: At VT of 10 mL/kg in all subjects, chest and upper abdominal wall excursions were 4.4 and 9.4 mm, respectively. The same pattern (upper abdominal wall excursions were twice as much as those of the chest wall) was noted in all groups and all VTs. CONCLUSION: Upper abdominal wall excursions were significantly larger than those of the chest wall in mechanically ventilated paralyzed patients, regardless of BMI. Assessment of breathing by clinical examination should avoid emphasis on "chest" wall movement alone, and instead include upper abdominal wall movement.

Landiolol has a less potent negative inotropic effect than esmolol in isolated rabbit hearts.

PURPOSE: We compared the negative chronotropic and inotropic effects of landiolol and esmolol, two clinically available short-acting beta1-blockers with high beta1-selectivity, using whole isolated rabbit heart preparations. METHODS: Tachycardia was induced by continuous perfusion of 10(-7) M isoproterenol, and we used concentrations of landiolol or esmolol in ascending steps (1 . 10(-6), 3 . 10(-6), 1 . 10(-5), 3 . 10(-5), and 1 x 10(-4) M). Heart rate (HR), left ventricular developed pressure (LVDP), the maximal rates of left ventricular force development (LVdP/dt(max)), and myocardial oxygen consumption (MVO2) were measured and compared. RESULTS: Both landiolol and esmolol produced dosedependent decreases in HR, LVDP, LVdP/dt(max), and MVO2. The HR lowering effects of the two agents were comparable. At concentrations of 3 . 10(-5) and 1 . 10(-4) M, esmolol produced more profound depression of LVDP (47 +/- 26 and 12 +/- 11 mmHg, respectively; mean +/- SD) and reduction of LVdP/dt(max) (650 +/- 287 and 120 +/- 103 mmHg x s(-1)) than landiolol (68 +/- 20 and 64 +/- 20 mmHg, and 897 +/- 236 and 852 +/- 240 mmHg.s(-1), respectively). At the same concentrations, esmolol caused more profound reduction in MVO(2) (40 +/- 11 and 35 +/- 10 microl x min(-1) x g(-1)) than landiolol (50 +/- 8 and 48 +/- 8 microl x min(-1) x g(-1)), respectively. CONCLUSION: Our results indicate that in the isolated rabbit heart, landiolol and esmolol had equipotent negative chronotropic effects, however, landiolol had a less potent negative inotropic effect than esmolol.