Comparison of inhalation inductions with xenon and sevoflurane

Background: Xenon is an odorless gas with low blood-gas solubility coefficient and without occupational and environmental hazards. This investigation was performed to evaluate the speed of induction, and respiratory and cardiovascular reactions to inhalation induction with xenon compared to an equianesthetic concentration of sevoflurane.
Results: Compared to equianesthetic sevoflurane, xenon produced a faster induction of anesthesia (14759 versus 71221 s, respectively) with smaller decreases in respiratory rate, tidal volume and minute ventilation. Both agents showed comparable cardiovascular stability and oxygen saturation during induction. One patient in the sevoflurane group had breath-holding and movements of extremities and another had only breath-holding. No patients in the xenon group experienced any complications.
Conclusion: Xenon produced a faster induction of anesthesia without any complications than sevoflurane. Xenon had smaller decreases in tidal volume and respiratory rate during induction than sevoflurane. Xenon might offer an alternative to sevoflurane for an inhalation induction.
Method Twenty-four adult ASA 1–2 patients premedicated with 0.05 mg/kg of midazolam were instructed to take vital capacity breaths of 1 minimum alveolar concentration (MAC) of either xenon or sevoflurane until they lost consciousness. Induction time, total ventilatory volume, tidal volume, respiratory rate, minute ventilation, end-tidal MAC fraction, cardiovascular parameters and oxygen saturation were recorded. The patients were interviewed on the following day to evaluate their acceptability rating of the inhalation inductions.     

Effects of participatory workplace improvement program on stress-related biomarkers and self-reported stress among university hospital nurses: a preliminary study

Although participatory workplace improvement programs are known to provide favorable effects on high stress occupations like nursing, no studies have confirmed its effect using biomarkers. The aim of this study was to determine whether a participatory workplace improvement program would decrease stress-related symptoms as evaluated by biomarkers and self-reported stress among hospital nurses. Three actions to alleviate job stress, which were determined through focus group interviews and voting, were undertaken for two months. A total of 31 female Japanese nurses underwent measurement of inflammatory markers, autonomic nervous activity (ANA), and perceived job stress (PJS) at three-time points; before the program (T1), within a week after the completion of the program (T2), and three months after the program (T3). A series of inflammatory markers (Interferon-γ, Interleukin (IL)-6, and IL-12/23p40) decreased significantly at T2, and IL-12/23p40 and IL-15 significantly decreased at T3 compared to T1, while ANA and PJS remained unchanged. Our participatory program exerted beneficial effects in reducing inflammatory responses, but not for ANA and PJS. Further investigations with a better study design, i.e., a randomized controlled trial, and a larger sample size are warranted to determine what exerted beneficial effects on inflammatory markers and why other outcomes remained unchanged.     

Uterine metastasis from hepatocellular carcinoma: a case report

The extrahepatic spread of hepatocellular carcinoma (HCC) is uncommon. Moreover, metastatic uterine tumor from extragenital primaries is rare. We report a 63-year-old woman with uterine metastasis from HCC. She had undergone transcatheter arterial embolization four times and surgery for HCC from 2-4 years before. This time, she underwent resection of a newborn, head-sized uterine tumor that was proven to be metastasis from HCC. This is the first described case of metastatic uterine tumor originated from HCC.     

VDD Pacing with a Previously Implanted Single Lead System

Three patients who had undergone implantation of a rate modulated, afrial sensitive RS4 pacemaker, with a single orthogonal lead underwent replacement of a depleted unit with a DDD pulse generator, reusing the original lead with an adapter that allowed conversion of the bipolar atrial electrode into unipolar configuration. The mean atrial electrogram amplitude was 1,8 mV and no significant atrial sensing defects were found during Holler monitoring. As the RS4 pulse generator is no longer available, continued VDD pacing is possible by replacing it with a DDD pulse generator using the previously implanted single lead system.     

Relationship of Helicobacter pylori-associated Gastritis and Polymorphonuclear Leukocyte Elastase

Abstract: Background: Much remains to be clarified about the mechanisms of Helicobacter pylori (H. pylori)-associated gastritis. We considered the possibility of neutrophil involvement and investigated the role of polymorphonuclear leukocyte elastase (PMN-E) in the etiology of H. pylori-associated gastritis. Methods: In 60 patients with gastritis, infection by H. pylori was diagnosed by a combination of the ELISA method and conventional culture method. The hexosamine contents of the mucosal tissues and plasma polymorphonucler leukocyte elastase complexes (PMN-EC) were determined. Results: PMN-EC was found to be elevated in H. pylori-positive gastritis patients, and the degree of elevation was proportionately related to the grade of gastritis inflammation. The hexosamine concentration of the gastric antral mucosa was significantly lower in H. pylori-positive patients than in the H. pylori-negative patients. The ratio of PMN-EC/gastric mucosal hexosamine concentration was significantly higher in the H. pylori-positive group than in the negative group. Conclusion: These data suggest that one of the mechanisms of the H. pylori-associated gastritis may be the infiltration of neutrophils into the gastric mucosa followed by the release of PMN-E which is responsible for the degradation of gastric mucosal proteins and resultant tissue damages.     

Assessment of Angiographic Coronary Calcification and Plaque Composition in Virtual Histology Intravascular Ultrasound

Objectives

We assessed the relation between coronary plaque composition and angiographic calcification by using virtual histology intravascular ultrasound (VH‐IVUS).

Background

The plaque vulnerability according to angiographic calcification is unclear.

Methods

Subjects were 140 consecutive patients (145 lesions) undergoing VH‐IVUS before percutaneous coronary intervention. Subjects were divided into 4 groups: no calcification group (n = 27), spotty group (n = 65) that had calcium deposits under 90° in grayscale IVUS, intermediate group (n = 37) had calcium deposits with 90° or more and under 180°, and extensive group (n = 16) had calcium deposits with 180° or more.

Results

The number of VH thin‐cap fibroatheromas in spotty group was significantly larger than no calcification group, intermediate group, and extensive group (0.66 ± 0.71 vs 0.22 ± 0.42 [P < 0.01], 0.32 ± 0.48 [P < 0.05], 0.13 ± 0.34 [P < 0.01], respectively). Spotty group without angiographic calcification had significantly larger %necrotic core than with angiographic calcification (24.5 ± 6.7% vs 19.9 ± 7.2%, P < 0.05). Intermediate group without angiographic calcification had significantly larger necrotic core area than with angiographic calcification (2.5 ± 0.9 mm² vs 1.7 ± 0.9 mm², P < 0.05). Extensive group with angiographic calcification had significantly larger %dense calcium than without angiographic calcification (18.3 ± 4.0% vs 13.4 ± 4.4%, P < 0.05).

Conclusions

Lesions with spotty calcification was highly vulnerable in VH‐IVUS. Spotty or intermediate plaque calcification without angiographic calcification was more vulnerable than those with angiographic calcification. Extensive plaque calcification with angiographic calcification had more dense calcium than those without angiographic calcification.

     

Fluctuations in plasma macrophage colony‐stimulating factor levels during autologous peripheral blood stem cell transplantation for haematologic diseases

Plasma macrophage colony‐stimulating factor (M‐CSF) levels were measured in 13 haematologic patients treated with autologous peripheral blood stem cell transplantation (PBSCT). Six of the patients showed an increase in M‐CSF peak levels (> 3000 pg/ml) during the conditioning and stem cell infusion period. The peak levels of M‐CSF in this phase correlated with thrombomodulin levels, indicating the endothelial origin of plasma M‐CSF. However, the M‐CSF levels were not influenced by TNFα. More patients with high M‐CSF levels (> 5000 pg/ml) suffered from organ failure than those with lower M‐CSF levels. These results suggest that high M‐CSF levels may correlate with cellular or organ damage in patients treated with PBSCT.     

Role of hepatic artery in haemodynamics in normal and cirrhotic livers in rats

To examine the degree of influence of the hepatic artery on microcirculation in the liver, microscopic observation of blood flow in the hepatic minute blood vessels and the sinusoids and pressure measurements at key points in hepatic vascular pathways in vivo were performed before and after hepatic artery ligation in normal and cirrhotic rats. In normal rats, portal vein pressure (109 mmH2O) fell 10 mmH2O after hepatic artery ligation, but the pressures of the terminal portal venule, the terminal hepatic venule and the inferior vena cava did not change. In cirrhotic rats, portal vein pressure (206 mmH2O) and terminal portal venule pressure (106 mmH2O) fell 23 and 10 mmH2O after hepatic artery ligation respectively: the pressures in the terminal hepatic venule and the inferior vena cava did not change. These results suggests that the pressure transmitted from the hepatic artery was mostly supplied to the intrahepatic portal vein in normal rats and both to the intrahepatic portal vein and to the sinusoids in cirrhotic rats. In both normal and cirrhotic rats, however, the pressure transmitted from the hepatic artery was about 10 per cent of the initial portal vein pressure, and the blood flow in minute vessels and sinusoids did not change after hepatic artery ligation. Accordingly, it is believed that the hepatic artery plays only a small role in the haemodynamics of the liver in both normal and cirrhotic rats, irrespective of the distribution and manner of the hepatic arterial termination.