Bronchial hyper-responsiveness to inhaled histamine in children with congenital heart disease

In order to assess bronchial responsiveness in patients with congestive heart failure secondary to congenital heart disease, we performed a histamine inhalation test while monitoring transcutaneous oxygen tension and compared the respiratory threshold to histamine with that obtained in patients with bronchial asthma. The inhalation test was performed by doubling concentrations of histamine solution for 2 min at 1 min intervals. The respiratory threshold of histamine was defined as the minimal concentration causing a drop in transcutaneous oxygen tension greater than 10% from baseline. Six of 10 patients with congenital heart disease and all of 12 patients with bronchial asthma had bronchial hyper-responsiveness to histamine. The mean of histamine concentration was 2750μg/mL and 937μg/mL, respectively. During the histamine inhalation test, respiratory resistance gradually increased in congenital heart disease patients. This was measured by the linear slope of transcutaneous oxygen pressure (-1.08 ± 0.75 mmHg/min), whereas in the bronchial asthma patients it rapidly decreased at the inflection point (-4.19 ± 1.86 mmHg/min). We conclude that children with congestive heart failure had bronchial hyper-responsiveness. We suggest bronchial hyper-responsiveness to inhaled histamine in congestive heart failure was caused by the gradual increased respiratory resistance, which was different from that of bronchial asthma.     

Urinary N-acetyl-beta-D-glucosaminidase excretion in term and preterm neonates

Urinary N-acetyl-beta-D-glucosaminidase (NAG) excretion was measured in term and preterm neonates on days 1, 4, 7, 14 and 28 of life. Urinary NAG showed a peak level on day 4 or 7 in these infants. In addition, it tended to be higher with the degree of prematurity. In sick preterms who were depressed at birth and had respiratory failure, the NAG activity was further elevated during the first 2 weeks, suggesting the presence of renal tubular injury in this period. These observations thus suggest that urinary NAG may be a sensitive measure of renal maturation or damage in neonates.     

Comparison of Arrhythmogenicity of Atrial Pacing at Several Right Atrial Pacing Sites: Evaluation of Canine Atrial Electrograms During Atrial Pacing and Arrhythmogenicity for Atrial Fibrillation

The changes in the duration of atrial electrograms and the appearance of AF during atrial pacing were compared among five atrial pacing sites in dogs to clarify the arrhythmogenicity of atrial pacing at different atrial pacing sites. In seven mongrel dogs (15–20 kg), the right atrial surface was exposed by right thoracotomy. Atrial electrograms were recorded via bipolar electrodes with an interelectrode distance of 1.2 mm at four right atrial sites: (1) the high right atrium (HRA), (2) the mid-right atrium (MRA), (3) the low right atrium (LRA), and (4) the center of the pectinate muscle (PM). The duration of the atrial electrograms at these four recording sites were measured during atrial pacing with fixed cycle lengths of 200, 150, and 120 ms delivered at five atrial sites: (1) the HRA, (2) the inferior vena cava (IVC), (3) the right atrial appendage (RAA), (4) Bachman's bundle (BB), and (5) the atrial septum (AS). In each dog, the atrial pacing with the 120-ms cycle length was performed five times at each pacing site to evaluate the in-ducibility of AF. When AF was induced, the atrial recording site which first showed a fragmented atrial electrogram was considered the initiation site of the AF. AF was induced during 9 of 35 episodes of atrial pacing at the HRA site, 11 of 35 at the IVC site, 5 of 35 at the RAA site. 3 of 35 at the BB site, and none at the AS site. The initiation site of AF was in the HRA site in 11 of 28 episodes of induced AF, in the MRA site in 9 of 28, and in the LRA site in 8 of 28. At each recording site, the shorter the paced cycle length, the longer the duration of the atrial electrogram regardless of the pacing site. During the atrial pacing with the 200-ms cycle length, the HRA pacing resulted in the shortest duration of the atrial electrogram at each recording site in comparison with the other pacing sites. However, during atrial pacing at the two shorter paced cycle lengths, the duration of the atrial electrogram was shorter during the pacing at the BB or AS sites in comparison with the other three pacing sites, i.e., the HRA, IVC, and RAA sites. These results were the same for all atrial recording sites, but the prolongation of the atrial electrogram was most prominent at the HRA and MRA recording sites, which are most likely initiation sites of the induced AF. In the canine atria, (1) the initiation sites of AF were likely to be the HRA, MRA, or LRA sites in comparison with the PM site; and (2) the atrial pacing at the BB or AS sites was considered less arrhythmogenic for AF than the pacing at the HRA, LRA, or RAA sites.     

Influence of Mobile Magnetic Resonance Imaging on Implanted Pacemakers

KISHI, R., et al.: Influence of Mobile Magnetic Resonance Imaging on Implanted Pacemakers. Purpose: Mobile magnetic resonance imaging (MRI) systems will be widely used in Japan. When traveling, mobile MRI generate alternating electromagnetic waves which may cause electromagnetic interference (EMI). This study was designed to determine whether this may influence the function of implanted pacemakers (PM). Methods and Results: The influence of the static magnetic fields was tested in the first method using a PM-human model (Phantom). Magnetic force was simultaneously measured. The PM was switched to the magnet mode within 90 cm from the vehicle, where the magnetic force was = 2 mT. In the second method, six phantoms were placed on the side of the road, facing in three different directions in X-Y-Z axis orientations, at 1.3 m and 2.0 m above the ground. The mobile MRI passed by at a distance of 1 m from the phantoms at the speed of 20 or 40 km/h. In these experiments, magnet mode switch of the PM was observed for 2 seconds when the vehicle passed close to the phantoms, though no electrical noise was recorded. Conclusion: Mobile MRI vehicles can switch a PM to magnet mode when the distance between patient and vehicle is <90 cm, regardless of whether the vehicle is moving or at a stop. Patients with implanted PM should not approach within <1 m of a mobile MRI. No other EMI-induced PM dysfunction was detected. (PACE 2003; 26[Pt. II]:527–529)     

Autoantibodies against a 210kDa glycoprotein of the nuclear pore complex as a prognostic marker in patients with primary biliary cirrhosis

It has been reported that the presence of anti-nuclear antibody against a 210kDa glycoprotein of nuclear pore complex (anti-gp210) is highly speci?c for primary biliary cirrhosis (PBC). The aim of the present study was to investigate the signi?cance of anti-gp210, especially as a prognostic marker. The presence of anti-gp210 was ascertained in 113 patients with PBC and 162 controls by indirect immuno?uorescence assay using HepG2 cells and immunoblotting analysis using nuclear extracts from HeLa cells. Anti-gp210 was detected in 25 of the 113 (22.1%) patients. None of the 162 controls was positive for anti-gp210. The appearance and titre of anti-gp210 in the patients with PBC did not vary from the time of diagnosis and through their clinical course. Anti-mitochondrial antibodies (AMA), including antibodies against pyruvate dehydrogenase complex, branched chain α-ketoacid dehydrogenase complex and α-ketoglutarate dehydrogenase complex, were not detected by enzyme-linked immunosorbent assay in ?ve of the 113 (4.4%) patients with PBC. However, anti-gp210 alone was positive in one of these ?ve patients. The difference in prognosis was statistically signi?cant; patients with PBC positive for anti-gp210 died from hepatic failure more frequently than those who were negative (P < 0.01), although there were no statistically signi?cant differences in the frequency of jaundice and the histological stage at the time of diagnosis between the two groups. We suggest that the presence of anti-gp210 is one of the independent prognostic markers able to predict, at the time of diagnosis, a poor outcome in patients with PBC.     

Decreased arteriovenous flow resistance in the left gastric venous area in cirrhotic patients

Abstract. To assess the relationship between the fluid mechanics in the left gastric venous area and the portal trunk, manometric measurements were made in patients with or without cirrhosis of the liver. In ten normal subjects, temporary portal vein occlusion produced comparable elevation in both the occluded left gastric venous pressure (OLGP) and the portal vein pressure (PVP); 152–4129 mm of water in OLGP and 115–452 mm of water in PVP. In sixty cirrhotic patients, however, the portal vein occlusion resulted in far less increase in OLGP than that in PVP; 281–365 mm of water in OLGP and 281–540 mm of water in PVP. In other words, regarding pressure measurements, the relationship was 'separated' in cirrhotics, but 'continuous' in normal subjects. Mathematical analysis of the data using a modification of Wheat-stone bridge model suggested that the arteriovenous flow resistance in the left gastric venous area of cirrhotics was reduced to less than one fifth of that in the controls. It would appear that the increased flow capacity as a result of a reduced arteriovenous flow resistance is responsible for the functional 'separation' from the portal trunk.     

Prediction of interferon-alpha-induced thyroid dysfunction in patients with chronic hepatitis C

To predict interferon-alpha (IFN-α)-induced thyroid dysfunction, anti-thyroglobulin (anti-TgAb) and anti-thyroid peroxidase antibodies (anti-TPOAb) were determined by radio-immunoassay (RIA) before IFN-α treatment in 30 patients with chronic hepatitis C in whom the conventional haemagglutination test had failed to detect anti-thyroid auto-antibodies. Seven patients developed thyroid dysfunction during IFN-α treatment (transient thyrotoxicosis in four patients, transient hypothyroidism in two, and Graves’ disease in one). Anti-TgAb and/or anti-TPOAb were detectable before IFN-α treatment in six of these seven patients, while these antibodies were detected before treatment in only four of 23 patients who did not develop any thyroid dysfunction. The prevalence of these antibodies was significantly higher (P= 0.002) in the former group of patients than in the latter. In four patients with detectable anti-TgAb before treatment but no subsequent thyroid dysfunction, the antibody disappeared during IFN-α treatment. Haemagglutination tests for anti-thyroid microsomal antibodies have previously been reported to be a useful predictive marker of IFN-α-induced thyroid dysfunction. In conclusion, sensitive detection of anti-thyroid auto-antibodies using RIA may also be useful for the prediction of IFN-α-induced thyroid dysfunction in patients with a negative haemagglutination test.     

Interleukin-6 inhibits the chemotaxis of human malignant plasma cell lines

The chemotaxis of human malignant plasma cells is promoted by two extracellular matrix proteins (ECMs): fibronectin (FN) and laminin (LN). We examined the effect of the supernatant from a bone marrow stroma cell line, KM-101, on the chemotaxis of human malignant plasma cell lines to assess the chemotaxis-regulatory roles of the bone marrow microenvironment. Five human malignant plasma cell lines, FR4ds, OPM-1ds, U266/B1, RPMI-8226 and ARH-77 showed different profiles of the expression of β1 integrins of FN and LN receptors. FR4ds, OPM-1ds and U266/B1 cells showed chemotaxis promoted by FN (Ch^FN) and LN (Ch^LN). ARH-77 cells showed Ch^FN but not Ch^LN. RPMI-8226 cells did not show either Ch^FN or Ch^LN. The supernatant from KM-101 cells inhibited the chemotaxis of each of these cell lines regardless of whether the chemotaxis was promoted by FN or LN. Among the cytokines produced by KM-101 cells, it was postulated that IL-6 mediated this inhibitory effect because anti-IL-6 monoclonal antibody (MoAb) and anti-IL-6 receptor MoAb significantly reversed the inhibition. Recombinant IL-6 (rIL-6) also exhibited a similar inhibitory effect. Because anti-gp130 MoAb significantly reversed the chemotaxis inhibitory effect of rIL-6, the inhibitory signal is probably transduced via the signal transducing receptor component, gp130. The chemotaxis-regulatory effect is another previously unrecognized function of this pleiotropic cytokine, IL-6. High levels of IL-6 in the bone marrow microenvironment of patients with multiple myeloma appears to be favourable for the localization of myeloma cells there.     

Midline extraperitoneal approach to upper urinary tract surgery: Anatomical basis of surgical technique

Aim: To overcome the disadvantages inherent in the standard surgical approach to the kidney, we introduced a novel surgical technique via a midline extraperitoneal approach. The surgical technique is not substantially different from that of the standard midline transperitoneal approach, except no entry is made into the peritoneal cavity. Although the peritoneum itself is extremely thin and fragile, the peritoneum together with underlying subperitoneal fascia can be dissected readily as a substantial layer, if the proper plane is dissected. Further medial mobilization of the peritoneal sac en bloc by pursuing the fusion fascia plane allows full exposure of the kidney, ureter and great vessels. This approach was adopted for consecutive 51 patients during a 10-month period in 2003. All operations, including 33 radical nephrectomies and 11 nephroureterectomies were completed successfully without significant technical difficulties and differences in operation time and estimated blood loss compared to the transperitoneal approach. No intra- or perioperative complication occurred. All patients did seem to have a much more comfortable postoperative period with minor pain and few abdominal complaint, and the clinical impression was that they resumed the physical activity and oral intake earlier than those after the transperitoneal approach (P = 0.056). There are no operation-related problems such as intra-abdominal adhesion or abdominal muscle weakness resulting in some deformity at 2-year or more follow up. This approach combines the advantages of the transperitoneal midline and extraperitoneal flank approach. Its use will undoubtedly reduce the complications inherent in the transperitoneal approach or the flank approach.     

Sudden Cardiac Death: Future Approaches Based on Identification and Control of Transient Risk Factors

Sudden Cardiac Death . Future progress in the ability to control the problem of sudden cardiac death will require new approaches in applied epidemiology, methods of accurately evaluating therapeutic outcome, and techniques to identify and control those transient risk factors that are responsible for the initiation of fatal arrhythmias. In regard to the latter, transient risk factors are distinguished from classical risk factors in two ways: (1) they are not present continuously over time, thus confounding sampling techniques among a population; and (2) their dynamic nature suggests a proximate role in the initiation of potentially fatal arrhythmias in contrast to the role of classical risk factors in the genesis of the underlying diseases. Transient risk factors derive from the structure/function model of sudden cardiac death, which places structural abnormalities in a conditioning role, establishing the sensitivity to a transient destabilizing influence. In contrast, functional abnormalities are those conditions immediately responsible for destabilizing the system, establishing vulnerability to potentially fatal arrhythmias. They include four categories of risk: (1) transient ischemia and reperfusion; (2) systemic abnormalities, such as hemodynamic dysfunction and fluid and electrolyte imbalance; (3) autonomic fluctuations, both central and cardiac; and (4) cardiac toxic states, including proarrhythmic effects of antiarrhythmic drugs and arrhythmogenic effects of other substances. Sudden cardiac death is a dynamic problem, and its pathogenesis contains dynamic features. The ability to identify transient risk factors and to control them before they exert their influence on a conditioned electrophysiologic system will provide new inroads into the problem of sudden cardiac death.