Effect of single-administration captopril on plasma and urinary vasopressin in normotensive subjects and patients with essential hypertension and primary aldosteronism

Effects of a single administration of captopril on plasma and urinary vasopressin (AVP) were examined in 8 normotensive (NT) female volunteers, 17 patients with essential hypertension (EHT) and 2 patients with primary aldosteronism (PA). Orally-administered captopril (25 mg) had no effect on plasma AVP levels in the three groups. However, urinary excretion of AVP decreased significantly after use of captopril in both NT and EHT subjects (-57% and -67%, respectively), and also in PA subjects. The magnitude of reduction in urinary AVP was significantly correlated with the pretreatment levels of plasma renin activity (r = 0.85) and plasma aldosterone concentration (r = 0.88) in NT subjects. Such correlation was not found in EHT subjects. These results suggest that captopril decreases AVP secretion in both normotensive and hypertensive subjects, but the relation of the magnitude in AVP reduction by captopril to the peripheral renin-angiotensin system might be different.     

Postural effects on electromyographic activity of the transversus abdominis muscle]

During breathing at rest in humans, electromyographic activity of the expiratory muscles (EMGem), tidal volume (VT), and minute ventilation (V(I)) are higher when standing than when supine. EMGem is known to correlate with VT and V(I). It is not known whether increased EMGem when standing results directly from the change in posture or indirectly from postural changes in ventilatory pattern. Moving average electromyographic activity of the transversus abdominis (EMGta) was recorded using a pair of fine wire electrodes during carbon dioxide (CO2) rebreathing both while standing and while supine. At matched end-tidal CO2 (ETCO2), VT, or V(I) values, EMGta was significantly higher when standing than when supine. Postural differences in EMGta had no correlation with increasing ETCO2, VT, or V(I) during CO2 rebreathing. These results suggested that both the direct effect of the postural change and an indirect effect through changes in ventilatory pattern contribute to the increased EMGem observed when standing compared to that when supine.     

Serum Lysozyme Levels and Clinical Features of Sarcoidosis

Serum lysozyme is used as a marker of sarcoidosis disease activity. In this study we examined the association between lysozyme levels and the clinical features of sarcoidosis and thus the clinical usability of this parameter in a large population. One hundred ten sarcoidosis patients from central Japan were examined for clinical features and serum lysozyme level at the first visit to our hospital and on a regular basis thereafter. The sensitivity of lysozyme for predicting sarcoidosis was 79.1%, whereas that of serum angiotensin-converting enzyme (ACE) was 59.0%. Even in the cases without an elevated serum ACE level, a value of 72.1% was obtained. The serum lysozyme level demonstrated a significant tendency to increase with the number of organs involved (p < 0.01). There were significant differences among the four radiographic stages (p < 0.05). The maximum serum lysozyme levels of patients without a disappearance of abnormal shadows on chest radiography within 5 years were significantly greater than those of individuals with a disappearance (p < 0.05). A positive correlation between serum lysozyme and serum ACE levels was observed. Because serum lysozyme is much less specific for sarcoidosis than serum ACE, its diagnostic value may be limited. However, the sensitivity was high even when serum ACE levels were within normal limits and correlated well with clinical features in sarcoidosis. Therefore, this parameter seems suitable for disease monitoring in proven cases. Accepted for publication: 19 November 1998     

Immunolocalisation of PIVKA-II in paraffin-embedded specimens of hepatocellular carcinoma

Abstract: Aims/Background: Although serum PIVKA-II has been widely used as a tumor marker for hepatocellular carcinoma (HCC), little information is available concerning tissue PIVKA-II, and detection of tissue PIVKA-II in paraffin-embedded tissue specimens of HCC is also considered difficult. Methods: Paraffin-embedded HCC tissues obtained at autopsy from 22 patients were subjected to immunohistochemical staining using the antibody MU-3 (Eisai Co., Ltd.) after microwave antigen retrieval. Results: PIVKA-II was mainly detected in the cytoplasm of HCC cells. The intensity of tissue PIVKA-II staining was not correlated with serum PIVKA-II levels or with the histological differentiation of HCC. However PIVKA-II staining tended to be more intense in tissue from patients with portal tumor thrombus, distant metastases, or a longer duration of HCC. Conclusion: This method of immunohistochemical staining is easy and simple to use and may be helpful for detecting tissue PIVKA-II in paraffin-embedded HCC specimens.     

Purification and partial characterization of a cellular inhibitor of the interferon-induced protein kinase of Mr 68,000 from influenza virus-infected cells.

A number of eukaryotic viruses have evolved mechanisms to downregulate activity of the interferon-induced, double-stranded RNA-activated protein kinase (referred to as P68 based on its Mr of 68,000 in human cells). This control is essential because once activated, the P68 kinase phosphorylates its natural substrate, the alpha subunit of the eukaryotic protein synthesis initiation factor 2 (eIF-2), limiting functional eukaryotic protein synthesis initiation factor 2 available for protein synthesis initiation. We have previously shown that influenza virus encoded a specific mechanism to repress the autophosphorylation and activity of P68. Using in vitro assays for P68 inhibition, we now have purified, to near homogeneity, the P68 repressor from influenza virus-infected cells. The purified product inhibited both the autophosphorylation of P68 as well as phosphorylation of the alpha subunit of eukaryotic protein synthesis initiation factor 2 by the kinase. We tested for both protease and phosphatase activity but found neither activity associated with the purified inhibitor. Surprisingly we found the purified repressor, which had an apparent Mr of approximately 58,000, was a cellular and not a viral-encoded protein. Possible mechanisms by which influenza virus activates this cellular regulator of the protein kinase, thereby minimizing potential antiviral effects of interferon, are discussed.     

Clinical impact of complete atrioventricular block in patients with ST‐segment elevation myocardial infarction

Complete atrioventricular block (CAVB) is a common complication of ST‐segment elevation myocardial infarction (STEMI). Although STEMI patients complicated with CAVB had a higher mortality in the thrombolytic era, little is known about the impact of CAVB on STEMI patients who underwent primary percutaneous coronary intervention (PCI). The study aimed at evaluating the clinical impact of CAVB on STEMI patients in the primary PCI era. We consecutively enrolled 1295 STEMI patients undergoing primary PCI within 24 hours from onset. Patients were divided into two groups according to the infarct location: anterior STEMI (n = 640) and nonanterior STEMI (n = 655). The outcomes were all‐cause death and major adverse cardiocerebrovascular events (MACCE) with a median follow‐up period of 3.8 (1.7–6.6) years. Eighty‐one patients (6.3%) developed CAVB. The incidence of CAVB was lower in anterior STEMI patients than in nonanterior STEMI (1.7% vs 10.7%, p < .05). Anterior STEMI patients with CAVB had a higher incidence of all‐cause deaths (82% vs 20%, p < .05) and MACCE (82% vs 25%, p < .05) than those without CAVB. Although higher incidence of all‐cause deaths was found more in nonanterior STEMI patients with CAVB compared with those without CAVB (30% vs 18%, p < .05), there was no significant difference in the incidence of MACCE (24% vs 19%). Multivariate analysis showed that CAVB was an independent predictor for all‐cause mortality and MACCE in anterior STEMI patients, but not in nonanterior STEMI. CAVB is rare in anterior STEMI patients, but remains a poor prognostic complication even in the primary PCI era.