1992年 · 第105卷第11期

A close or even causal relation between myocardial adenosine and bradyarrhythmias during acute myocardial hypoxia was testified in guinea pig, rabbit and dog mainly by using specific competitive antagonist and synchronous quantitative analysis of 3 variables: intensity of myocardial hypoxia, degree of endogenous adenosine increment and severity of bradyarrhythmias. Results disclosed: A) striking resemblance of the bradyarrhythmias with hypoxic origin to those caused by exogenous adenosine, B) same locality of A-V conduction block induced by both myocardial hypoxia and exogenous adenosine, C) precise parallelism among the above-listed 3 variables with very high correlativity (r = 0.99, P<0.01), D) frequent accompaniment of reversal of hypoxic bradyarrhythmias through resupply of 21% O2 with normalization of preexisted increase in myocardial adenosine, E) satisfactory blockade of hypoxic bradyarrhythmias by adenosine's specific antagonist--aminophylline and their augmentation by adenosine's uptake inhibitor--dipyridamole, F) close similarity of the characteristic curve representing relation among the above 3 variables to that among intensity of myocardial hypoxia, degree of endogenous adenosine increment and amount of coronary blood flow in which adenosine's role as a mediator has been well documented and G) reproducible persistence of bradyarrhythmias during myocardial hypoxia irrespective of preliminary vagotomy and atropinization, denoting independence of the occurrence of such dysarrhythmias upon vagal drive, suggestive of a mechanism other than vagotonia. We advocated that hypoxia-induced bradyarrhythmias was caused by increment in endogenous adenosine.

To explore the effect of chronic converting enzyme inhibition on the macro- and microcirculation, normotensive rats were chronically given 100 mg/kg/day of captopril in their drinking water beginning one day before uninephrectomy. Cremaster arteriolar dimensions were measured 2, 4, or 8 weeks later by intravital microscopy, before and after topical application of 10-3 M adenosine. Mean blood pressure were significantly decreased at 4 (17%) and 8 (18%) weeks in treated rats vs age-matched control. Structural diameter reductions occurred in large arterioles starting 4 weeks in treated rats, and in small arterioles at 8 weeks. The cross-sectional wall area of large arterioles increased with age in control animal, but not in captopril treated one. Eight weeks of captopril treatment also decreased the cross-sectional wall area in small arterioles. Measured by stereological techniques, small arteriolar density decreased 17% at 4 weeks and 13% at 8 weeks in treated rats. Using histological techniques, a marked reduction of medial-intimal area of the abdominal aorta was found in treated rats at 4 (24%) and 8 (15%) weeks without a significant change in internal diameter.

Serum ferritin (SF), alpha-1-antitrypsin (AAT) and alpha-fetoprotein (AFP) were examined preoperatively in 66 patients with intrahepatic space-occupied lesions revealed by B-real time ultrasonography. Elevated SF levels (>300 μg/L in males and>180 μg/L in females), AAT levels (4.2 g/L), and AFP levels (>20 μg/L) were shown in 84%, 71% and 66% respectively of 55 patients with liver cancer. Combined analysis indicates that if all the three tests are negative, liver cancer can be essentially excluded; and positive AFP can rule out hepatic hemangioma. So combined assays of SF, AAT and AFP are valuable in the diagnosis and differential diagnosis of liver cancer.

The levels of tumor-associated antigens (TAAS) corresponded to monoclonal antibodies WLA-2C4 and CL-3 in sera of 57 lung cancer patients, 100 healthy adults and 50 non-tumor disease patients were assayed with SABC-ELISA of immunobinding inhibition test. The threshold values of WLA-2C4 and CL-3 (RBI) were 12% and 36%, respectively. The positive results of lung carcinomas with at least one of the two TAAS were as follows: squamous cell carcinoma 89%; adenocarcinoma 83%; small cell carcinoma 67% and their mean positive rate was 79%. Whereas the positive rate in healthy adults and non-tumor disease patients was only 6%. These results indicate that using monoclonal antibodies WLA-2C4 and CL-3 simultaneously may be helpful to the serological diagnosis of lung carcinoma.

To testify whether primary changes caused by the virus with its related factors and secondary changes caused by hypotension in the brains of patient with epidemic hemorrhagic fever (EHF) could be repeated in the animal model, suckling Balb/c mice were inoculated IP with 100 LD50/0.05 ml of Chen strain of hemorrhagic fever virus. After the onset of the disease, paraformaldehyde and glutaraldehyde were used for fixation by perfusion through left ventricle. Sections stained with HE and MAb against EHF virus by immunocytochemical method (4-step PAP) showed diffuse viral antigen deposition. All brains were diffusely scattered with single cell acidophilic necrosis which are believed to be caused primarily by the virus. 33.3% of the brains also showed symmetrical distribution of cerebral infarct-like necrosis which are believed to be caused secondarily by hypotension. This result supports our previous study on the autopsy of brains of EHF patients.

Psoralen (PSO) was found cytotoxic against in vitro cultured human mucoepidermoid carcinoma cells of MEC-1 cell line. Its IC50 value was 8.6 μg/ml, and relative antitumor activity (RAA) 15. PSO suppressed DNA synthesis, damaged microvilli and cell membrane, and induced degeneration of mitochondria. It inhibited the growth of MEC-1 cells transplanted in nude mice by 79.1% which was as strong as pingyanmycin (PYM 81.4%). The body weight loss of PSO treated tumor-bearing mice was 5%, whereas that of PYM treated ones 13.3% (P<0.01). PSO may be an effective agent for the treatment of human mucoepidermoid carcinoma.

The effect of hamster liver passage on the isoenzyme patterns of isolates of Entamoeba histolytica was investigated. Three isolates, F, G and T were originally obtained from patients with acute amebic dysentery and another strain, C, was obtained from an asymptomatic carrier. All these strains were maintained for over two years in axenic culture. The isoenzyme pattern (zymodeme) of hexokinase (HK), phosphoglucomutase (PGM) and glucose phosphoisomerase (GPI) of these strains was found to belong to non-pathogenic group X, but the isoenzyme pattern of GPI resembled less pathogenic zymodeme XX and might be an intermediate type. Following inoculation of trophozoites into hamster livers and recovery after abscess formation, their isoenzyme pattern changed and revealed that they belonged to pathogenic type XIV. Liver passage caused an enhancement in amebic virulence as evidenced by their increased ability to destroy leukocytes. The results indicate that isoenzyme pattern is not a stable property of E. histolytica.

The cerebral arteries in seven cases of Moyamoya disease, demonstrated by angiography were observed by light, transmission and scanning electron microscopy. In two cases, the lumen of the terminal portion of the internal carotid artery was completely occluded by proliferated connective tissue. The characteristic pathologic change was extensive destruction of the smooth muscle cells and the elastica interna. Degeneration and necrosis of smooth muscle cells were obvious in the media. Many condensed organelles and other elements of cellular destruction were dispersed throughout the interstitium. The media was thinned. The proliferated smooth muscle cells in the intima showed the same destructive changes as in the media. The elastica interna was excessively infolded and was thickened or thinned, disrupted or disintegrated in some segments. Identical, but less severe and more localized changes were seen in three middle cerebral arteries (M2 and M5 segments) and two collateral arteries at the base of brain. These changes suggest that Moyamoya disease is a progressive disorder characterized by repeated destruction of smooth muscle cells occurRing over a long time period. The pathogenesis of these changes is discussed.

A prospective double-blind study was carried out in 136 women 0.5 to 21 years since menopause (YSM) in order to demonstrate the effects of a long-acting estriol derivative-Nylestriol (CEE3) on bone loss and lipoprotein lipids. They were orally administered at 2 mg of CEE3 or placebo every 2 weeks. Among 90 subjects who finished 1 year of medication, 49 received CEE3 and 41 placebo. The results were: 1. Serum ALP, Ca/Cr and Hop/Cr in fasting urine decreased in 3 months (P<0.05); 2. Menopause-related reduction of forearm bone density was restrained; 3. LDL-C decreased in 3 months and HDL-C increased in 6 months (P<0.05), with no significant changes in TC and TG; 4. Side effects were mild. 1/3 of those with intact uterus had spotting and another 1/3 had moderate withdrawal bleeding after the addition of medroxyprogesterone acetate at the end of 12 months of CEE3 therapy. This study demonstrates that CEE3 is effective and acceptable for preventing osteoporosis and lipoprotein lipids disorder in postmenopausal women. Long-term application awaits further studies.

The author's approach and technique in the treatment of complex liver abscesses that persisted or recurred following percutaneous drainage are described. Six patients were treated by percutaneous debridement using an instrument specially designed for that purpose. Four patients were chronically ill but stable, while the other two were septic, hypotensive and considered to be life threatened. All patients had primary pyogenic abscesses. Four had demonstrated mixed bacterial flora consisting of E. coli, Klebsiella, Proteus and gram-positive cocci and two were caused by E. coli only. Contrast enhanced CT of the abdomen in all cases revealed multiloculated or septated abscesses containing large central debris and peripheral shell or halo of compromised hepatic parenchyma. Debridement was successful in all cases, resulting in complete healing within 12 days. Follow-up for 1-4.5 years revealed no recurrences. Three cases of infected tumors of the liver were referred for treatment. CT findings in these cases demonstrated a well developed external capsule and internal septations, and the absence of a surrounding halo of compromised parenchyma distinguishes them from primary abscesses. This preliminary experience makes the authors to conclude that percutaneous debridement of pyogenic liver abscesses is a safe and curative procedure in selected cases of life-threatening chronic liver abscesses.