Effect of tumour necrosis factor in the mouse-tail model of psoriasis.

The effects of local and systemic administration of tumour necrosis factor (TNF) on the mouse-tail model of psoriasis were examined histologically at 4 days after administration. Subcutaneous injection of TNF at 1 x 10(1) to 1 x 10(4) units/mouse resulted in dose-dependent formation of a granular layer in the tail scales, which was quantified as the percentage of tail scales having granular layer formations extending over half or more of their surface and was larger than that occurring in untreated mice and in mice receiving injections of vehicle solution alone. Daily intraperitoneal injection of TNF at 1 x 10(3) or 1 x 10(4) units/mouse for 28 days resulted in similar granular layer formation and in a significantly reduced mitotic index of the tail keratinocytes, indicating an antiproliferative effect of TNF. The lowered mitotic index and the induction of granular layers, apparently attributable to a modulation of keratinocyte proliferation and differentiation by TNF, suggest that TNF may be effective as a drug for treatment of psoriasis.

[Assessment of beta-methyl lodophenyl pentadecanoic acid myocardial scintigraphy in patients with chronic pulmonary diseases].

The purpose of this study was to determine whether impaired fatty acid metabolism occurs in the right ventricle of patients with chronic pulmonary diseases (TB sequelae, TB seq.; 8, and chronic pulmonary emphysema. CPE; 14). 123I-BMIPP myocardial scintigraphy was performed on 22 subjects. The RV-BMIPP index (ratio of radioactivity in the right ventricle to that in the upper mediastinum), LV-BMIPP index (ratio of radioactivity in the left ventricle to that in the upper mediastinum), and RVc/LVc (ratio of radioactivity in the right ventricle to that in the left ventricle) were calculated to compare the distribution of radioactivity in the right and left ventricles. We also examined the correlations between these parameters and parameters of blood gas analysis and pulmonary hemodynamics. The RV-BMIPP index. LV-BMIPP index, and RVc/LVc were elevated in the TB seq. and CPE patient groups compared to the control group. The RV-BMIPP and LV-BMIPP indices demonstrated significant, negative correlations with PaO2; also a significant positive correlation was observed between the RV-BMIPP index and mean pulmonary arterial pressure. On the other hand, no significant correlation was found between the LV-BMIPP index and mean pulmonary arterial pressure. In the arm-stretching test under right heart catheterization, the RV-BMIPP and LV-BMIPP indices demonstrated significant, positive correlations with the cardiac index during exercise. These results suggest that hypoxemia accelerates fatty acid metabolism in the myocardium, and that local pressure overloading accelerates fatty acid metabolism in the right ventricle. Anomalies of fatty acid metabolism in the right ventricle may appear in patients with chronic pulmonary disease, and could be an adaptation to hypoxemia and overload, not an impairment.

[Analysis by two-dimensional electrophoresis of the cause of myocardial dysfunction in aging rat hearts].

The severity and frequency of atherosclerosis, diabetes, and ischemic heart disease, which affect cardiac function, increase with aging. Although there are many reports about hemodynamic and histopathological studies about aging hearts, there are very few studies on changes in structural proteins in aging hearts. We investigated the contractile proteins of the left ventricles in rats aged 6, 12 and 125 weeks using two-dimensional electrophoresis. There were no difference in structural proteins in heart between 6-week and 12-week-old rats. The contents of myosin heavy chain, myosin light chain 2, actin, troponin-I in 125-week-old rats decreased compared with those of 12-week-old rats. Myosin heavy chain, which is one component of myosin, interacts with actin and changes chemical energy to mechanical energy. Therefore its decrease leads to a decline in myocardial contractility. These results seem to indicate one of the most important changes in the aging rat heart, as well as impairment in relaxation by the increase of interstitial fibrosis and decline of Ca uptake by sarcoplasmic reticulum.

[Left ventricular aneurysm with normal coronary arteriogram after myocardial infarction].

Left ventricular aneurysms after myocardial infarction are generally considered one of the complications of severe coronary artery disease. Postinfarction ventricular aneurysms with normal coronary arteriogram are rare. Only a few cases have been reported previously in Japan. We examined the incidence and the clinical characteristics of postinfarction ventricular aneurysms without coronary obstruction. Among the consecutive 1800 patients studied in our laboratory with selective coronary cineangiography and left ventriography, we found 5 (4 male, 1 female) patients with left ventricular aneurysms with no or minimal coronary arterial obstruction. The patient's ages ranged from 34 to 83 with a mean of 59. Interestingly, no patient had prior anginal history, and every case occurred with a first sudden attack of chest pain. The likely mechanisms causing the development of myocardial infarction were coronary spasm and/or thromboembolic accident. One patient, in whom a coronary induction test was performed, showed positive findings. It is possible that poor collateral circulation and well preserved contraction of viable myocardium in these patients bring about the formation of left ventricular aneurysm after myocardial infarction with normal coronary arteriogram.

[Myocardial structural proteins in cor pulmonale. Analysis by two-dimensional electrophoresis].

Changes in cardiac structural proteins caused by cor pulmonale were studied with two-dimensional electrophoresis. Sprague-Dawley rats were exposed to an oxygen-poor gas mixture (10% O2/90% N2) for three weeks. These rats (the hypoxic group) were compared to a control group that was kept in room air. Hemoglobin, hematocrit, and right ventricular systolic pressure were greater in the hypoxic group than in the control group. After the third week, desmin content of both ventricular muscles had increased in the hypoxic group, and was significantly greater in the hypoxic group than in the control group. The contents of other cardiac structural proteins did not change. These data suggest that increases in desmin are caused by adaptation of the myocardium to pressure overload associated with pulmonary hypertension. However, increases in the desmin content of the left ventricular muscle might be caused by volume overload, humoral factors, or might be a direct effect of hypoxemia.