[Experimental study of the cellular response on the intraocular lens surface].
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Biomedical subjects
Publications and source records attributed to Y Enomoto.
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The effects of several saponins of animal and plant origin on the contractile activity of atrial and papillary muscles of the guinea-pig were tested. In a concentration of 1 X 10(-5)M, holothurin-A (HL-A), holothurin-B, echinoside-A, echinoside-B and sakuraso-saponin (Saku) exhibited positive inotropic and chronotropic actions whereas desacyl-jego-saponin and ginsenoside-Rd did not. Saponins having a positive inotropic action caused haemolysis of rabbit erythrocytes whereas those without inotropic action did not cause haemolysis. The positive inotropic action of saponins was not affected by practolol, chlorpheniramine, cimetidine and indomethacin. Verapamil (10(-6)M) inhibited the inotropic actions due to HL-A and isoprenaline (10(-8)M) to the same extent but had a small effect on those due to ouabain (10(-7)M). In high K+ (30 mM K+) medium where the action potential and the contraction were depressed, HL-A, Saku and isoprenaline restored the action potential and the contraction of the 'slow response' type whereas ouabain failed to do so. In normal medium HL-A and Saku reduced the resting membrane potential by 15-20 mV. These results suggest that modification of the Ca channel is involved in the positive inotropic action of saponins.
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The purpose of this study was to determine the immunoreactivity of myocardial actin filaments with actin antiserum and to examine the significance of its application to diseased human cardiac muscle. The actin was extracted and purified from chicken gizzards. Anti-actin rabbit serum was prepared and purified by affinity chromatography and defined by an immunoblotting test. Using the avidin-biotin-peroxidase complex (ABC) method, the actin antiserum was applied to paraffin sections prepared from hearts taken from routine autopsies of patients who had died of myocardial infarction. Reactivity was shown to be completely lost, not only in necrotized fibers, but also in non-specific degenerative fibers which could be identified by their eosinophilic cytoplasm with pyknotic nuclei, and clearly remaining and/or diminished cross-striations stained with hematoxylin-eosin. In contrast, hypertrophic myocardial fibers adjacent to granulation or scar tissue and those adjacent to infarcted foci exhibited a more intense reaction. These results indicated that the immunohistochemical reaction of actin filaments can be used for the easy detection of very mild degrees of degeneration of cardial muscle fibers, and for hypertrophic fibers adjacent to diseased foci. Studies of the immunoreactivity of actin protein suggestive of alteration at the molecular level might yield morphological clues regarding the nature of functional activity in the contraction of cardiac fibers.
The relationship between endothelial reactivity to Ulex europaeus agglutinin-1 (UEA-1) and the permeability of the vascular wall in human autopsied cases of cerebral infarction was studied. Sections from the cerebral cortex were reacted with horseradish peroxidase UEA-1 to demonstrate the surface membrane of endothelial cells. Albumin in the neuropil of sections was demonstrated for the estimation of increased vascular permeability. The results showed that endothelial reactivity to UEA-1 was reduced in cases where death had occurred 3 to 5 days after onset of cerebral infarction. Reactivity was also diminished in cases where death had occurred after 13 and 25 days; these cases showed fresh ischemic lesions caused by re-attacks of infarction. Albumin extravasation into the neuropil was demonstrated in these intermediate cases. Chronic cases, dying after more than 52 days, showed no reduction of endothelial reactivity to UEA-1 and no albumin extravasation was proved. It was concluded that UEA-1 can be employed as a useful morphological marker for evaluation of endothelial function and vascular permeability.
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The mode of depolarizing action of palytoxin (PTX) was compared with that of grayanotoxin-I (GTX-I) to examine the site of action of PTX in cardiac tissues isolated from dogs and guinea pigs: PTX at above 1 X 10(-10) mol/l depolarized the membrane of canine Purkinje fibres, canine and guinea-pig ventricular muscles regardless of stimulation. The PTX-induced depolarization was resistant to 1 X 10(-5) mol/l tetrodotoxin (TTX) but was attenuated by low Na medium. GTX-I at 1 X 10(-5) mol/l depolarized the membrane of ventricular muscles from dogs and guinea pigs only when they were stimulated. Although GTX-I caused depolarization in Purkinje fibres in both stimulated and rested conditions, the effect was greater in stimulated fibres. In the presence of GTX-I, ventricular muscles generated long-lasting action potentials as a response to stimuli. TTX antagonized the GTX-I-action. After treatment of PTX, GTX-I still induced the long-lasting action potential and TTX could antagonize it. Ouabain at 1 X 10(-6) or 3 X 10(-6) mol/l partially inhibited the PTX-induced depolarization in guinea-pig papillary muscles. The data suggest that the TTX-sensitive Na channel is intact after treatment with PTX and that PTX acts on a site different from the Na channel, possibly on the Na+, K+-ATPase in cardiac cells.
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Semiquantitative analysis of lactoferrin deficiency in neutrophil polymorphonuclear leucocytes in various haematological and non-haematological disease was carried out by scoring polymorphonuclear leucocytes stained for lactoferrin by the immunoperoxidase method. The staining patterns for lactoferrin were classified into four types (0-III) based on the intensity of reaction, and the sum of the ratings of 100 polymorphonuclear leucocytes was considered as "lactoferrin score" with a possible range of 0-300. As a result, significantly low lactoferrin-scores were frequently observed in acute leukaemias and the acute phase of chronic leukaemias. Of 35 cases with leukaemias, lactoferrin-negative polymorphonuclear leucocytes (type 0) were observed in the following cases: eight cases of acute myelogenous leukaemia (8/14), a case of chronic myelogenous leukaemia (1/10) in blast crisis, one of acute promyelocytic leukaemia (1/1), one of acute monocytic leukaemia (1/2), and a case of chronic myelomonocytic leukaemia (1/2) in a transitional phase to an acute myelomonocytic leukaemia. In two cases of acute myelogenous leukaemia, in which the majority of polymorphonuclear leucocytes were negative for lactoferrin, ultrastructural cytochemical study revealed total lack of specific granules in these polymorphonuclear leucocytes. This suggests that lactoferrin is localised in the specific granules of neutrophils as has been postulated previously by others.