JOURNAL OF THE KYORIN MEDICAL SOCIETY

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This study investigated whether the immunologic response and cellular reaction including mononuclear cells and neutrophil leukocytes which operate to host defense against Y. enterocolitica infection are modified by use of betaadregenic drugs which regulate intracellular cyclic AMP accumulation. The pharmacologic effects to the infection were observed on both magnitude of antibody production against Y. enterocolitica and SRBC antigens and histopathologic findings in the liver, spleen, mesenteric lymph node, lung and thymus of the infected mice. Theophilline and isoproterenol which effectively stimulate intracellular cyclic AMP accumulation induced an evident splenomegaly with prominent proliferation of splenic eukaryocytes and pyroninophilic cells in the thymus dependent areas, whereas magnitude of antibody production did not demonstrate any sufficient elevation. Furthermore, inflammatory reaction in the various organs caused by the infection was rather inhibited. In the infected mice treated with propranolol which inhibites intracellular cyclic AMP, proliferation of the splenic cells and magnitude of antibody production were more effectively suppressed than that of the theophilline treated mice. On the contrary, acute exudative inflammation in the lung and focal necrosis in the liver were noted in the ropranolol group of mice. This experiment indicates that theophilline, isoproterenol and propranolol are able to modify the immunologic response and cellular reaction in the tissue against Y. enterocolitica infection.

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Lead-inhibited ALA-D is reactivated by heat treatment (60℃, 5 min) and addition of zinc chloride in vitro. These restorations seem to be specific for the lead-inhibited enzyme. In the inhibited ALA-D with copper and mercury, these restorations were not characteristic. Addition of 100-200 μmoles/liter of zinc chloride in incubation mixture, reactivated ALA-D, inhibited with lead acetate, nearly to the extent of control values, while heat treatment method was not found so effective. When the incubation mixture with zinc in lower level (50-100 μmoles/liter) was heated directly before determination of the enzyme activity, the effect was remarkable. The erythrocyte ALA-D of a lead worker showed a similar result. This restored ALA-D activity may reflect concentration of the enzyme. In the lower Ht, concentration of zinc obtaining the maximal effect is said to be in lower level (Sakai et al, 1976), but the effect of zinc addition with heat treatment was less influenced by Ht value. ALA-D values for this effect are negatively correlated with the concentrations of lead added.

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In Japan the first documented instance of botulism was recorded in 1951. The majority of cases occurring thereafter have been of type E. No type A cases have been reported. With this information as background, we would like to present what we believe to be is the first occurrence of type A botulism in Japan. On August 11, 1976 two sisters living in Tokyo, aged 11 and 15 years, presented with malaise, ptosis, dysphasia, and dyspnea approximately 24 hours after eating bitter tasting, spoiled "Satsuma-age" (chopped-up fish rolled into the shape of balls and fried). Both patients were hospitalized and diagnosed as having botulism. Type E botulinum antitoxin was given but there was no clinical improvement. The younger sister died on day 8. The elder sister remained conscious but progressively developed generalized motor paralysis, respiratory paralysis, and paralysis of the throat and intestinal tract. She required ventilatory support by means of a respirator attached to a nasotracheal tube for 145 days, intravenous hyperalimentation for 115 days, and antibiotic therapy for 95 days. She was discharged 220 days after the onset of disease. Serum samples taken from both patients on August 16 were positive for type A botulinum toxin. Cl. botulinum spores were also found in the stools of the younger sister on August 17. We believe that these cases represent the first confirmed instance of type A botulism in Japan.

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A capillary devided in parallel with an A-V anastmosis at both bifurcation and series with arteriole and venule was designed here. An capillary flow ratio α denotes the capillary flow Fc devided by an input arteriolar flow F (α=Fc/F). This ratio is obtainable from the fact that artificial decrease in arteriolar flow makes an oxygen utilization ratio nearly equal to the capillary flow ratio. By this method an experiment was carried out on the thigh of a dog under the condition induced by drugs and stimulation of the sciatic nerve as follows : capillary flow ratios were ca. 0.4 for control, ca. 0.3 for papaverine hydrochloride, and ca. 0.8 for 10-Hz stimulation.

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