Takeshi Muto

High sensitivity to salt in kininogen-deficient brown Norway Katholiek rats.

Brown Norway Katholiek rats, which have very low levels of plasma kininogens, excreted a much smaller amount of kinin in the urine than normal rats of the same strain. The systolic blood pressure of 7-week-old kininogen-deficient rats fed low (0.3%) NaCl diets (131 +/- 4 mm Hg, n = 12) was not different from that in normal rats. Two percent NaCl diets given from 7 weeks of age for 4 weeks caused rapid increases in blood pressure (167 +/- 4 mm Hg, n = 12, 9 weeks old) in deficient rats, although the same diets induced no blood pressure increase in normal rats. Urinary excretion of active kallikrein and prokallikrein remained constant in both rat groups throughout NaCl loading. During this period, the deficient rats secreted less urine (9 weeks old, P < .05) and less urinary sodium (11 weeks old, P < .05). Serum levels of sodium in deficient rats were higher (P < .05) than in normal rats at 9 weeks of age. Intracellular concentrations of sodium in the erythrocytes of deficient rats were higher (P < .05) than in normal rats throughout NaCl loading. Subcutaneous infusion of bovine low molecular weight kininogen with an osmotic pump in NaCl-loaded deficient rats induced a reduction (P < .01) in blood pressure and increases (P < .05) in urine volume and urinary sodium and kinin levels. By contrast, subcutaneous infusion of the bradykinin antagonist Hoe 140 or of aprotinin in NaCl-loaded normal rats induced a hypertensive response. This antagonist treatment reduced urine volume and urinary sodium. These results indicate that the lack of kinin generation observed in the kininogen-deficient rats was related through sodium retention to the hypertensive response to NaCl loading.

Experimental feline toxoplasmosis.

The route of inoculation as well as stage of inoculated organism in its life cycle influenced the pathogenicity or infectivity of Toxoplasma in cats. All 6 cats administered orally with Toxoplasma cysts were infected without any clinical symptoms and excreted oocysts in the feces at the early stage of infection (5-12 days after administration). Of 3 cats administered orally with Toxoplasma oocysts, only one animal developed latent infection excreting oocysts in the feces at the end of 5th week after administration (38th, 40th day). On postmortem examination, none of infected animals showed abnormalities. Toxoplasma was recovered from the lung, striated musculatures and others. When cats were inoculated intraperitoneally with cysts, all of them developed fatal infection. Clinical signs were manifested by fever, anorexia, lethargy and dyspnea, which were similar to those of cats infected naturally. On postmortem examination, a large amount of fluid was found to have accumulated in the pleural and peritoneal cavities. Cloudy swelling of the liver and inflammatory edem of the lung were also observed. The level of SGOT and SGPT values was elevated significantly. None of animals inoculated intraperitoneally with cysts excreted oocysts in their feces though Toxoplasma was recovered from all tissues and organs of them. Intramusculally inoculation of cortisone acetate did not affect on relapsing or oocyst reproduction.

Ourrccence of Sick Animals in Conventional Guinea Pigs Obtained from Commercial Breeders during 1964 to 1982

A quarantine was performed on conventional Hartley guinea pigs free from Streptococcus zooepidemicus, Bordetella bronchiseptica and Salmonella spp., but infected with Eimeria caviae, which were purchased from twenty-five commercial breeders by the National Institute of Health. Physical examinations revealed an incidence of 0.88 per cent or 1,461 sick animals in 166, 050 guinea pigs quarantined during the period 1964 to 1982. The result obtained showed the following significant differences between the periods 1964 to 1971 and 1972 to 1982: Annual incidence of sick animals in the period 1972 to 1982 increased twice as many as 0.56 to 0.81 per cent during the 1964 to 1971, and monthly incidence showed bimodal occurrence at April and October in the former period but continual occurrence from November to April in the latter period. Major clinical signs in the former period were death and diarrhea, which occurred usually within a week after arrival of the guinea pigs at our institute and caused significant decrease of body weight, but those in the latter period were retarded growth and weakness which became detectable during 1-3 weeks after arrival of the animals. Discussions were made on possible reasons concerning the differences in incidence of sick animals during the two periods.