The cardiovascular effects of medetomidine, detomidine, and xylazine in horses were studied. Fifteen horses, whose right carotid arteries had previously been surgically raised to a subcutaneous position during general anesthesia were used. Five horses each were given the following 8 treatments: an intravenous injection of 4 doses of medetomidine (3, 5, 7.5, and 10 microg/kg), 3 doses of detomidine (10, 20, and 40 microg/kg), and one dose of xylazine (1 mg/kg). Heart rate decreased, but not statistically significant. Atrio-ventricular block was observed following all treatments and prolonged with detomidine. Cardiac index (CI) and stroke volume (SV) were decreased with all treatments. The CI decreased to about 50% of baseline values for 5 min after 7.5 and 10 microg/kg medetomidine and 1 mg/kg xylazine, for 20 min after 20 microg/kg detomidine, and for 50 min after 40 microg/kg detomidine. All treatments produced an initial hypertension within 2 min of drug administration followed by a significant decrease in arterial blood pressure (ABP) in horses administered 3 to 7.5 microg/kg medetomidine and 1 mg/kg xylazine. Hypertension was significantly prolonged in 20 and 40 microg/kg detomidine. The hypotensive phase was not observed in 10 microg/kg medetomidine or detomidine. The changes in ABP were associated with an increase in peripheral vascular resistance. Respiratory rate was decreased for 40 to 120 min in 5, 7.5, and 10 microg/kg medetomidine and detomidine. The partial pressure of arterial oxygen decreased significantly in 10 microg/kg medetomidine and detomidine, while the partial pressure of arterial carbon dioxide did not change significantly. Medetomidine induced dose-dependent cardiovascular depression similar to detomidine. The cardiovascular effects of medetomidine and xylazine were not as prolonged as that of detomidine.
To evaluate the effect of third eyelid removal on the ocular surface of dogs, we operated on five young Beagle dogs and observed changes to tear function using the following tests: phenol red thread test (PRT), Schirmer tear test (STT-1), modified Schirmer tear test (STT-2), pH and tear break-up time (BUT). There was a significant decrease (37%) in STT-2 within 2 weeks after the excision and this declined further to 60% at 1 year. The pH value increased after excision. Presurgical pH was 7.17 +/- 0.20 (mean +/- SD), which increased to 7.55 +/- 0.24 in the 14-60 days following removal, and further increased to 7.77 +/- 0.65 at 1 year. The PRT and STT-1 decreased by 26% within 3-7 months compared to pre-excision values, but by 1 year the values recovered to near normal. The BUT pre-excision value was 24.0 +/- 8.1 s, which shortened to 13.5 +/- 4.5 s after 5 months and continued to decrease further during the study. There were no overt visual signs of KCS during the observational period. However, microinjury of the keratoconjunctival epithelium was observed for all operated eyes when vital staining was used at 1 year post surgery. Surgical excision of the third eyelid in Beagle dogs influenced tear quality level and affected the stability of the tear layer, and at 1 year there was evidence of microinjury to the keratoconjunctival epithelium.
Immunohistochemical detection of inhibin-alpha, -betaA and -betaB chains and 3beta-hydroxysteroid dehydrogenase (HSD) was carried out on primary testicular tumors from 15 dogs and normal testes from three adult dogs. Histopathologically, the tumors were composed of three types: Leydig cell tumors in five dogs, Sertoli cell tumors in five dogs, and seminoma in five dogs. In normal testes, immunostaining against inhibin-alpha, -betaA, and -betaB chains and 3beta-HSD revealed positive reactivity in the cytoplasm of Leydig cells. In testicular tumors, immunoreactive cells against inhibin-alpha, -betaA, and -betaB chains and 3beta-HSD were localized in all Leydig cell tumors but not in any Sertoli cell tumors or seminomas. The results of radioimmunoassay for plasma inhibin in dogs with Leydig cell tumors showed higher concentrations than those in dogs with Sertoli cell tumors and seminomas and those in normal dogs. The concentration of inhibin in the plasma was markedly decreased by the surgical removal of the Leydig cell tumor in one dog. Our findings suggest that inhibin is synthesized by normal and neoplastic Leydig cells in the canine testis, and the secreted inhibin may be inhibin A and inhibin B.
Lacaziosis, formerly called lobomycosis, caused by Lacazia loboi, is a zoonotic mycosis found in humans and dolphins and is endemic in the countries on the Atlantic Ocean. Although the Japanese coast is not considered an endemic area, photographic records of lacaziosis-like skin lesions were found in bottlenose dolphins (Tursiops truncatus) that were migrating in the Goto Islands (Nagasaki Prefecture, Japan). We diagnosed 2 cases of lacaziosis in bottlenose dolphins captured simultaneously at the same coast within Japanese territory on the basis of clinical characteristics, cytology, histopathology, immunological tests, and detection of partial sequences of a 43 kDa glycoprotein coding gene (gp43) with a nested-PCR system. The granulomatous skin lesions from the present cases were similar to those found in animals from endemic areas, containing multiple budding and chains of round yeast cells and positive in the immune-staining with anti-Paracoccidioides brasiliensis serum which is a fungal species related to L. loboi; however, the gp43 gene sequences derived from the present cases showed 94.1% homology to P. brasiliensis and 84.1% to L. loboi. We confirmed that the causative agent at the present cases was different genotype of L. loboi from Amazon area.
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