The oral administration of phenylbutazone at a dose rate of approximately 10 mg per kg per day for seven to 14 days resulted in the development of signs of toxicity in seven of eight ponies treated. Clinical signs included anorexia, depression and abdominal oedema. Blood biochemical determinations showed a decrease in total plasma protein and calcium concentrations with an increase in urea concentration. These changes were considered indicative of water retention. Three of the ponies died during treatment following the development of shock. Shock was considered to arise from the submucosal oedema of the large intestine observed on necropsy. Oral ulceration was also found in these animals. In two ponies intravenous administration of phenylbutazone (4.0 mg per kg) for seven days was studied. In one of these ponies a marked decrease in total plasma protein concentration occurred.

Invest. 1995Invest. . 95:2573Invest. -2580

The K+ efflux that mediates sickle-cell dehydration may occur through several pathways, including two with a high capacity for mediating rapid K+ loss, KCl cotransport and the Ca(2+)-dependent K+ channel [K(Ca2+)]. The rate and pathway of red blood cell (RBC) dehydration most likely depends on cell age and hemoglobin (Hb) composition, with the presence of HbF playing an important role. Oxygenated sickle RBCs have relatively stable cell volume during incubation in vitro, whereas deoxygenated cells become dehydrated, and therefore more dense, due to activation of one or more K+ efflux pathways. In this investigation, sickle RBCs were deoxygenated either continuously or in 15-minute cycles for 4 hours, and the density increases of very young, transferrin receptor-positive (TfR+) cells and the remaining TfR-cells were determined. The contribution of KCl cotransport was estimated by replacing Cl-with NO3-.K(Ca2+) was inhibited by removal of Ca2+ or addition of charybdotoxin (ChTX). For both continuous and cyclic deoxygenation, TfR+ cells had a greater density increase when compared with TfR-cells. The lower percentage of HbF found in the TfR+ population may contribute to this difference. With continuous deoxygenation, the density shift was decreased by inhibition of K(Ca2+), but not by inhibition of KCl cotransport. With cyclic deoxygenation, the density shift was decreased in an independent, additive manner by inhibition of both pathways. Thus, cyclic deoxygenation of sickle cells under these conditions appears to activate both K(Ca2+) and the KCl cotransporter.

FIG 1: Magnetic resonance imaging (T1-weighted with gadolinium) of the brain of a dog, showing significant uptake of contrast by the tumour (arrow) FIG 2: Sagittal section of the brain of a dog, revealing the tumour (black arrow) situated above the pituitary gland. Pituitary oedema (white arrow) is also present (Magnevist; Schering), differentiating the abnormal tissue from normal tissue with clearly defined margins and suggesting a neoplastic lesion with surrounding oedema. Due to the likelihood of an intracranial neoplasm, the owner declined a cerebrospinal fluid (CSF) tap and requested that the dog be euthanased.On gross postmortem examination the dog was in good body condition. The bladder was distended and filled with dilute urine. The brain was removed. The pituitary gland was swollen secondary to oedema and discoloured reddishbrown. The whole brain and samples of peripheral lymph node, spleen, kidney, liver and lung were fixed in 10 per cent neutral buffered formalin. CSF was not examined. A midsagittal section of the fixed brain revealed a white nodular mass measuring 0·75 cm in diameter in the hypothalamus (Fig 2). The neurohypophysis was swollen. The optic chiasm and the medullary body were not involved, but the anterior commissura had been displaced dorsally. There were no other pathological findings. Histological sections of all tissues were stained with haematoxylin and eosin and examined. Immunohistochemical staining was performed on paraffinembedded sections of the tumour using the modified avidin-biotin-peroxidase complex method (Hsu and others 1981). Immunohistochemical staining was performed with antibodies to B cell antigen (CD79a), T cell antigen (CD3) and CENTRAL diabetes insipidus is an uncommon condition characterised by polyuria due to a deficiency in the secretion of antidiuretic hormone from the posterior pituitary gland. The causes of central diabetes insipidus in dogs include intracranial tumours, such as craniopharyngioma, meningioma, pituitary chromophobe adenoma, pituitary chromophobe adenocarcinoma and metastatic tumours (Neer and Reavis 1983, Davenport and others 1986, Goossens and others 1995. The condition has also been reported secondary to non-neoplastic lesions, such as head trauma, brain surgery and congenital anomalies (Authement and others 1989, Harb and others 1996, Ramsey and others 1999). However, in many dogs with central diabetes insipidus the cause is not identified. This short communication describes a case of central diabetes insipidus in a dog secondary to a focal pituitary and hypothalamic B cell lymphoma.A six-year-old female neutered Bernese mountain dog was presented with a history of profound polydipsia, polyuria and lethargy of approximately one month's duration. The referring veterinarian had treated the dog empirically with desmopressin (DDAVP; Ferring Pharmaceuticals) for one week. This had reduced the polyuria and polydipsia but the dog was still very dull. There had been no environmental or dietary changes before the development of clinical signs, and t...

The K+ efflux that mediates sickle-cell dehydration may occur through several pathways, including two with a high capacity for mediating rapid K+ loss, KCl cotransport and the Ca(2+)-dependent K+ channel [K(Ca2+)]. The rate and pathway of red blood cell (RBC) dehydration most likely depends on cell age and hemoglobin (Hb) composition, with the presence of HbF playing an important role. Oxygenated sickle RBCs have relatively stable cell volume during incubation in vitro, whereas deoxygenated cells become dehydrated, and therefore more dense, due to activation of one or more K+ efflux pathways. In this investigation, sickle RBCs were deoxygenated either continuously or in 15-minute cycles for 4 hours, and the density increases of very young, transferrin receptor-positive (TfR+) cells and the remaining TfR-cells were determined. The contribution of KCl cotransport was estimated by replacing Cl-with NO3-.K(Ca2+) was inhibited by removal of Ca2+ or addition of charybdotoxin (ChTX). For both continuous and cyclic deoxygenation, TfR+ cells had a greater density increase when compared with TfR-cells. The lower percentage of HbF found in the TfR+ population may contribute to this difference. With continuous deoxygenation, the density shift was decreased by inhibition of K(Ca2+), but not by inhibition of KCl cotransport. With cyclic deoxygenation, the density shift was decreased in an independent, additive manner by inhibition of both pathways. Thus, cyclic deoxygenation of sickle cells under these conditions appears to activate both K(Ca2+) and the KCl cotransporter.