Hyperadrenocorticism is a frequent disease in dogs. The excess of circulating cortisol affects different organs and metabolic pathways, producing severe adverse effects that endanger the animal’s life. Among these effects, hypertension and renal damage can be mentioned. A group of 20 dogs with pituitary dependent hyperadrenocorticism (PDH) and 12 control dogs were used to study the following parameters: cortisol and nitric oxide (NO nit/nit) concentrations, diastolic and systolic blood pressure, renal artery resistance index by Doppler ultrasound, the rate of glomerular filtration by radio-renogram excretion and the presence of proteins in urine. Dogs with PDH showed a significantly lower NO nit/nit (P<0.0001) than the controls and this correlated with high values of diastolic and systolic pressure (r = -0.87; P<0.0001 and r = -0.81; P<0.0001 respectively). Most dogs (80%) are hypertensive mainly due to an increase in diastolic pressure, which correlated positively with the UPC (r = 0.8; P<0.001) and negatively with the glomerular rate of filtration (r = -0.58; P=0.007). Systolic pressure only increased in 60% of the cases and did not correlate with the mentioned variables. In PDH the decrease of NO affects blood pressure. The diastolic pressure would seem to have the greatest impact on the kidneys, therefore its evaluation and control are important to avoid and/or control renal damage.
The purpose of this study was to evaluate the neuroprotective effects of intranasally delivered recombinant human neuronal erythropoietin (Neuro-EPO) on brain injury induced by unilateral permanent ischemia in the Mongolian gerbil. Expression of EPO receptor (EPOR) and neuroglobin (Ngb) over 5 weeks after intranasal treatment with Neuro-EPO was determined using immunohistochemistry. Mortality of Neuro-EPO-treated gerbils decreased after surgery, and the sensory and motor function was significantly improved. Histopathological mapping showed that Neuro-EPO significantly reduced delayed neuronal death in the brain. Expression of Ngb was upregulated in the cerebral cortex at most time points (expect for 10 min and 48 hr) and in the hippocampus at 10 min and from 48 hr to 5 weeks, whereas EPOR was almost downregulated or unchanged in the brain (expect for 48 hr). The 10 min and 48 hr seemed to be two time points for the brain to switch the expression of both Ngb and EPOR to early and late recovery phase, respectively. In addition, there were two phases, 10 min to 1 hr and 24 hr to 72 hr, respectively, closing to the "golden hour" of about 60 min and the "silver day" of 1 to 3 days, for the brain to recover from stroke onset with intranasal Neuro-EPO treatment. Therefore, the results suggest that the intranasal administration of Neuro-EPO is effective in the treatment of acute brain ischemia. The different expression patterns of Ngb and EPOR is probably due to ischemic tolerance in the cerebral cortex and ischemic sensitivity in the hippocampus.
Ectopic ACTH secretion is provoked by extra-pituitary tumours that secrete ACTH, constituting an infrequent type of Cushing Syndrome in the dog. Neuroendocrine tumours (NET) are characterised by the synthesis of peptides with hormone activity. A dog with clinical diagnosis of Cushing's syndrome and presenting an abdominal tumour located in the area of the left adrenal gland was sent to the hospital. Cortisol was not inhibited at four and eight hours after the application of low-dose dexamethasone and the cortisol/creatinine ratio was elevated (93 × 10 -6 , reference values < 10 × 10 -6 ). Plasma ACTH measurements were high (28.6 pmol/l, reference values 5.5-14.3 pmol/l). On computed tomography, the tumour was found in the meso-epigastrium, with both adrenal glands hyperplasic and no alteration of the pituitary image. The tumour was located between the two layers of the meso-colon and was removed using laparoscopy. After surgery, ACTH concentrations became normal and clinical signs remitted. The histopathological diagnosis was NET, with positive ACTH immunostaining.
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