A fatal response to xylazine and ketamine in a group of rabbits.
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Biomedical subjects
Publications and source records attributed to W P Palmore.
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Four adult, castrated, male ferrets were studied in two similar trials for effects of food intake on variables hypothesized to promote struvite (ammonium, magnesium, phosphate hexahydrate) crystal formation in urine. Struvite crystalluria occurred in three of the four ferrets. Urine pH (UpH) averaged 6.6 for these ferrets. UpH in the ferret without crystalluria was 6.0. By simple linear regression analysis, no relationship was found between the amount of food ingested and the urinary concentration and excretion of magnesium and phosphorous. However, urine osmolality and excretion of both protein and ammonium were correlated to food intake (P less than .05). Ways in which these effects could promote struvite crystal formation are discussed.
1. The renal circulatory instability that some believe is inherent in rabbits was studied. 2. In five, conscious rabbits, glomerular filtration rate (GFR) averaged 4.2 +/- 0.6 ml/min/kg body wt after 1 hr, but changed to an overall average of 3.5 +/- 1.5 ml/min/kg wt after 3 hr. 3. Between-measurement coefficient of variation for GFR was more than 30% for three rabbits and 10% or less for two. 4. Renal blood flow (RBF) was even more variable. 5. The renal circulatory instability may be associated with differences in sympathetic activity by mechanisms not existing in other mammals.
Control of blood flow in the renal portal circulation of turkeys given epinephrine was evaluated by determining the distribution of injected radiopaque contrast medium within the portal circulation. Radiopacity in the region of the renal parenchyma and/or the caudal renal portal vein was increased in each of the 6 birds after epinephrine (4.0 micrograms/kg of body weight) was injected into the wing vein. In 1 bird, the contrast medium also was distributed into the mesenteric vein. Thus, epinephrine not only induced flow of blood from the pelvic limb (leg) to the kidneys, but to the abdominal viscera as well. Regulation of the patency of the renal portal valve is thought to be one means by which renal portal blood flow is controlled. However, epinephrine had no consistent effect on the valve. Thus, epinephrine seemed to control renal portal blood flow and, perhaps, blood flow to other abdominal viscera at sites other than the renal portal valve.
Renal responses to intravenous DL-alanine (ala) and glucagon (GLN) infusions were compared in conscious dogs. Doses of GLN (0.1 microgram/min) that did not increase plasma glucose (PG) concentrations, a physiological effect of GLN, stimulated glomerular filtration rate (G.F.R.). Higher GLN infusion rates (1.0 and 10.0 micrograms/min) stimulated G.F.R., renal plasma flow (R.P.F.), PG, and potassium and urea clearances. Ala infusions (1.3 mmol/min) had similar effects if the dogs had been pre-conditioned by feeding of corn starch, but not if they had been fed a normal diet. This level of ala infusion increased plasma alpha amino nitrogen to levels equivalent to plasma ala levels reported to stimulate GLN secretion. The reason for the lack of responsiveness to ala infusion when the normal diet was fed was not clear. When somatostatin (3.8 micrograms/min), an inhibitor of GLN secretion, and ala were infused simultaneously, G.F.R. was lower than when ala alone was infused. The data suggested that the ala-induced renal effects were mediated by GLN.
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Urine specific gravity, osmolality, and the incidence of proteinuria were assessed in 18 caged cats. The values for these parameters were increased when dry, as compared to moist, cat food was fed. Failure to recognize these characteristics of feline urine could lead to erroneous interpretations of laboratory data since elevation of these values, particularly protein, has been associated with renal disease.
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In the rat, the pituitary gland is essential for the stimulation of aldosterone secretion by sodium depletion. Hypophysectomy abolishes the response to sodium depletion, whereas whole pituitary gland injections partially restore it. The response cannot be restored by injections of either adrenocorticotropin or growth hormone, nor by adrenocorticotropin plus thyroxin. The pituitary gland must secrete a hormone or possibly several hormones which are necessary for the adrenal gland to respond to sodium depletion.