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Biomedical subjects

W L Spangler

Publications and source records attributed to W L Spangler.

At least 37 records · Page 2Linked to original sources
PubMed1979

Crystalline corneal opacities in the Siberian Husky.

Bilaterally symmetric opacities were detected in the corneal stroma of 78 (14%) of 560 Siberian Huskies, aged 7 months to 12 years, examined in ophthalmology screening clinics. The opacities were round or horizontally oval and consisted of a diffuse gray homogeneous haze in the anterior stroma or an array of fine polychromatic crystals in the posterior stroma, or both. The corneas were not inflamed. The frequency of occurrence and density of the opacities increased with age. Several affected dogs were closely related, but a specific inheritance pattern could not be established. Light and electron microscopy disclosed clusters of extracellular, thin, needle-shaped, crystalline clefts. Histochemical stains on frozen sections identified neutral fats, phospholipids, and cholesterol as components of the crystals.

Animals↗
PubMed1979

Influence of the ambient acceleration field upon acute acceleration tolerance in chickens.

It has been demonstrated both in the Russian and in the American space programs that there is a progressive deconditioning of the circulatory system with exposure to weightlessness. Astronauts and cosmonauts returned to Earth have a significantly reduced orthostatic tolerance which will persist for a few days. We have measured the acceleration tolerance of domestic fowl, acutely exposed to a 6 g+z field, as the time over which a normal heart rate can be maintained. This period of circulatory accommodation ends abruptly with a marked bradycardia, which with continued treatment is terminal. For animals which have been previously chronically accelerated (e.g., physiologically adapted to a 2.5 g field) the acute acceleration tolerance is greatly increased. It appears that the influence of the ambient acceleration field in conditioning the responsiveness of the circulatory system is a general phenomenon.

Acceleration↗
PubMed1979

Furosemide enhancement of experimental gentamicin nephrotoxicity: comparison of functional and morphological changes with activities of urinary enzymes.

Dogs were given gentamicin (10 mg/kg) intramuscularly every 8 hr for 10 days. Levels of serum creatinine rose by day 6 (0.91 +/- 0.08 vs. 0.75 +/- 0.02 mg/dl for controls, P less than 0.05) and of blood urea nitrogen by day 8 (24.3 +/- 4.80 vs. 16.1 +/- 0.90 mg/dl for controls, P less than 0.05). Gentamicin nephrotoxicity occurred earlier and was more marked when furosemide (2 mg/kg) was added: the level of serum creatinine by day 6 was 1.62 +/- 0.25 mg/dl (P less than 0.05), and the level of blood urea nitrogen by day 8 was 181 +/- 23.5 mg/dl (P less than 0.01). Elevations in the activities of the urinary enzymes beta-glucuronidase, N-acetyl-beta-glucosaminidase, and muramidase preceded rises in levels of serum creatinine and blood urea nitrogen. Examination of serial percutaneous renal biopsy specimens showed that gentamicin administration was associated with hyaline droplet degeneration, lysosomal changes, and, later, cell necrosis (primarily of the proximal tubules). Changes in renal morphology were more severe and occurred earlier when furosemide was administered concomitantly. In summary, furosemide enhanced gentamicin nephrotoxicity. Enzymuria was an early sign of gentamicin nephrotoxicity.

Acetylglucosaminidase↗
PubMed1979

Tolerance of domestic fowl to high sustained +Gz.

A system is described for the acceleration treatment of domestic fowl. A reasonable endpoint for acceleration tolerance is provided by a bradycardia which occurs fairly close to the lethal limit. In a group of 61 male Rhode Island Red chickens exposed to 6 Gz, the mean tolerance (+/- S.D.) was 11.1 +/- 10.6 min. Among individuals, the acceleration tolerance is inversely related to both body size and age, and positively to pre-treatment heart rate.

Acceleration↗
PubMed1979

Vitamin D intoxication and the pathogenesis of vitamin D nephropathy in the dog.

Dogs given excess vitamin D (500 or 1,000 micrograms/kg of body weight each day for 1 to 3 weeks were observed for clinical and pathologic changes of increased blood pressure and of characteristic nephropathy associated with vitamin D toxicosis or hypercalcemia. Serum calcium and serum urea nitrogen (UN) increased throughout the treatment period, but serum phosphorus remained within the normal range. Plasma renin activity increased markedly. Blood pressure showed only insignificnat changes (P = greater than 0.05). Gross and microscopic examination of the kidneys suggested vascular-oriented changes with an ischemic basis. Glomerular vascular poles showed hypertrophy and hyperplasia of juxtaglomerular cells. Ultrastructually, an increase in the number of secretory granules was noticed in these cells. A hypothesis regarding the mechanism of renal injury during vitamin D toxicosis is presented.

Animals↗
PubMed1979

Ultrastruct of the juxtaglomerular apparatus in the dog in a sodium-balanced state.

The ultrastructure of juxtaglomerular apparatuses (JGA) from four dogs in a state of sodium balance were examined. Plasma renin activity and urinary sodium excretion in the dogs were within normal values. At the vascular pole of the glomerulus, circumferentially oriented smooth muscle cells in the wall of the glomerular arteriole were abruptly replaced by modified smooth muscle cells with complicated interwoven cell processes. These modified cells were indistinguishable from the juxtaglomerular cells of the lacis region (extraglomerular mesangium). The basal lamina surrounding these modified smooth muscle cells in the wall of the glomerular arteriole was continuous with the basal lamina of the juxtaglomerular cells of the lacis (extraglomerular mesangium) and the macula densa. The most striking differences in the JGA of the dog, when compared with the JGA of other laboratory animals, are related to the observation that cytoplasmic secretory granules are less abundant in the dog, are generally smaller than the practical resolving capability of the light microscope, and are restricted to cells of the lacis area in the JGA.

Animals↗
PubMed1979

Pathophysiologic response of the juxtaglomerular apparatus to dietary sodium restriction in the dog.

Pathophysiologic changes in the juxtaglomerular apparatus (JGA) of the dog were induced by 10 days of dietary sodium restriction (less than 1 mEq of Na+/day). Plasma renin activity increased 12-fold and plasma aldosterone values increased 60-fold, whereas urinary sodium excretion decreased precipitously. Urinary potassium excretion remained within normal values throughout the period of sodium restriction. The JGA cell counts, determined by light microscopy, were significantly (P = less than 0.05) increased after 2 days of sodium restriction and remained increased through day 10. Adrenal gland weights and the cross-sectional width of the zona glomerulosa were not altered. Ultrastructurally, JGA cells showed progressive hypertrophy and hyperplasia. The Golgi apparatus became more prominent. The endoplasmic reticulum increased, as did the number of ribosomes. Cytoplasmic secretory granules increased in number and size from day 2 through day 6. On days 8 and 10, fewer and smaller secretory granules were encountered, even though plasma renin and aldosterone values continued to increase. In the dog maintained in a balanced sodium state, little renin is stored in cytoplasmic granules of the juxtaglomerular cells. Short-term stimulation results in increased plasma renin values and increased production and storage of renin in JGA cells. Continued stimulation results in depletion of cytoplasmic stores, although plasma renin content continues to rise, suggesting that renin is produced and secreted directly during more prolonged stimulation.

Aldosterone↗
PubMed1979

Responses of domestic fowl to repeated +Gz acceleration.

The responses of domestic fowl to repeated exposures of 4 min to +6Gz (8 times daily, 5 d weekly) are reported. Survivorship curves for the test group of 48 birds divided into three response categories: mode I, highly susceptible, with all individuals dying on the first day; mode II, more tolerant, with mortality occurring within the first 20 d of treatment; and mode III, highly tolerant, with mortality occurring only after 20 d of treatment. Observations of lymphocyte frequency, an index of systemic stress, and postmortem observations indicate that this heterogeniety has a biological basis.

Acceleration↗
PubMed1979

Effects of brief exposure of domestic fowl to very intense acceleration fields.

Since biological responses to high sustained Gz (HSGz) are determined largely by field intensity and duration of exposure, a series of experiments was arranged to emphasize the effects of field intensity. Male Rhode Island Red chickens were given a single standard exposure of 1 min to a field, which increased from 5-18 +Gz for the series. Acceleration-induced changes were observed in heart rate during and after the treatment, and in lymphocyte frequency and body mass maintenance subsequently. Generally, there was an increasing bradycardia and lymphopenia, which was proportional to field strength. Above 13 G, normal growth and even the maintenance of a pre-treatment body mass were impaired.

Acceleration↗
PubMed1978

Seizure-induced rhabdomyolysis accompanied by acute renal failure in a dog.

Secondary complications from extreme and prolonged convulsive seizures occurred in a young dog. Physical exertion resulted in necrosis of a substantial amount of skeletal muscle. The release of large quantities of myoglobin into the circulation caused severe impairment of renal function. Anoxia, apparently associated with the inability to breathe during seizures, resulted in brain damage. It was concluded that, although primary therapy must be directed toward alleviation of intense seizure activity, subsequent screening for renal disease and corollary supportive therapy would be appropriate.

Acute Kidney Injury↗
PubMed1978

Plasmodium knowlesi malaria in the Rhesus monkey.

Twelve Rhesus monkeys were inoculated intravenously with about 500 000 malaria parasites, Plasmodium knowlesi. Acute hemolysis occurred 5 days later, and all animals died on the 6th or 7th day after inoculation. All organs were gray-green to gray-brown because of deposition of hemoglobin and malaria pigments. This deposition was particularly striking in the lung, brain, abdominal fat and serous surfaces. Microscopic changes indicative of acute hypoxia were found in the liver (centrilobular necrosis) and kidneys (acute tubular necrosis). Terminal intravascular coagulopathy was evidenced by widely distributed, recently formed, fibrin thrombi.

Animals↗
PubMed1977

Blood pressure measurement in the dog.

An indirect method of blood pressure measurement was evaluated in 169 dogs, including 114 that were hospitalized because of a variety of diseases, 10 clinically normal dogs presented for neutering, and 45 privately owned, clinically normal dogs. Measurements correlated well with values obtained by simultaneous direct arterial puncture. Normotension was considered to be 130 to 180 mm of Hg, systolic, and 60 to 95 mm of Hg, diastolic. As a group, 20 dogs with advanced renal disease had significant (P less than 0.001) hypertension, compared with the groups of clinically normal dogs. Of 94 dogs with a variety of diseases exclusive of renal disease, 10 had hypertension and 2 had hypotension.

Animals↗