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Biomedical subjects

K C Bovée

Publications and source records attributed to K C Bovée.

At least 19 recordsLinked to original sources

Norepinephrine kinetics in dogs with experimentally induced renal vascular hypertension.

OBJECTIVE: To determine norepinephrine (NE) kinetics in dogs with experimentally induced renal vascular hypertension. ANIMALS: 4 mixed-breed dogs. PROCEDURE: The study comprised a control and hypertensive period. The hypertensive period followed induction of renal vascular hypertension achieved by surgical placement of clips on both renal arteries to reduce diameter by approximately 80%. Arterial blood pressure, renal clearance, and NE kinetics were measured during each period while dogs were receiving a low-sodium diet. Measurements of NE kinetics and renal clearance during the hypertensive period were made 5 days after induction of hypertension. RESULTS: Five days after induction of hypertension, arterial blood pressure increased by 15 to 20 mm Hg. Mean (+/- SEM) plasma NE concentration and NE spillover rate increased significantly from 151.5+/-14.1 pg/ml and 8.03+/-0.62 ng/kg/min, respectively, during the control period to 631.4+/-30.5 pg/ml and 54.0+/-5.2 ng/kg/min, respectively, during the hypertensive period. Norepinephrine clearance rate also increased (54.0+/-2.4 vs. 86.0+/-9.3 ml/kg/min). Positive associations between mean arterial pressure (MAP) and NE concentration and spillover rate were detected. However, MAP and NE clearance rate were not associated. CONCLUSIONS AND CLINICAL RELEVANCE: Increased blood pressure during the hypertensive period was likely attributable to increased NE spillover rate, which resulted in a significant increase in plasma NE concentration. Analysis of these results suggests that central sympathetic outflow was increased and may be responsible for the pathogenesis of high blood pressure during the acute phase of renal vascular hypertension in dogs.

Animals↗

Influence of dietary protein on renal function in dogs.

Two previously published studies in dogs with reduced renal function are reviewed. In the first study, renal function and biochemical responses to dietary changes were studied in four dogs with stable chronic renal failure. The objective was to determine if dogs with moderate stable failure adjust to diets with varied protein and electrolyte content. These dogs were found to have the capacity to adapt to a wide range of dietary protein and electrolyte intake. The only exception was found in dogs fed a reduced-protein diet, which failed to appropriately adjust renal tubular excretion of sodium and phosphate. The only advantage of reduced dietary protein in this study was a reduction in blood urea nitrogen (BUN). Disadvantages of reduced-protein diets were reduced glomerular filtration rate (GFR) and renal plasma flow. In the second study, the hypothesis that large amounts of dietary protein sustain renal hyperfunction and produce progressive glomerulosclerosis in dogs as previously reported in rats was tested. Results failed to find a pattern of deterioration of renal function over 4 y. Light microscopic changes and electron microscopy also failed to find glomerular injury similar to that reported in rodents. These results do not support the hypothesis that feeding a high protein diet had a significant adverse effect on renal function or morphology.

Amino Acids↗

Renal dysfunction in dogs with pyometra.

Renal function and pathologic changes in 27 dogs with pyometra were studied. Evaluation included CBC; serum biochemical evaluation; urinalysis; urine and uterine bacteriologic culture; uterine morphologic features; and light, electron, and immunofluorescent microscopic evaluation of renal tissues. Measurements of 24-hour creatinine clearance, protein excretion, Na excretion, and urine volume were made in 12 dogs without azotemia. Of 27 dogs, 26% were azotemic and 89% had a urine sp gr less than 1.035. Glomerular filtration rate was reduced in 75% of 12 dogs without azotemia. None of these 12 dogs was proteinuric. Examination of renal biopsy specimens revealed a high prevalence of mild tubulointerstitial nephritis, but few specific glomerular lesions. Minimal immunofluorescence was detected within the mesangium in 18% of the dogs. Immunofluorescence was not associated with the interstitium or tubules. Urinary tract infection was detected in 22% of the dogs. Escherichia coli and Klebsiella were recovered from the uterus in 59 and 15% of the dogs, respectively. Low urine specific gravity values were obtained from dogs without azotemia and from dogs with uterine cultures considered negative for E coli and other gram-negative bacteria. The reduction in glomerular filtration rate was a functional abnormality not correlated with structural damage in the glomerulus.

Animals↗

Spontaneous systemic hypertension in dogs: five cases (1981-1983).

Spontaneous (not experimentally induced) systemic hypertension was detected in 5 male dogs that were examined because of apparent blindness caused by intraocular hemorrhage and/or retinal detachment. Secondary causes of hypertension, including renal, adrenal, and thyroid disease, were investigated. Four of the dogs had glomerulonephropathy, renal insufficiency, and proteinuria. Four dogs had compensatory cardiac hypertrophy. Hypertension in 4 of 5 dogs was associated with glomerulosclerosis with chronic renal insufficiency, bilateral adrenocortical hyperplasia, adrenocortical adenoma with renal amyloidosis, and immune-mediated glomerulonephritis with chronic renal insufficiency, respectively. The fifth dog was determined to have essential hypertension. The dogs were treated for their primary diseases. Sodium restriction alone was inadequate to reduce blood pressure; 4 of the dogs also required antihypertensive medications.

Animals↗

Ureterocolonic anastomosis in clinically normal dogs.

Ureterocolonic anastomosis was evaluated in 13 clinically normal dogs. Urinary continence was maintained after surgery, and the procedure was completed without technique errors in all but 2 dogs. Three dogs died within 5 weeks (2 of undetermined causes and 1 of aspiration pneumonia and neurologic disease), and 1 dog was euthanatized 4 months after surgery because of neurologic signs. Two healthy dogs were euthanatized 3 months after surgery for light microscopic evaluation of their kidneys. Five dogs were euthanatized 6 months after surgery for light microscopic evaluation of their kidneys. Gastrointestinal and neurologic disturbances developed in 4 dogs at various postoperative intervals. Plasma ammonia concentration measured in 2 dogs with neurologic signs was increased. Plasma ammonia concentration measured in 5 dogs without neurologic signs was within normal limits. All 5 dogs, in which metabolic acidosis was diagnosed, had high normal or above normal serum chloride concentration. Serum urea nitrogen values were increased after surgery because of colonic absorption of urea. Serum creatinine concentration was increased in 1 dog 6 months after surgery. Individual kidney glomerular filtration rate was reduced in 38% (3/8) of the kidneys from 4 other dogs at 6 months after surgery. Of 5 dogs euthanatized at 3 to 4 months after surgery, 4 had bilateral pyelitis, and 1 had unilateral pyelonephritis. Six months after surgery, pyelonephritis was diagnosed in 40% (4/10) of the kidneys from 5 dogs. The ureterocolonic anastomosis procedure is a salvage procedure that should allow complete cystectomy. However, variable degrees of metabolic acidosis, hyperammonemia, and neurologic disease may result.

Anastomosis, Surgical↗

Canine cystine urolithiasis.

Cystine uroliths form as a result of a complex metabolic disturbance in amino acid metabolism and transport. The inheritance of this disease is obscure because it does not follow a standard mendelian pattern. Uroliths are a vexing clinical problem because the recurrence rate is high. Accurate diagnosis of uroliths requires use of crystallographic methods. The renal defect leading to excessive excretion of cystine is variable. The only effective method of prevention of recurrence is use of D-penicillamine, which is poorly tolerated by some dogs.

Animals↗

Essential hereditary hypertension in dogs: a new animal model.

The objective of this project is to characterize a genetically determined model of essential hypertension in dogs. A pair of unrelated dogs with essential hypertension were identified. Breeding of these dogs and back-cross matings have resulted in 24 offspring, approximately half of which have essential hypertension (systolic blood pressure 170 mmHg, diastolic 105 mmHg). Other offspring are either borderline hypertensive or normal. Blood pressure is measured in the trained, unanaesthetized state by direct arterial puncture. Offspring have normal plasma chemistries, electrolytes, glomerular filtration rate, plasma renin activity, aldosterone and catecholamines. These dogs appear to salt-sensitive compared with normal dogs. Further breeding studies will characterize this new model of hereditary essential hypertension.

Animals↗

Cystinuria in the maned wolf of South America.

Of 42 maned wolves in zoos or live-trapped in Brazil, 34 had excessive cystine in their urine. Renal clearance studies of five of the affected wolves revealed a variable defect for the reabsorption of cystine and dibasic amino acids. The renal tubular handling of other solutes including glucose, phosphate, sodium, potassium, and uric acid was considered normal. Urinary calculi composed of cystine were found in four wolves and proved fatal in three of them. With the exception of the high incidence in this species, this hereditary disease resembles the disorder described in dogs and humans.

Amino Acids↗

Characterization of renal defects in dogs with a syndrome similar to the Fanconi syndrome in man.

Ten adult dogs with multiple spontaneous defects of renal tubular reabsorption were studied. Clinical signs included polydipsia, polyuria, and glycosuria for 2 to 12 months. Eight of the dogs were Basenjis. Urinalyses revealed hyposthenuria, glycosuria, and amino aciduria in most dogs. Renal function was normal in 5 dogs and slightly reduced in the remainder. Moderate metabolic acidosis had developed in 3 dogs. Renal clearance studies revealed reduced tubular reabsorption of glucose, phosphate, sodium, potassium, and uric acid. Abnormal glucose tubular maximal curves were found. Results of oral glucose tolerance tests were normal. Two patterns of abnormal amino aciduria were evident: generalized amino aciduria and a pattern similar to that of cystinuria in dogs. Radiography of long bones and bone densitometry did not reveal any skeletal abnormalities. Five of the dogs died within 90 days of diagnosis; death was due to acute renal failure associated with profound dehydration, acidosis, and papillary necrosis. The other dogs remained stable without treatment after 18 months. Histopathology of kidneys did not reveal uniform abnormalities; some dogs had variable and nonspecific changes and others were normal. Electron microscopy did not reveal ultrastructural abnormalities in renal tubular cells. It was concluded that the syndrome in these dogs represents a new entity of renal disease in dogs, similar to idiopathic Fanconi syndrome in man.

Animals↗

Clinical evaluation of glomerular function: 24-hour creatinine clearance in dogs.

Methods of renal clearance to measure glomerular filtration rate (GFR) were compared with plasma creatinine concentration in clinically normal and partially nephrectomized dogs. Glomerular filtration rate was measured by use of a simple 24-hour creatinine clearance method in 36 normal female Beagles. Mean values were 57.6 +/- 9.3 ml/minute/m2 of body surface or 3.7 +/- 0.77 ml/minute/kg of body weight. Variability of this measurement was considerable, as determined in 4 dogs studied on 4 consecutive days. Glomerular filtration rate was measured in the same 36 dogs while they were under anesthesia, using short clearance periods to compare inulin and endogenous creatinine clearance. Mean values for inulin were 41.8 +/- 13.9 ml/minute/m2 of body surface. A close agreement with creatinine clearance was found (correlation coefficient, 0.998). Mean plasma creatinine concentration was 0.82 (range, 0.5--1.0) mg/100 ml. The value of GFR measurement compared with plasma creatinine concentration was determined in 10 dogs after 75% nephrectomy. Sixty days after partial nephrectomy, GFR was reduced to 61% of normal. Mean plasma creatinine and blood urea nitrogen were 1.2 +/- 0.14 mg/100 ml and 20.4 +/- 7.1 mg/100 ml, respectively. Thus, the detection of reduced renal function may be uncertain when plasma creatinine or blood urea nitrogen are used as a means of evaluating renal function. It was concluded that a simple method of creatinine clearance is a sensitive and useful measurement to detect early or borderline reduction in glomerular function.

Anesthesia↗

Trigonal-colonic anastomosis: a urinary diversion procedure in dogs.

Trigonal-colonic anastomosis for diversion of urine into the colon was performed in 12 clinically normal dogs and in 10 incontinent dogs with diseases of the urinary bladder or urethra. Dogs were studied from 1 to 30 months after surgery. The surgical procedure was technically satisfactory. Fifteen of 22 dogs were studied with intravenous urography, and only 1 case of hydronephrosis was found. Pyelitis was a common histopathologic finding in both groups of dogs. Pyelonephritis developed in 30% of dogs, regardless of duration of anastomosis. Glomerular filtration rate was reduced in all dogs studied, but renal failure was infrequent. Values for blood urea nitrogen and serum inorganic phosphorus were elevated due to intestinal recycling of nitrogenous products and phosphate. Electrolyte imbalances were not a problem, but gastrointestinal disturbances developed in 3 of the 10 diseased dogs. Six of 10 diseased dogs survived from 9 months to more than 3 years. Trigonal-colonic anastomosis appears to be a satisfactory salvage procedure for incontinent dogs with diseases of the urinary bladder or urethra that do not respond to other forms of therapy.

Animals↗

Characterization and treatment of acid-base and renal defects due to urethral obstruction in cats.

In 23 cats, urinary obstruction of 24 to 48 hours' duration caused marked azotemia, hyperphosphatemia, hyperkalemia, and metabolic acidosis. The metabolic acidosis was a consistent finding and was severe in all cats (venous pH, 7.11 +/- 0.09). Serum sodium and chloride were normal. Glycosuria was found in 17 (74%) of the cats. There was no clear difference in blood pH, serum chemical values, or electrolyte concentrations between cats obstructed 24 hours and those obstructed 48 hours or longer. At a mean of 8.4 hours after relief of obstruction, acid-base status was corrected to normal, using fluid replacement and sodium bicarbonate therapy. Blood urea nitrogen serum creatinine, and serum inorganic phosphorus improved significantly (P less than 0.01) at a mean of 19.5 hours after treatment. Variation in azotemia after fluid replacement suggested variable decreases in glomerular filtration rate after relief of obstruction. Hypokalemia occasionally developed after relief of obstruction during the postobstructive diuresis. It was concluded that fluid and electrolyte therapy must be regulated in response to the postobstructive diuresis, to ensure proper medical management.

Acid-Base Imbalance↗

Spontaneous Fanconi syndrome in the dog.

Three dogs with spontaneous renal tubular defects similar to idiopathic Fanconi syndrome are characterized. Renal clearance studies revealed a fractional reabsorption of glucose ranging from 31% to 82%. Abnormal glucose thulium values were present in all dogs. A generalized aminoaciduria occurred in two dogs while one had aminoaciduria characteristic of canine cystinuria. Fractional reabsorption of phosphate ranged from 47% to 79%. In vitro uptake of alpha-methyl-D-glucoside was significantly depressed (p less than 0.001). In vitro uptake of amino isobutyric acid was similar to controls. Renal biopsy revealed nonspecific interstitial change in two dogs and normal histology in the other. These animals represent a useful new model for the study of renal tubular transport defects.

Amino Acids↗