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Biomedical subjects

M Kaye

Publications and source records attributed to M Kaye.

At least 91 records · Page 5Linked to original sources

Depth perception, eye alignment and cortical ocular dominance of dark-related cats.

On first exposure to light, animals that have been reared from birth until about 4 months of age in total darkness exhibit substantial visual and visuomotor deficits, which decline in severity during the first few months following exposure to light. In order to determine whether dark-reared animals eventually acquire stereoscopic vision following exposure to light we examined the binocular status of 5 dark-reared animals two of which developed convergent eye alignment. The binocular status was assessed behaviorally by measurements of the ability of each animal to perceive depth using either one or both eyes, and physiologically by documentation of the distribution of cortical ocular dominance of a sample of visual acuity, their binocular depth perception remained very poor, comparable to the monocular performance of normal cats. In marked contrast to normal animals none of the dark-reared animals, even those with normal eye alignment, performed substantially better binocularly than monocularly, a result indicating the absence of a uniquely binocular mechanism for depth perception in these animals. Although the dark-reared animals were found to retain a substantial (but reduced) complement of binocularly influenced cortical neurons, the tuning of these cells for retinal disparity must be insufficiently precise to mediate depth perception under binocular viewing conditions that is superior to that which can be achieved monocularly.

Animals↗

The role of phosphorus in the genesis of azotemic osteodystrophy.

There is good evidence for a role for phosphate retention in the genesis of secondary hyperparathyroidism. It exerts its effect directly by lowering the ionized calcium, thereby stimulating parathyroid secretion, and indirectly by causing skeletal resistance to the calcemic action of parathyroid hormone. The resistance phenomenon may be due in part to a direct effect of phosphorus on the skeletal resorbing action of parathyroid hormone and in part to an indirect effect of phosphorus on 1,25(OH)2D3 production. As well as causing parathyroid resistance, low serum 1,25(OH)2D3 is also responsible for decreased calcium absorption and may have a role in the mineralization disturbance seen in most cases of severe uremia. In the occasional instance, hypophosphatemia induced by phosphate-binding agents may contribute to uremic osteomalacia.

Animals↗

Evidence that resistance to the calcemic action of parathyroid hormone in rats with acute uremia is caused by phosphate retention.

An animal model was developed to examine the cause of resistance to the calcemic action of PTH in renal failure. Thyroparathyroidectomized (TPTX) rats were repeatedly reinfused with their excreted urine, over a 5-hour period, to produce an acute uremic animal with normal kidneys. Nonuremic controls were infused with equivalent volumes of a simple electrolyte solution. Using this model, we have demonstrated impaired calcemic response to PTH (Lilly Parathyroid Extract, 80 U/100 g) in urine-infused rats compared with electrolyte-infused rats. The final plasma calcium concentrations were 12.0 +/- 0.3 and 14.9 +/- 0.3 mg/dl, respectively (P less than 0.001). The cause of this impaired calcemic response was investigated by reinfusing rats with their own urine that had been pretreated with either activated charcoal or zirconium oxide in two different anionic forms, or urine that had been ultrafiltrated through an Amicon membrane of which the stated molecular-weight cut-off of the smallest pore-size membrane was 500 daltons. It was found that charcoal and ultrafiltration techniques had no effect, whereas the zirconium oxide treatment completely corrected the impaired calcemic response and returned the plasma phosphorus to a concentration similar to that in nonuremic controls. This can be explained by the fact that the principal effect of zirconium oxide on urine is to remove inorganic phosphate. Other groups of TPTX rats given PTH extract were infused with an electrolyte solution containing varying amounts of phosphate up to a maximum similar to the amount that a urine-infused rat would receive. A highly significant inverse relationship was found between the dose of phosphate infused with the electrolyte solution and the measured calcemic response to PTH. This relationship is represented by the following equation: calcium (mg/dl) = 14.84 - 0.139 inorganic phosphate; r = 0.915, P less than 0.001. From these series of studies, we conclude that phosphate retention is the cause of resistance to the calcemic action of PTH extract in this acute uremic model.

Acute Kidney Injury↗

Assessment of depth perception in cats.

A behavioural method is described for the assessment of depth perception of kittens. Measurement is made of the smallest separation in depth that can be discriminated between two adjacent stimuli under both monocular and binocular viewing conditions. Normal animals can discriminate much smaller separations in depth when using two eyes than with monocular viewing, implying the presence of a cue to depth that is uniquely available with binocular viewing. The test provides a quick and reliable way of screening animals for stereopsis.

Animals↗

Experience with polytetrafluoroethylene grafts in patients on long-term hemodialysis.

Expanded polytetrafluoroethylene (PTFE) is a new material now being used to create subcutaneous arteriovenous anastomoses for vascular access in hemodialysis. The authors have been impressed with the versatility of grafts made from this material and, where failure occurs, the ease with which surgical revision can be carried out. Two cases are described to illustrate the adaptability of this material to reconstruction. The authors' initial impression based on 22 months' experience is that PTFE grafts have appreciably modified the management with respect to vascular access, of many patients on long-term hemodialysis.

Aged↗

Two year sequential haemodynamic data on polytetrafluoroethylene (PTFE) grafts used for haemodialysis.

Forty-one PTFE grafts were studied prospectively with measurement of intragraft pressure and flow. As well, cardiac function was assessed by measuring cardiac output, ejection times and ejection fraction. It was shown that graft failure was associated with changes in graft pressures and flow. No untoward effects of graft flows of 1-2L/min were found on cardiac function.

Brachial Artery↗

Changes in the red cell, plasma and inulin spaces and in the total water contents of rat femurs in cortisone induced osteoporosis.

Measurements of the bone vascular space by use of 99mTc-labelled red cells and 131I-serum albumin, and of the 3H-inulin spaces and total water contents were carried out in female rats treated for four weeks by daily subcutaneous injections of 15 mg cortisone acetate. Significant decreases in bone vascularity, inulin space and water contents were noted as compared to controls. These changes were not associated with differences in plasma calcium values, or parathyroid gland weights. They were found to be present together with significant decreases in bone density and ash contents of the femoral shafts in the steroid-treated animals. It is suggested that the changes in the vascular and extravascular fluid spaces of bones were probably consequent upon a generally depressed level of cellular activity and bone turnover, which could be found in steroid induced osteoporosis.

Animals↗

Resistance to parathyroid hormone in renal failure: role of vitamin D metabolites.

Resistance to the calcemic action of parathyroid extract (PTE) was shown in thyroparathyroidectomized rats after 5 hr of renal failure that was induced by either bilateral nephrectomy (NPX) or ureter ligation (UL). Studies were carried out to investigate the relationship of parathyroid resistance to the vitamin D status of the animal. Concentrations of 1,25-dihydroxycholecalciferol (1,25(OH)2D3) and 24,25-dihydroxycholecalciferol (24,25(OH)2D3) were similar in pooled sera samples from rats either UL or sham-operated and treated with PTE. Pretreatment with oral 25-hydroxycholecalciferol or with a combination of i.v. 24,25(OH)2D3 and 1,25(OH)2D3 prior to UL failed to alter the resistance. Resistance was also present in a group in vitamin-D-deficient rats. A similar group given 1 microgram of vitamin D2 showed more parathyroid resistance than did the group not given vitamin D2. In chronic renal failure of 28 day's duration, parathyroid resistance was again demonstrated, but, in contrast to the acute renal failure models, this was partly corrected by prior 1,25(OH)2D3 administration. These studies show that parathyroid resistance is not caused by an abnormality of vitamin D metabolism in the acute renal failure model, and we suggest that the phenomenon is due to the accumulation of one or more uremic factors.

Acute Kidney Injury↗

Changes in red cell space of bone in hypocalcemic states: studies in rat femur.

With the use of technetium-99m-labeled red cells, the red cell space of the femur was found to be increased in rats fed a 0.01 percent Ca diet for 4 wk, at which time they were also hypocalcemic. Rats fed the same diet for 2 wk did not demonstrate hypocalcemia nor hypervascularity of the femur. Thyroparathyroidectomized (TPTX) rats fed the calcium-deficient diet produced hypocalcemia nor hypervascularity as did TPTX rats fed a normal diet for 4 wk. However, bone vascularity was normal at 2 wk post-TPTX (normal diet) when the degree of hypocalcemia was less marked. Inhibition of prostaglandin synthetase with oral indomethacin 0.2 mg/100 g per 12 h for 60 h did not alter the red cell space estimates but did increase bone blood flow in both normal and calcium-deficient animals. Acute restoration of normocalcemia with CaCl2 orally in the calcium-deficient rats did not revert the bone hypervascularity. The evidence suggests that in these models of hypocalcemic states, the rise in the vascular space of bone does not result from the influence of PTH, calcitonin, diet, or prostaglandins.

Animals↗

Complications in expanded polytetrafluoroethylene arteriovenous grafts: an angiographic study.

Expanded polytetrafluoroethylene grafts were used for creation of arteriovenous shunts in 35 patients on chronic hemodialysis. When flow studies or mechanical factors indicated abnormal flow in the graft, angiography was performed. Detection of venous backflow or obstruction, arterial stenosis, aneurysm formation, or graft kinking facilitated correction and thus salvage of the grafts.

Aneurysm↗

Natural fluorescence in serum of patients with chronic renal failure not to be confused with creatine kinase-BB isoenzyme.

We assessed the reported presence of creatine kinase-BB isoenzyme in the serum of patients with chronic renal failure. Our study showed that the blood of these patients contains a fluorescent material with an electrophoretic mobility similar to that of the BB isoenzyme on cellulose acetate strips. The fluorescing material is, however, completely distinct from BB isoenzyme and its nature is as yet undetermined.

Creatine Kinase↗

Polytetrafluorethylene (PTFE) grafts for hemodialysis. 18 months' experience.

18 months clinical experience with 6 mm polytetrafluorethylene forearm grafts for hemodialysis access has been described. 35 grafts were implanted, all in patients who had unsuitable vessels for construction of a regular Brescia-Cimino forearm fistula. The overall patency was 71% with mean duration of 10.3 months, and at any one time more than 85% of the grafts at risk were functional. Complications, including undesirable flow rates, edema, thrombosis, aneurysm and cardiac failure have been discussed and rational methods of avoidance described. We believe the polytetrafluorethylene (PTFE) graft represents an important advance in hemodialysis access.

Adult↗

Hemodynamic studies in patients with expanded polytetrafluoroethylene (PTFE) forearm grafts.

21 patients with polytetrafluoroethylene grafts inserted for hemodialysis access were studied to assess the hemodynamic parameters. Mean graft flow was 1.9 l/min with a range of 0.2-3.8 l/min. Intragraft pressure varied from 1 to 83 mmHg and was dependent on systemic pressure, graft flow and the presence of stenotic lesions. Mean cardiac output was 7.1 l/min and index 4.0 l/min and was positively correlated with graft flow. By obtaining this data surgical corrective action was taken in several patients prospectively thus removing the abnormalities and ensuring continued graft patency. The techniques described are reproducible and simple and can be carried out in less than five minutes with minimal patient discomfort or hazard.

Adult↗

Changes in red cell, plasma, inulin, and total water compartments in rat femurs. Comparison of vitamin D deficiency and diphosphonate induced rickets.

The vascular space, as measured with the use of 99m-technetium-labelled red cells and 131I-serum albumin, as well as the 14C-inulin and 3H2O fluid compartments were measured in rats which had been made rachitic by the use of a low phosphate vitamin D-deficient diet. A similar group of rachitic animals fed vitamin D2 50 IU, 5 and 3 days prior to sacrifice and a weight-matched control group were also studied. The same spaces were measured in rats made rachitic by daily s.c. injections of ethane-1-hydroxy-1,1-diphosphonate (EHDP) for 4 weeks and a weight-matched saline injected control group. Findings indicated that the red cell and RISA spaces were unchanged in the untreated D-deficient group as compared to controls but increased after being repleted with vitamin D. By contrast, the vascular space was depressed in the EHDP-treated group. The water content was elevated in D-deficient rickets returning towards normal on healing, whilst both inulin and water spaces were increased in the EHDP-treated animals. Thus, while the extravascular space reflected the presence of osteoid, the vascular space depended on cellular turnover and the process of mineralization.

Animals↗

Hypomagnesemic hypocalcemia. Early serum calcium and late parathyroid hormone increase with magnesium therapy.

A patient with short-bowel syndrome developed severe hypomagnesemia (0.2 mEq/liter) associated with symptomatic hypocalcemia (6.1 mg/100 ml). Parathyroid hormone (PTH) levels were normal but inappropriately low. During therapy with magnesium sulfate, an initial hypocalcemia was followed by a calcemic response without a change in PTH levels. This indicates improved bone responsiveness to circulating low levels of endogenous PTH with magnesium replenishment, which appears to be related to the restoration of magnesium-dependent cellular mechanisms. The additional observation of a slow and delayed increase in PTH, despite normal calcium levels, indicates improvement of hormone synthesis.

Calcium↗