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Biomedical subjects

R A Fattor

Publications and source records attributed to R A Fattor.

3 recordsLinked to original sources
PubMed1990

Effects of calcium loading and impaired energy production on metabolic and ultrastructural features of cell injury in cultured neonatal rat cardiac myocytes.

We evaluated the contributions of calcium loading and impaired energy production to metabolic and ultrastructural manifestations of cell injury in a cultured neonatal rat ventriculocyte model. Direct calcium loading was produced by incubation in K(+)-free medium to inhibit the Na+,K(+)-ATPase and promote Na(+)-Ca2+ exchange, and inhibition of energy metabolism was produced by incubation with 30 microM iodoacetic acid (IAA). Measurements were made of total cell calcium, [3H] arachidonic acid (AA) release (an index of membrane phospholipid degradation), ATP, and ultrastructural features of cell damage. Inhibition of the Na(+),K(+) pump resulted in the rapid onset of cellular calcium loading, increased [3H]AA release, and moderate ATP reduction. After return to control medium for 24 hours, myocytes previously exposed to K(+)-free medium for 1 hour showed recovery of ATP level and little additional [3H]AA release. However, after 2 to 3 hours of calcium loading, the ATP level remained moderately depressed, residual [3H]AA release was greater, and a mixed population of relatively normal and severely damaged myocytes was observed by electron microscopy. IAA treatment for 1 hour resulted in moderate ATP reduction without calcium accumulation or [3H]AA release, whereas IAA treatment for 3 hours resulted in marked ATP reduction associated with calcium accumulation and [3H]AA release. Reversal experiments showed substantial recovery of ATP level after 1 hour of IAA exposure, and marked ATP depression and [3H]AA release associated with widespread irreversible injury after 3 hours. Thus, the data indicate that increased calcium accumulation itself can initiate accelerated membrane phospholipid degradation, but that progression to irreversible injury is influenced by other factors, including the magnitude of ATP depression associated with calcium loading.

Adenosine Triphosphate↗
PubMedDate not supplied

Effect of unilateral nephrectomy on three patients with histopathological evidence of diabetic glomerulosclerosis in the resected kidney.

Diabetes mellitus and surgical ablation of renal tissue are two independent influences associated with hyperfiltration and elevated levels of the glomerular transcapillary hydraulic pressure differential (delta P). There is increasing evidence that hyperfiltration with elevated delta P is pathogenic and leads to glomerular damage. The authors questioned whether these two influences (surgical ablation of renal tissue and diabetes mellitus) would act in an additive fashion in human patients to produce an accelerated decline in renal function. Three patients with non-insulin-dependent diabetes mellitus who had undergone a unilateral nephrectomy (for a variety of reasons) were (retrospectively) identified. In each patient, morphologic evidence of diabetic glomerulonephropathy was present in the resected kidney. The charts from these patients were reviewed and post-nephrectomy renal function was estimated over time by plotting reciprocal serum creatine values versus time. Follow-up intervals after nephrectomy varied from 4 to 15 years. The results of our follow-up showed no obvious detrimental effect on renal function (as measured by 1/serum creatinine) attributable to the unilateral nephrectomy. The authors conclude that residual renal function (and ultimate outcome) in patients with non-insulin-dependent diabetes mellitus is highly variable, but does not seem to be adversely affected (at least over the time span of observation in these patients) by unilateral nephrectomy.

Diabetes Mellitus, Type 2↗