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Biomedical subjects

N C Brackett

Publications and source records attributed to N C Brackett.

At least 19 recordsLinked to original sources
PubMed1993

Essential hypertension: historical perspective, mechanisms and an approach to treatment.

The mechanisms of essential hypertension have been reviewed and drugs useful in treatment discussed. Although much is known therapy remains largely empiric. Future control of hypertension depends on developments from the laboratory and carefully designed clinical trials that support the empirical. On the horizon, molecular biology promises to be progressing toward unraveling the tangle of the genetic origins of the disease. Perhaps only with this knowledge will completely rational therapy emerge.

Humans↗
PubMed1990

Acid-base disturbances in acute asthma.

The clinical features, arterial blood gases, and acid-base profile were examined in 229 consecutive episodes of acute asthma in 170 patients who required hospitalization. A simple respiratory alkalosis was the most common acid-base disturbance, occurring in 48 percent of the episodes. Metabolic acidosis, either alone or as part of a mixed disturbance, was noted in 28 percent. Of 60 episodes presenting with respiratory acidosis, 37 (62 percent) had a coexistent metabolic acidosis. Metabolic acidosis was more likely to occur in male subjects and in patients with evidence of more severe airflow obstruction. Patients with metabolic acidosis had an average anion gap of 15.8 mEq/L; these patients were more hypoxemic than those without metabolic acidosis and there was a significant inverse correlation between the anion gap and the degree of hypoxemia. We conclude that metabolic acidosis is a common finding in acute, severe asthma and suggest that the pathogenesis of lactic acidosis is multifactorial and includes contributions from lactate production by respiratory muscles, tissue hypoxia, and intracellular alkalosis.

Acid-Base Equilibrium↗
PubMed1982

Diabetic glomerulonephropathy: histopathologic, immunofluorescent, and ultrastructural studies of 16 cases.

Sixteen cases of diabetic glomerulopathy are reported. Direct immunofluorescent and ultrastructural studies of renal biopsy tissues demonstrated that two patients had linear deposits of IgM and C'3 in the absence of IgG, four diabetic patients had sclerosis-induced entrapment of immunoglobulins and complement, and one patient had granular immune complexes in the subepithelial and intramembranous portion of the glomerular basement membrane. In one patient, who had nodular glomerular lesions, diffuse fibrillar deposits of electron-dense material were observed in the mesangium. In this mesangial infiltrate, light microscopy revealed the absence of amyloid and direct immunofluorescence revealed the absence of all immunoglobulins, complement components, and fibrinogen. Our study suggests that the morphologic alterations observed in diabetic glomerulopathy might be mediated by either immune mechanism or by abnormal biochemical or functional factors, such as impairment of the mesangial IgA clearance mechanism.

Antigen-Antibody Complex↗
PubMed1982

Evidence for extrarenal production of 1 alpha ,25-dihydroxyvitamin D in man.

Recent studies provide evidence for extrarenal production of 1 alpha ,25-dihydroxyvitamin D [1 alpha ,25(OH)2D]. To investigate this possibility, serum vitamin D, 25-hydroxyvitamin D (25-OHD), 24,25-dihydroxyvitamin D [24,25(OH)2D], and 1 alpha ,25(OH)2D were measured in eight adult anephric subjects. All were undergoing hemodialysis and three of them were receiving vitamin D, 50,000 or 100,000 U/d. Serum vitamin D was elevated in two of the patients given vitamin D and was abnormally low in the others. Mean serum 25-OHD was increased in patients given vitamin D (94.0 +/- 7.6 ng/ml) and was normal in the others (16.4 +/- 0.9 ng/ml, P less than 0.001). Mean serum 24,25(OH)2D was normal in patients given vitamin D (1.38 +/- 0.27 ng/ml) and was low in the others (0.25 +/- 0.08 ng/ml, P less than 0.001). Serum 24,25(OH)2D correlated significantly with serum 25-OHD (r = 0.848, P less than 0.01). Mean serum 1 alpha ,25(OH)2D determined by receptor assay was 5.8 +/- 1.9 pg/ml in patients who were not given vitamin D and was 14.1 +/- 0.6 in those who were given vitamin D (P less than 0.001). Serum 1 alpha ,25(OH)2D correlated significantly with serum 25-OHD (r = 0.911, P less than 0.01). Mean serum 1 alpha ,25(OH)2D, measured by bioassay, was 8.3 +/- 1.9 pg/ml in patients who were given vitamin D and was 15.9 +/- 2.4 pg/ml in those who were given vitamin D (P less than 0.05). There was a significant correlation between the values for serum 1 alpha ,25(OH)2D obtained with the two methods (r = 0.728, P less than 0.01). The results (a) provide evidence in man for extrarenal production of both 24,25(OH)2D and, by two independent assays, of 1 alpha , 25(OH)2D, and (b) indicate that serum values of the two dihydroxy metabolites of vitamin D in anephric subjects vary with the serum concentration of the precursor 25-OHD.

Adult↗
PubMed1981

Gold nephropathy. Ultrastructural, fluorescent, and energy-dispersive x-ray microanalysis study.

The nephrotic syndrome developed in a patient receiving therapy with gold for rheumatoid arthritis. The results of a histopathological examination of the renal biopsy specimen were unremarkable. Immunofluorescent studies showed deposits of immunoglobulins and C3 in a granular pattern in the glomerular basement membranes. Ultrastructurally, the discrete osmiophilic immune complexes were epimembranous. By x-ray microanalysis, gold that was complexed with sulfur was present in proximal tubular cytoplasmic vacuoles and nuclei. Gold and sulfur could not be demonstrated in glomerular epimembranous deposits. The results of these studies suggest that immune complex deposition does not involve gold and sulfur acting as haptens. Gold-salt therapy may result in damage to proximal tubules that leak renal tubular antigens, which in turn complex with autoantibody and produce an autoimmune membranous nephropathy. The evidence for this mechanism is not convincing. Although the data indicate an immune-complex cause for gold-salt nephropathy, the incident antigen (or antigens) and mechanism of action remain unidentified.

Adult↗
PubMed1978

Role of sodium intake in the antihypertensive effect of propranolol.

Twelve hypertensive patients had measurements of body weight, blood pressure, plasma renin activity, and plasma volume during periods of normal sodium intake and acute sodium depletion. After receiving propranolol orally for four to 14 weeks, repeat measurements were obtained under identical conditions of sodium intake. During normal sodium intake, propranolol therapy was associated with a decrease in plasma renin activity, a variable tendency to an increase in body weight and plasma volume, and a decrease in mean arterial pressure of 5 mm Hg (NS). During sodium restriction, blood pressure was decreased significantly from that observed during normal sodium intake and propranolol added a further significant decrease of 8 mm Hg (P less than .01). Blood pressure reductions obtained with sodium depletion and acute diuretic therapy were approximately the same with or without propranolol. The increase in plasma renin activity expected with sodium depletion and diuretic therapy was not blunted by propranolol.

Adult↗
PubMed1975

Incomplete renal tubular acidosis: some clinical and physiological features.

17 patients with recurrent calcium-containing renal calculi were studied using the short NH4Cl test and one subject with 'incomplete renal tubular acidosis' was identified. In retrospect the only clue to this diagnosis was a fasting, morning urine pH exceeding 6.0 units. Fasting morning urine pH, which is usually less than 6.0 in subjects who acidify normally, is proposed as a simple screening test for 'incomplete RTA'. Modified high dose NH4Cl tests and Na2SO4 tests were performed in this subject and other patients with either complete or incomplete distal renal tubular acidosis. These studies suggest that the ability to lower urine pH is impaired less with the incomplete than with the complete form of the disease.

Acidosis, Renal Tubular↗