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Biomedical subjects

J R Luderer

Publications and source records attributed to J R Luderer.

30 records · Page 2Linked to original sources
PubMed1982

Converting enzyme inhibition with captopril in patients with primary hyperaldosteronism.

The humoral and hemodynamic effects of converting enzyme inhibition captopril are presented in two patients with primary hyperaldosteronism (PHA). In all, 20 patients with resistant hypertension were treated with the angiotensin converting enzyme inhibitor captopril. In 18 patients with essential or renovascular hypertension mean (+/- SEM) plasma renin activity (PRA) rose from 5.0 +/- 1.4 to 35.3 +/- 5.3 ng/ml/hr (P less than 0.01) and mean (+/- SEM) plasma aldosterone (PA) declined from 25.8 +/- 2.9 to 15.1 +/- 1.9 ng/ml (P less than 0.01) after captopril. In two patients with PHA the PRA was not stimulated by converting enzyme inhibition, although there was modest decline in PA and a temporary reduction in blood pressure. After surgical removal of aldosterone-producing adenomas, PRA responsed appropriately to captopril. These cases illustrate that a disease process can modify the response to a drug and demonstrate that, in patients with PHA, captopril does not stimulate PRA, induces only minor decrements in PA, and is relatively ineffective as an antihypertensive.

Aldosterone↗
PubMed1981

Rational use of drug levels.

Considerable strides have been made in pharmacokinetics the last decade. Such techniques as gas chromatography and radioimmunoassay can measure minute quantities of drugs in serum and other body fluids. These assays are now available in many community hospitals. Therapeutic serum concentrations have been established for many drugs. Proper interpretation of serum drug levels permits precision in the use of drugs and minimizes adverse effects.

Drug Administration Schedule↗
PubMed1980

The effect of hydralazine on arachidonic acid metabolism in isolated, washed human platelets.

The effects of hydralazine on arachidonic acid metabolism were studied in isolated washed human platelets. The washed platelets (10(9)/ml) were exposed to 14C-arachidonic acid and incubated for 15 minutes in a platelet aggregometer (37 degrees C). The media was then extracted and the reaction products separated by means of reversed phase high pressure liquid chromatography. In this system, hydralazine inhibited the production of TXB2 (the stable metabolite of TXA2) and enhanced the production of PGF2 alpha and PGE2 in a dose dependent fashion. Indomethacin, blocked the production of all prostaglandin compounds normally synthesized by platelets. These results suggest that hydralazine is a specific thromboxane synthetase inhibitor and that its vasodilatory effects might be related to its ability to block the production of an endogenous vasoconstrictor (i.e. TXA2).

Arachidonic Acids↗
PubMed1977

Plasma prostaglandins in hypercalcemic patients with neoplastic disease.

Peripheral plasma prostaglandin E (PGE) determinations were performed on a series of 79 patients with solid tumor neoplasms and correlated with their serum calcium levels. Fourteen patients were hypercalcemic and 11 of these had significant elevations in circulating plasma PGE. Ten of the hypercalcemic group had extensive metastases to bone. These findings support the recently developed hypothesis that prostaglandins are causally related to the genesis of hypercalcemia in malignancy.

Adult↗
PubMed1977

Immunosuppression and human cancer: role of prostaglandins.

Prostaglandins, unsaturated fatty acid derivatives with diversified pharmacologic activity, have been implicated in the pathophysiology of many diseases. Prostaglandin E (PGE) levels were measured by radioimmunoassay in the plasma of 41 normocalcemic patients with various stages of malignancies. Delayed hypersensitivity was assessed by a battery of six recall skin test antigens (ST) and by Dinitrochlorobenzene (DNCB) sensitization and challenge. Twenty-five patients with one or more positive skin tests had a mean PGE level of 87+/-8 pg/ml, whereas 16 patients with negative ST had a mean PGE level of 96+/-12 pg/ml. Twenty-one DNCB negative patients had a mean PGE level of 98+/-12 pg/ml and eight totally anergic patients had a mean PGE of 96+/-12 pg/ml. All PGE values were within the normal range and there was no statistical difference between the four groups. (p less than 0.1). We concluded that circulating PGE does not correlate with the non-specific immunosuppression seen in cancer patients.

Adult↗
PubMed1977

Immunologic myopathy. Linear IgG deposition and fulminant terminal episode.

The histopathologic characteristics of a patient with progressive myopathy, renal failure, hemoptysis, and a fulminant terminal event demonstrated a diffuse vasculitis, type 2 fiber atrophy of muscle, and linear IgG staining of the basement membranes of skeletal muscle fibers and of glomerular capillary basement membranes. Interpretation of electron micrographs confirmed that there was thickening of muscle basement membranes. The data suggest the presence of an antibody to a basement membrane antigen shared by muscle and kidney.

Aged↗