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Biomedical subjects

A L Aronson

Publications and source records attributed to A L Aronson.

At least 37 records · Page 2Linked to original sources

Altered hemoglobin-oxygen affinity with long-term propranolol therapy in patients with coronary artery disease.

Pharmacologic agents that alter hemoglobin affinity for oxygen may affect systemic or myocardial oxygen delivery. In vitro, and in normal man propranolol shifts the oxyhemoglobin equilibrium curve to the right, thus increasing the partial pressure of oxygen at which hemoglobin is 50% saturated (P50) and enhancing oxygen delivery. The effect of propranolol on hemoglobin P50 was evaluated in 12 patients with angina pectoris and documented coronary artery disease. Determinations were made during oral propranolol therapy (mean daily dose 152 mg) of at least 3 months' duration and after administration of propranolol had been discontinued for at least 4 days. Hemoglobin P50 and erythrocyte 2,3-diphosphoglycerate (DPG) were measured. Data in 12 patients were: the mean P50 after discontinuation of propranolol was 28.2 mm Hg+/-0.9 (standard error of the mean) and during propranolol therapy 31.7+/-0.7; P less than 0.001; red blood cell 2,3-DPG did not change to explain the increase in P50. This demonstrated shift could increase systemic oxygen delivery and thus benefit marginally perfused myocardium while sparing coronary flow. Propranolol, in addition to its negative chronotropic and inotropic effects, may increase tissue oxygen delivery in patients with the anginal syndrome.

Coronary Disease↗

Sinoventricular conduction in atrial standstill.

Sinoventricular rhythm implies preserved sinus node function with conduction of impulses to the A-V junction without generalized atrial excitation. Impulse propagation in such cases is presumably via specialized internodal tracts. In this present case, synchronized but localized activation from an area of the right atrium preceded each QRS, without generalized atrial depolarization. These recordings are offered as further evidence for the clinical occurrence of sinoventricular rhythm in humans.

Aged↗

Pathogenesis of lead shot poisoning in the mallard duck.

Adult mallard ducks were administered steel pellets to determine the rate of excretion from the gastrointestinal tract. In separate studies the ducks were administered 5 number 6 lead pellets. Birds were examined for clinical signs and sacrificed at given intervals over a 20 day period to assess changes in tissue structure and concentrations of lead with time. The above studies were conducted in 2 groups of ducks, fed a low or a high fiber diet. The rate of steel pellet excretion on birds on the low fiber diet decreased with an increase in pellet size. Pellet excretion was greatly reduced in birds fed the high fiber diet. Administration of lead shot resulted in the development of green diarrhea, anorexia and weakness. It also produced high concentrations of lead in the blood, kidney, liver and bone with lower concentrations in skeletal muscle. The major lesions were destruction of the mitotically active proventricular epithelium and medullary osteocytes, destruction of pectoral muscle cells and the presence of intranuclear inclusion bodies in the proximal tubular epithelium of the kidneys. Birds on the high fiber diet demonstrated more severe clinical signs and higher concentrations of lead in the tissues.

Animals↗