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Biomedical subjects

A Olmos

Publications and source records attributed to A Olmos.

At least 55 records · Page 3Linked to original sources
PubMed1984

[Measured and estimated sinoatrial conduction during variations in rhythm. Microelectrode study of the isolated rabbit atrium].

Strips of isolated atrium were obtained from 10 rabbits to study the validity of indirect methods of estimating sinoatrial conduction time during variations of the sinus rhythm. Direct recordings of the trans-membrane action potential of the sinus node were made. Mapping of the sinus region was undertaken to determine the site of the dominant pacemaker. A quadripolar surface electrode was positioned on the lower part of the crista terminalis for stimulation and recording of the atrial potential. This enabled a comparison to be made between the indirect estimated and the directly measured conduction times. An intrasinusal shift of the dominant pacemaker was obtained by cooling from 38 degrees C to 35 degrees C. This shift occurs progressively in the cranino-candal direction. The estimated and measured conduction times were compared under basal conditions and after cooling. The sinus cycle was significantly longer (p less than 0.001) at 35 degrees C (318 +/- 68 ms) than at 38 degrees C (255 +/- 48 ms). The mean measured anterograde conduction time also decreased from 36 to 31 ms (p less than 0.01) and the mean measured retrograde conduction time also decreased from 39 to 33 ms (p less than 0.02); the total conduction time decreased from 75 to 64 ms (p less than 0.001). The results of the total estimated conduction times were discordant. The associated effects of stimulation and cooling can cause conduction defects and an overestimation of the conduction time.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1981

[A study of anemia in 86 patients on hemodialysis (author's transl)].

Anemia is one of the complications of terminal chronic renal failure that may worsen with periodical hemodialysis because of residual blood losses in the dialyzers that may be significant if clotting occurs within the circulation system. The potential iron deficiency component of the anemia has been studied in 86 patients submitted to periodic hemodialysis by measurement of hemoglobin, serum iron, transferrin saturation, total iron binding capacity, and ferritin. The following correlations were investigated: degree of anemia and type of renal disease, months on hemodialysis and hemoglobin, months on hemodialysis and serum ferritin, and liters of blood transfused and serum ferritin. Statistically significant correlations were found between months on hemodialysis and hemoglobin, and between liters of blood transfused and serum ferritin. From the correlation between serum iron and ferritin the patients could be classified in three groups: 1, with either normal or low serum iron and ferritin, candidates to iron therapy; 2, with elevated serum iron and ferritin, needing no iron treatment; and 3, with unequal changes of serum iron and ferritin, in whom iron kinetic studies are indicated in order to discover the patents that may benefit from iron therapy.

Adolescent↗
PubMed1980

Identification of two types of porphyria cutanea tarda by measurement of erythrocyte uroporphyrinogen decarboxylase.

1. Erythrocyte uroporphyrinogen decarboxylase activity has been measured in 27 patients with porphyria cutanea tarda, of whom 11 had a family history of overt porphyria cutanea tarda. 2. Eight patients from six families had erythrocyte uroporphyrinogen decarboxylase activities that were decreased to about half of control values. This decrease was shown by family studies to be inherited as an autosomal dominant characteristic. Two of these patients had no family history of overt porphyria cutanea tarda. 3. Nineteen patients had uroporphyrinogen decarboxylase activities close to or within the range found in 18 control subjects. Of these, five patients had a family history of porphyria cutanea tarda. 4. Inheritance of an autosomal dominant gene which decreases uroporphyrinogen decarboxylase activity in erythrocytes and liver is an uncommon cause of porphyria cutanea tarda and may not explain all cases of familial porphyria cutanea tarda. The hepatic enzyme defect in the common type of porphyria cutanea tarda, in which erythrocyte uroporphyrinogen decarboxylase activity is normal, may be caused either by inheritance of a gene whose effect is restricted to the liver or by gene whose effect is restricted to the liver or by chemicals that selectively inhibit the hepatic enzyme.

Adolescent↗
PubMed1980

Follow-up studies of porphyrin excretion in porphyria cutanea tarda treated with p-aminobenzoic acid.

The treatment of porphyria cutanea tarda (PCT) with p-aminobenzoic acid (PABA) was suggested because PABA is capable of reversing the porphyrinogenic action of 3,5-dicarbethoxy-1,4-dihydrocollidine (DDC) in rats. Three patients with PCT were treated with 3 g of PABA daily during 6 and 12 months and the urinary and faecal porphyrin excretion were serially analyzed by solvent extraction techniques and by thin layer chromatography of their methyl esters. PABA treatment did not show any apparent effect on porphyrin excretion.

4-Aminobenzoic Acid↗