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Biomedical subjects

A A Mathe

Publications and source records attributed to A A Mathe.

5 recordsLinked to original sources
PubMed1987

Electroconvulsive therapy and plasma prostaglandin E2 metabolite in major depressive disorder.

1. Animal experiments show that PGE2 affects the release of ACTH and corticosteroids. In depressed subjects, plasma concentrations of the same hormones are increased immediately following ECT. Consequently we explored possible effects of ECT on PGE2. 2. The major plasma PGE2 metabolite (PGEM), ACTH, and cortisol were determined by RIA. 3. PGEM did not change with time alone and anesthesia without ECT also did not have a consistent effect. PGEM was significantly elevated at all post ECT sampling times. The maximum increase, about fifty percent, was attained at 15 and 30 minutes. Similar changes were observed following ECT-I and ECT-VI. 4. Positive correlations between PGEM, ACTH and cortisol were obtained. 5. The results demonstrate that following ECT stimulus there is a robust increase in circulating PGEM. The increased release of PGE2 may, in part, account for the elevated plasma ACTH and cortisol.

Adolescent↗
PubMed1978

Effect of dihomo-gamma-linolenic acid on the canine pulmonary vascular bed.

The effect of dihomo-gamma-linolenic acid (DGLA), the precursor of the monoenoic prostaglandins (PG), F1alpha and E1, on the pulmonary vascular bed of the intact dog was studied under conditions of controlled pulmonary blood flow. DGLA increased pulmonary vascular resistance in a dose-related manner by constricting intrapulmonary veins and upstream segments, presumably pulmonary arteries. Intrapulmonary injection of DGLA also increased transpulmonary injection of DGLA also increased transpulmonary airway pressure, presumably by increasing airway resistance and decreasing lung compliance or both. The vasoconstrictor response, however, was independent of changes in transpulmonary pressure since similar pressor responses were obtained in ventilated and nonventilated lungs. Further, the response was not dependent on factors or elements in whole blood, since the increase in pulmonary vascular resistance occurred during perfusion with saline or dextran and was enhanced in these media. Conversion of DGLA to PGs by a lung cyclo-oxygenase appears to mediate the response, since it was blocked by indomethacin and dose not occur with injection of nonprecursor long-chain fatty acids. These data suggest that the response to DGLA is due to formation of vasoactive products in the monoenoic PG pathway.

8,11,14-Eicosatrienoic Acid↗
PubMed1978

Modification of pulmonary vascular responses to arachidonic acid by alterations in physiologic state.

The effects of bolus injections of arachidonic acid and prostaglandins (PG) E2 and F2a on the pulmonary vascular bed were compared under resting conditions and after alteration in the physiologic state of the lung. Studies were carried out in the vascularly isolated lung lobe of the intact, anesthetized dog under conditions of controlled blood flow. Arachidonic acid, PGE2 and PGF2a increased pulmonary vascular resistance by constricting intrapulmonary veins and arteries in a dose-related manner, as did an analog of the endoperoxide, PGH2, whereas PGI2 dilated the pulmonary vascular bed. The response to arachidonate was associated with a 2- to 3-fold increase in levels of PGE- and PGF-like substances in pulmonary venous blood and was blocked by indomethacin. The effects of arachidonic acid, but not the PGs, were greatly enhanced during perfusion with either dextran or saline and the enhanced response in saline was associated with a 15 to 20-fold increase in levels of PG-like substances in the pulmonary effluent. Responses to arachidonate were not dependent upon the presence of formed elements in blood but were related to perfusate protein concentration. Alveolar hypoxia decreased responses to the precursor while those to PGE2 and PGF2a were enhanced. Responses to the PGs, but not those to arachidonate, were affected by changes in blood pH. Sublethal doses of Escherichic coli endotoxin increased the response to arachidonic acid, but not those to PGE2 and PGF2a. Results of the present study indicate that the effects of bolus injection of arachidonic acid on the pulmonary vascular bed are due mainly to formation of constrictor metabolites which may overshadow the actions of any dilator (PGI2) formed and suggest that metabolism of the precursor is altered by changes in physiologic state.

Animals↗