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Biomedical subjects

C M Ingerman

Publications and source records attributed to C M Ingerman.

18 recordsLinked to original sources
PubMed1982

Ophthalmic manifestations of the Hermansky-Pudlak syndrome (oculocutaneous albinism and hemorrhagic diathesis).

We report the association of oculocutaneous albinism and defective platelet function, the Hermansky-Pudlak syndrome, in two young Puerto Rican patients, a 17-year-old boy and a 9-year-old girl. Wide variation in pigmentation may obscure the diagnosis of albinism. Puerto Rican albinos are at increased risk of inheriting this autosomal recessive syndrome. Although usually mild, bleeding in affected patients can be life-threatening, especially after aspirin administration. Albino patients should be questioned about a history of bleeding and referred for hematologic consultation.

Adolescent↗
PubMed1980

Model system for the study of inital damage to arterial endothelial cells in situ by scanning electron microscopy.

The central artery of the rabbit ear was injected with either 1 ml of control or test solutions in a model system which allowed for the study of effluent fractions coming from a segment of the artery and for the examination of the vessel by electron microscopy. The procedure allowed for either mixing of blood with the test solution ("flow by") or injection of the solutions in the absence of blood ("no flow by"). Effluent fractions were collected and assayed for 6-keto-PGF1 alpha, and indicator of PGI2 production. After the collection of effluent fractions, the artery was perfused with 1% glutaraldehyde to begin fixation. Ultrastructural damage to endothelial cells was seen, by SEM, in a graded response to sodium arachidonate solutions at concentrations between 6.6 and 3.3 mM ("flow by"); and between 3.3 and 0.83 mM ("no flow by"). Lower concentrations of arachidonate did not cause damage. Damage included enucleation, separation or denudation of endothelial cells. Sodium linoleate produced similar damage. A burst of PGI2 production appeared to be associated with arachidonate-damaged endothelium. Injection of sodium arachidonate at lower concentrations (0.33 mM and 0.165 mM) resulted in continuous production of PGI2 over a period of 1 to 5 minutes.

Animals↗
PubMed1978

Hereditary abnormality of platelet aggregation attributable to nucleotide storage pool deficiency.

An abnormality of platelet aggregation has been detected in six family members with mild bleeding tendencies. In citrated platelet-rich plasma, primary aggregation induced by ADP or epinephrine and agglutination in response to ristocetin were present but second wave aggregation and aggregation in response to collagen suspension were absent or greatly reduced. Sodium arachidonate-induced aggregation was normal although aggregation in response to prostaglandin G2 was reduced and depended entirely on the presence of plasma or ADP. Further tests indicated that the platelets produced prostaglandins but did not release ATP in response to thrombin or sodium arachidonate. Platelets from the patients were found to contain reduced amounts of ADP and 5-hydroxytryptamine and to be unable to retain radioactivity during prolonged incubation at 37 degree C with radiolabeled 5-hydroxytryptamine. Although electron microscopy revealed an absence of very dense bodies, the platelets appeared otherwise normal. The findings are discussed in relation to previous studies of nucleotide storage pool deficiency and the light they shed on platelet physiology in general.

Adenosine Diphosphate↗
PubMed1976

Separation of prostaglandins E2 and F2alpha from their pulmonary metabolites by thin-layer chromatography.

A simple thin-layer chromatographic system has been developed separate PGE2 and PGF2alpha from 13, 14-dihydro-PGF2alpha, and other pulmonary metabolites of prostaglandins. The separation is achieved on Kieselgel-60 F-254 plates impregnated with both silver nitrate and boric acid. The system should be of use in the purification and tentative identification of primary prostaglandin.

Chromatography, Thin Layer↗
PubMed1976

Malondialdehyde formation as an indicator of prostaglandin production by human platelets.

The formation of malondialdehyde, a metabolite of prostaglandin endoperoxides, has been studied in platelet-rich plasma. Small amounts were produced in response to ADP, epinephrine, or collagen and larger amounts in response to thrombin. Arachidonic acid induced platelets to produce large amounts of malondialdehyde. Malondialdehyde formation by platelets was prevented by aspirin or indomethacin. The measurement of malondialdehyde in platelet-rich plasma may be used as an indicator of platelet prostaglandin synthesis, and is simpler than the measurement of prostaglandins.

Adenosine Diphosphate↗
PubMed1976

Platelet prostaglandin production and its implications.

Both aspirin and indomethacin abolish platelet shape change and aggregation induced by arachidonic acid, indicating that these effects are due to prostaglandin production. An unstable prostaglandin endoperoxide (PGG2 or PGH2) is probably the mediator of the arachidonic acid effects, and they can be mimicked by the stable synthetic prostaglandin, 11-deoxy-15-methyl-15RS-PGE2 (Wy-17, 186). All three of these prostaglandins induce platelet aggregation in the presence of aspirin. Neither aspirin nor indomethacin inhibits shape change or primary aggregation induced by ADP, which indicates that these effects are not due to prostaglandin production. Arachidonic acid, Wy-17, 186, and ADP require fibrinogen as a cofactor in order to aggregate washed human platelets. However, the combination of ADP and arachidonic acid or of ADP and Wy-17, 186 is synergistic and will aggregate washed human platelets in the absence of added fibrinogen. No synergism is observed between arachidonic acnd and Wy-17, 186. During platelet degranulation (i.e., the platelet-release reaction) induced by collagen both ADP and prostaglandin endoperoxides are made available, and collagen can induce the aggregation of washed human platelets in the absence of added fibrinogen. Prostaglandin endoperoxides, ADP, and fibrinogen probably act in concert to aggregate platelets in normal hemostasis since the absence of any one of these principles usually has an effect on the bleeding time.

Adenosine Diphosphate↗
PubMed1975

Uptake and inactivation of a-type prostanglandins by human red cells.

Incubation of A type prostaglandins with whole blood or washed red cells at 37 degrees C converted them to more polar products with negligible vasodepressor and smooth muscle-contracting activities. This conversion did not occur in platelet-rich plasma. Uptake of the prostaglandins by red cells was demonstrated at both 4 degrees C and 37 degrees C. The data suggest 1) that if PGA is released from tissues into the blood stream or is administered for therapeutic purposes, its biological activity would be diminished by human red cells, and 2) that development of an assay for PGA in blood should take into account its uptake and metabolism by human red cells.

Erythrocytes↗
PubMed1974

Arachidonic acid causes sudden death in rabbits.

Injection of sodium arachidonate (1.4 milligrams per kilogram) into the marginal ear veins of rabbits caused death within 3 minutes. Histological examination showed platelet thrombi in the microvasculature of the lungs. Rabbits were protected from the lethal effects of arachidonic acid by pretreatment with aspirin. Fatty acids closely related to arachidonic acid did not cause death.

Animals↗