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Biomedical subjects

A G Herman

Publications and source records attributed to A G Herman.

At least 217 records · Page 12Linked to original sources
PubMed1983

5-hydroxytryptamine and platelet aggregation.

5-Hydroxytryptamine (5-HT) activates blood platelets of various species including humans. In contrast to cat, pig, and sheep platelets, human blood platelets respond to 5-HT mainly with a shape change and a reversible aggregation only. However, depending on the concentration and the time interval between its addition and that of another agonist, 5-HT amplifies the human platelet aggregation induced by ADP, collagen, epinephrine, and norepinephrine; the monoamine itself induces strong aggregation of platelets presensitized with norepinephrine, lysolecithin, or Thrombofax. Prolonged exposure of platelets to 5-HT results in transient tachyphylaxis. Pharmacodissection and receptor-binding studies suggest the presence of functional receptors, possibly of the 5-HT2 (S2) type, different from the ones involved in the active uptake of the monoamine by the platelets. As a modulator of platelet reactions, 5-HT may be involved in secondary platelet aggregation, hemostasis, and thrombus formation.

Adenosine Diphosphate↗
PubMed1983

Accumulation and release of [3H]-5-hydroxytryptamine in saphenous veins and cerebral arteries of the dog.

Experiments were performed to examine whether isolated canine blood vessels have the ability to accumulate [3H]-5-hydroxytryptamine ([3H]-5-HT) and if so, whether the 3H-amine can be released from the tissues by stimuli known to evoke release of norepinephrine. Helical strips of saphenous veins and cerebral arteries obtained from dogs were incubated with [3H]-5-HT and mounted for superfusion. Both blood vessels take up [3H]-5-HT in a concentration-dependent manner; this accumulation is markedly reduced in veins and arteries denervated with 6-hydroxydopamine and in veins pretreated with cocaine. In saphenous veins and cerebral arteries labeled with [3H]-5-HT, a basal efflux of 3H, consisting mainly of [3H]-5-hydroxyindole-acetic acid, was observed. Electrical stimulation of the preparations evoked a frequency-dependent overflow of tritium due in part to an overflow of intact [3H]-5-HT. This stimulation-induced 3H-overflow was inhibited by tetrodotoxin and was nearly absent in denervated tissues and in veins pretreated with cocaine. In saphenous veins the overflow of 3H evoked by electrical stimulation was markedly augmented by phentolamine but not influenced by methiothepin. In the veins, both K+ and tyramine caused an overflow of [3H]-5-HT which was absent after denervation or after pretreatment of the preparations with cocaine. Our results show that the major part of the [3H]-5-HT which is taken up by the isolated blood vessels accumulates in the adrenergic nerves and that the indoleamine can be released from these nerves as a "false" transmitter, together with norepinephrine.

Animals↗
PubMed1982

Characterization of monohydroxylated lipoxygenase metabolites of arachidonic and linoleic acid in rabbit peritoneal tissue.

Rabbit peritoneal tissue contains a lipoxygenase which converts arachidonic acid preferentially into 15-hydroxy-5,8,11,13-eicosatetraenoic acid. Stereochemical analysis of the menthyloxycarbonyl derivative of this metabolite by means of a high-pressure liquid chromatography method, involving the use of a Ag+ -loaded cation-exchange column, indicated that it has mainly the 15-Ls-hydroxy configuration. The biosynthesis of 15-hydroxy-5,8,11,13-eicosatetraenoic acid could be confirmed during examination of the monohydroxy acids obtained without addition of fatty acids, thus formed from endogenously released substrate. However, the 9-and 13-hydroxy derivatives of linoleic acid were also formed and in quantities exceeding those of 15-hydroxy-5,8,11,13-eicosatetraenoic acid.

Animals↗
PubMed1982

Contribution of complement activation to the rise in blood levels of 6-oxo-prostaglandin F1 alpha during endotoxin-induced hypotension in rabbits.

Administration of endotoxin (lipopolysaccharide W E. coli O111 B4, 0.5 mg/kg i.v.) induced about 20% activation of the complement system (measured as CH50 and C3), a biphasic hypotension, thrombocytopenia and a significant rise in blood levels of 6-oxo-PGF1 alpha. Complement depletion (CH50 and C3 less than 3%) with Cobra Venom Factor significantly reduced the initial fall in blood pressure and the rise in 6-oxo-PGF1 alpha, and abolished the second phase of hypotension and the thrombocytopenia, due to subsequent injection of endotoxin. It is concluded that activation of about 20% of the complement system by endotoxin is a prerequisite for the occurrence of thrombocytopenia and secondary hypotension, and that it is involved in the increase in blood levels of 6-oxo-PGF1 alpha. The results of histamine determinations in rabbit blood and plasma indicate that, besides products derived from prostaglandin endoperoxides, other vasoactive substances, possibly released during complement-mediated adherence aggregation of platelets, might contribute to the endotoxin-induced hypotension.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

Arachidonic acid metabolism by cultured mesothelial cells. Different transformations of exogenously added and endogenously.

The capacity of cultured mesothelial cells to produce prostaglandins from both exogenous an endogenous arachidonic acid has been investigated. Incubations with labelled [1-14C]arachidonic acid and [1-14C]prostaglandin endoperoxide H2 indicated the formation of prostacyclin and prostaglandin E2. Evaluation of the transformation of endogenously released arachidonic acid, however, could only confirm the production of prostacyclin.

Animals↗
PubMed1982

Effect of dipyridamole on the formation of 6-oxo-prostaglandin F1 alpha by the rat isolated aorta and ram seminal vesicle microsomes.

1 Dipyridamole (1 and 10 muM) enhanced the production of 6-oxo-prostaglandin F1 alpha by rat aortic tissue. 2 Dipyridamole (5 to 40 muM) did not influence the PGI2-synthetase activity in ram seminal vesicle microsomes whereas, in concentrations ranging from 100 to 200 muM, it reduced the metabolism of exogenously added arachidonic acid. The latter effect may be due to an inhibition of the cyclooxygenase.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

15-Hydroxy-5,8,11,13-eicosatetraenoic acid (15-HETE) formation by rabbit peritoneal tissue.

The capacity of rabbit peritoneal tissue to produce lipoxygenase metabolites from exogenous arachidonic acid has been studied. The lipoxygenase pathway of arachidonic acid in this tissue is mainly directed to 15-HETE. Preliminary experiments with peritoneal macrophages indicate that these cells, just like PMN leukocytes, may contribute to the 15-HETE formation observed in peritoneal tissue.

Animals↗
PubMed1981

Prostanoids and hemostasis in chickens: anti-aggregating activity of prostaglandins E1 and E2, but not of prostacyclin and prostaglandin D2.

Aggregation of chicken thrombocytes was studied in whole blood using an electronic aggregometer. Serotonin (5-hydroxytryptamine, 5HT), arachidonic acid (AA) and collagen, but not adenosinediphosphate (ADP) induced aggregation. Prostaglandin (PG) endoperoxides were essential for arachidonic acid-induced aggregation, but were not involved in 5HT-induced aggregation, as indicated by inhibitory studies with indomethacin. Similar experiments indicated that biosynthesis of endogenous PG endoperoxides contributed to the aggregation induced by low concentrations of collagen, but was of little importance when high collagen doses were employed. PGE1 and PGE2 could abolish all types of aggregation studied, whereas prostacyclin (PGI2) and PGD2 were without any anti-aggregatory activity at 1 microgram/ml. Between 1 and 100 ng/ml PGE1 and PGE2 inhibited arachidonic acid- and 5HT-induced aggregation dose-dependently. The lack of any hemostatic function of PGI2 in chickens was also indicated by the absence of biosynthesis of endogenous PGI2 in chicken aorta. PGI2 was assessed as anti-aggregating activity, released by aortic fragments stirred in rabbit platelet rich plasma. Still, the presence of chicken aorta tissue in chicken whole blood inhibited 5HT-, but not arachidonic acid-induced aggregation. This inhibition was not affected by pretreatment of the aortic fragments with indomethacin or pargyline.

Alprostadil↗