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PubMed1982

Selective effect of microembolization on pulmonary removal of biogenic amines.

Pulmonary amine extraction (E) was measured by triple-indicator dilution techniques from bolus injections of trace amounts of 5-hydroxy[14C]tryptamine ([14C]HT)m [3H]norepinephrine ([3H]NE), indocyanine green dye before and after glass-bead embolization in 23 anesthetized dogs. Control E(5-[14C]-HT) was 89.7 +/- 1.7%; 10 min after embolization (which approximately doubled pulmonary artery pressure and pulmonary vascular resistance), E(5-[14C]HT) was significantly reduced to 65.9 +/- 3.0% (kappa +/- SE; n = 10) (P less than 0.01). Control E([3H]NE) (40.1 +/- 4.5%) was unaffected by embolization. Imipramine (8 mg/kg) depressed control E(5-[14C]HT) to 38.7 +/- 1.5% and control E([3H]NE)d to 35.0 +/- 3.9% (P less than 0.05; n = 4). In these animals, pulmonary hemodynamic changes secondary to embolization were comparable to those in non-drug-treated dogs, but E(5-[14C]HT) and E([3H]NE) were not further depressed. Progressive pulmonary lobar artery ligation (n = 5) did not affect amine extraction until perfusion was limited to one lobe. The selectivity of the effect of embolization on E(5-[14C]HT), the lack of an effect on imipramine-insensitive E(5-[14C]HT) extraction, and the much smaller changes after progressive lobar ligation indicate that, although derecruitment of vascular surface area secondary to mechanical obstruction may contribute to postembolization depression of E(5-[14C]HT), additional mechanisms such as local saturation of 5-HT uptake or selective damage to endothelial cell transport of 5-HT may underlie these observations.

Animals↗
PubMed1982

Comparison of pulmonary and extrapulmonary extraction of biogenic amines.

Multiple indicator-dilution technique was used to study the effect of altered blood flow and imipramine (8 mg/kg) on extraction (E) of trace amounts of 5-hydroxy[14C]tryptamine (5-[14C]HT) and [3H]norepinephrine ([3H]NE) in pulmonary (n = 6) and hindlimb (n = 6) circulations of anesthetized dogs. Increasing cardiac output (via right-heart bypass) from 63 to 112 ml.min-1.kg-1 did not significantly affect pulmonary amine extraction [E(5-[14C]-HT), 73 +/- 4%; E([3H]NE), 51 +/- 3%], whereas decreasing cardiac output to 13 ml.min-1.kg-1 led to significant increases in extraction of either amine (P less than 0.05). Imipramine significantly decreased pulmonary amine extraction with greatest inhibition noted at the lowest cardiac output. Hindlimb E(5-[14C]HT) and E([3H]NE) was 49 +/- 6 and 33 +/- 3%, respectively, at hindlimb blood flow of 104 ml/min and was not affected by changes in hindlimb blood flow from 47 to 202 ml/min. Although hindlimb (5-[14C]HT) was significantly less than pulmonary E(5-[14C]-HT), it was similar in that imipramine significantly decreased hindlimb E(5][14C]HT) to 26% (P less than 0.01) suggesting that part of hindlimb 5-HT extraction may involve a drug-sensitive carrier-mediated process as has been shown in lung. The difference in magnitude between the two beds may be a function of decreased endothelial cell surface area in the hindlimb compared with lung. Since pulmonary and hindlimb extraction of trace amounts of these amines appears to be insensitive to changes in blood flow near normal regional blood flow, indicator-dilution techniques appear to be useful in evaluating alterations in the metabolic capacity of the microcirculation of intact animals.

Animals↗
PubMed1983

Effects of chronic hypoxia on pulmonary vascular responses to biogenic amines.

The effects of chronic hypoxia on pulmonary vascular resistance changes (% delta Rpv) to histamine, 5-hydroxytryptamine (5-HT), norepinephrine (NE), and KCl were studied in isolated perfused lungs from control rats and rats exposed to 7, 14, and 28 days of hypoxia. Histamine, which produced linear increases in % delta Rpv with increasing doses in the control, was reversed to vasodilation by chronic hypoxia of 7 and 14 days and at 28 days, vasodilation to this amine still predominated (7 out of 10). Control responses to 5-HT were unaltered by 7 days of hypoxia but enhanced at 14 and 28 days. Control responses to NE showed either vasoconstriction or vasodilation; at 7 days of hypoxia, NE had no significant vasoactivity; however, at 14 days, vasoconstriction and vasodilation were both observed, with vasodilation being more effective. Lastly, the pressor responses to KCl were not affected by chronic hypoxia of any duration. These results suggest that chronic hypoxia: 1) does not alter pulmonary vascular contractility (KCl); 2) reduces H1 and alpha-receptor activity while enhancing H2- and beta-receptor activity; and 3) enhances the pressor responses to 5-HT by increasing either the efficacy of this amine or the number of 5-HT vasoconstrictor receptors.

Animals↗
PubMed1983

Effect of nomifensine on cortisol, prolactin and biogenic amines in neurotic depressed patients.

The effect of nomifensine on plasma levels of cortisol, prolactin, dopamine, noradrenaline, adrenaline and serotonin were studied in neurotic depressive patients. Cortisol levels were elevated in the morning and were significantly decreased by nomifensine treatment. Prolactin levels were within the normal range and nomifensine did not modify them. A significative increase in catecholamine plasma levels was observed at the 6th week of treatment in depressed patients (dopamine: 106%; noradrenaline: 14%; adrenaline: 10%) whose nomifensine plasma levels ranged between 84 and 105 ng/ml. No statistical differences were found between pre- and post-treatment serotonin concentration. Reduction of plasma cortisol and clinical improvement may be related to increased catecholamine levels.

Adult↗
PubMed1992

Effect of the duration of streptozotocin-induced diabetes on turnover of central biogenic amines in mice.

The relationship between central catecholaminergic and serotonergic neurons and the development of streptozotocin-induced diabetic mice was examined over periods of 3, 14, 50 and 100 days. The accumulation of 3,4-dihydroxyphenylalanine (DOPA) and 5-hydroxytryptophan (5-HTP) were measured after central decarboxylase activity was inhibited by m-hydroxybenzylhydrazine (NSD-1015). Results indicated that DOPA accumulation in the hypothalamus was not altered during the entire time course of the experiment. On the other hand, DOPA accumulation in the striatum was decreased in 50- and 100-day diabetic mice. The DOPA levels in the pons medulla were not increased until the mice had been diabetic for 100 days. The accumulation of 5-HTP was decreased in the hypothalamus of 14-day diabetic mice and was also present at 50 and 100 days, that in the striatum and pons medulla was not decreased until the mice had been diabetic for 50 days and persisted to 100 days in the striatum. These data showed that both DOPA and 5-HTP accumulation in the striatum and pons medulla were changed only in long-term diabetic mice and suggested that changes in catecholamine and serotonin turn-over rates are not generalized, but restricted only to some particular brain regions and time courses.

5-Hydroxytryptophan↗
PubMed1977

Reactivity of isolated human cerebral arteries to biogenic amines.

Serotonin (5-HT), histamine, norepinephrine, methoxamine and isoproterenol caused dose-dependent contraction of human cerebral arteries. The potency of 5-HT was greater among test agents in the basilar arteries, whereas it was equivalent to that of norepinephrine in human anterior, middle and posterior cerebral arteries. Acetylcholine and carbachol (10(-9)-10(-5) M) caused a negligible response in human cerebral arteries. Contractile response to 5-HT was greater in the distal rather than middle portion of the human basilar arteries while this order was reversed in the response to norepinephrine. Tyramine (10(-4) M) caused tonic contraction and nicotine (10(-4) M) and electrical transmural stimulation produced phasic contraction of arteries which were antagonized by adrenergic blocking agents. Adenine nucleotides failed to cause relaxation and only high concentration of adenosine caused a minute relaxation. However, papaverine and nitroglycerin caused marked relaxation. These results suggest that adrenergic mechanism may play a role in the regulation of vascular tone in human cerebral arteries.

Acetylcholine↗
PubMed1991

Biogenic amines.

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Biogenic Amines↗