Gunnar Unge

The 5-hydroxytryptamine take-up mechanism in normal platelets and platelets from migraine and asthmatic patients

Abstract The initial velocity for 5-HT take-up by platelets was studied in platelet rich plasma from healthy blood donors and patients with migraine or asthma. The kinetic data were analyzed according to Lineweaver-Burk and Eadie-Hofstee. The latter plot revealed only one mechanism for active transport of 5-HT through the outer membrane of the normal platelet. In most of the patients no distinct curves depicting a plain active take-up mechanism could be detected. The findings indicate that 5-HT clearance may be severely disturbed in migraine and asthmatic patients.

Defective serotonin transport mechanism in platelets from endogenously depressed patients

Abstract The 5-HT uptake kinetics in platelets from ten depressed patients were studied with a highly reproducible method which detects specific changes in the platelet 5-HT transport. The six patients with endogenous depression had a disturbed 5-HT-uptake. A passive diffusion of 5-HT predominated over the active 5-HT-transport. This disturbance was not found in the four non-endogenously depressed patients or in the fifty normal controls. These findings suggest that platelets from endogenously depressed patients may have abnormal physical membrane characteristics.

The proliferative activity of the heart tissues in various forms of experimental cardiac hypertrophy studied by electron microscope autoradiography.

SummaryCardiac hypertrophy was induced in rats by swimming exercise and by the production of aortic stenosis. After various intervals3H-thymidine was injected intraperitoneally and the hearts were removed and processed for electron microscope autoradiography. In the hearts from exercised rats numerous labelled cells were found in the interstitial tissue. Most of these cells were endothelial cells of blood capillaries, and others were capillary pericytes. In these hearts occasional lymphocytes and granulocytes were also labelled but no fibroblasts or striated heart muscle cells. In the hearts from rats with aortic stenosis no labelled cells were encountered, whereas two labelled endothelial cells were found in the heart of a normal rat. The findings lend further support to the proposal based on findings in light microscope autoradiograms that in cardiac hypertrophy induced by physical exercise there is a significant neoformation of myocardial blood capillaries, whereas any such capillary reaction in cardiac hypertrophy secondary to aortic stenosis is of minor degree and probably insignificant.

Myocardial blood capillary reaction in various forms of cardiac hypertrophy

SummaryThe ultrastructure of the myocardial blood capillary reaction in cardiac hypertrophy induced by physical exercise (swimming) and aortic stenosis was studied in the rat. Clear evidence of a neoformation of capillaries was obtained in the hearts of the swimming exercised rats, whereas no capillary reaction was observed in the hearts from rats with aortic stenosis. The growing capillaries first appeared as solid cords of pericyte-like cells in the interstitium. In the central core of these cords clefts appeared which were lined by endothelial-like cells containing pinocytotic vesicles. These cells might either be transformed pericytes or the result of endothelial proliferation along the interior of the cord. When the cleft established contact with the original capillary lumen it enlarged to form a continuation of this lumen.

The effect of various inhibitors on the 5-ht binding and uptake by human platelets

Abstract The effect of various potential inhibitors on the 14C-5-HT-hydroxytryptamine (5-HT) uptake in human platelets was studied in fresh undiluted platelet rich-plasma (PRP). The kinetic data, based on 5-HT concentrations ranging from 0.17 to 1.7 μmol/1, were analyzed according to Lineweaver-Burk , Scatchard and Sips. The inhibitors were: adenosinediphosphate (ADP), 5-HT, acetylsalicylic acid (ASA), dipyridamole, N-ethylmaleimid (NEM) and ouabain. In untreated PRP the mode of 5-HT transport corresponded to one active site. ASA did not interfere with the uptake mechanism. ADP in concentrations insufficient to cause platelet aggregation induced passive diffusion of 5-HT in addition to the active transport. All the other agents caused a disturbance in the active 5-HT transport without adding passive diffusion. The inhibitors were uncompetetive (ouabain, dipyridamole) or increased at rising 14 C-5-HT concentrations (5-HT, NEM, dipyridamole). It is concluded that the 5-HT uptake by platelets resembles a two-substrate reaction.

Ultrastructural aspects of cardiac lymphatic capillaries in experimental cardiac hypertrophy.

Abstract The lymphatic capillaries in normal rat hearts and hearts rendered hypertrophic by aortic stenosis and swimming exercise were studied in the electron microscope. No differences were found between the normal and hypertrophied hearts with respect to the ultrastructural aspects of the lymphatic capillaries. It was concluded that lymph stasis and cell proliferation in lymphatic capillaries do not contribute to the heart enlargement resulting from aortic stenosis and swimming exercise.

Dipyridamole suppresses uptake of thymidine in human and bovine cells in vitro.

Dipyridamole has been shown to induce proliferative activity in heart muscle capillary wall cells in the rat. To test whether this effect is due to direct cellular stimulation we tested the substance in various in vitro systems (human lymphocytes, glial cells and endothelial cells; and bovine endothelial cells). During these conditions dipyridamole did not influence cellular proliferation. In all cell systems tested, uptake of labelled thymidine showed an inhibition by dipyridamole. This confirms the earlier finding that dipyridamole inhibits nucleoside uptake, and extends the finding to human cells.