[Dark-field microscopic diagnosis as an aid in assessing periodontitis patients].
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Biomedical subjects
Publications and source records attributed to A Hefti.
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Sensitivity to adrenaline-antagonism of the inhibitory effect of PGI2 on thrombin-induced increase in [Ca2+]i was measured in platelets from normotensive and untreated hypertensive subjects. Platelets from hypertensive subjects exhibited an increased sensitivity to adrenaline. This effect was more pronounced in younger patients with hypertension, and suggests an increased adenylate cyclase sensitivity in the early hypertension. The data also indicate that a mechanism linked to calcium-influx plays an important role in older hypertensives. This may explain the greater efficacy of calcium entry blockers in older hypertensive patients with essential hypertension.
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That adrenaline is involved in the pathophysiology of essential hypertension (EHT) is suggested by the observed elevation of plasma adrenaline concentration in some patients. Adrenaline, by stimulating the alpha-2 adrenoceptor, causes vasoconstriction in the smooth muscle cell and initiates shape change and aggregation in platelets. Therefore, the effect of adrenaline on intracellular free calcium concentration ([Ca2+]i) in the platelets of hypertensive subjects was investigated as a model for vascular smooth muscle. Platelets from untreated patients with EHT had an elevated [Ca2+]i and incubation with adrenaline for 30 min caused a greater increase in [Ca2+]i in treated patients with EHT than in normotensive controls. This long-term effect of adrenaline was possibly linked to a defective calcium extrusion mechanism in hypertension. No immediate effect was observed on [Ca2+]i by PGI2 and adrenaline, while both modulated [Ca2+]i if the platelets were stimulated with thrombin. PGI2 prevented the thrombin-induced increase in [Ca2+]i and adrenaline antagonized the effect of PGI2. Platelets from untreated patients with EHT exhibited an increased sensitivity to thrombin and adrenaline when compared to normotensive and treated hypertensive subjects. It is suggested that these supersensitivities are related to the elevated [Ca2+]i in untreated hypertensive patients.
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The Papilla Bleeding Index (PBI) was measured on 95 interdental papillae, after which the results were compared to Sulcus Bleeding Index (SBI) scores, sulcus fluid (SF) amounts and pocket depth (PD) measurements. In 52 of the papillae, a histological evaluation of the degree of inflammation was also made, in which not only the expanse of the infiltrate but also its intensity were of interest. The PBI was positively correlated with all of the other clinical indices. Obvious and highly statistically significant correlations were demonstrated among PBI, SBI and SF. In contrast, between PBI and PD, and between SBI and PD, only weak correlations were found. The comparison of the PBI with the histological determination of inflammation revealed a clear increase in the absolute amount of inflammatory infiltrate as PBI scores increased. In addition, there was a definitive shift in the intensity of the infiltration; moderate and severe areas of infiltration became more common as PBI scores went up.
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