[Reflexion oximetry measurement of cutaneous hemoglobin saturation and concentration in patients with chronic venous insufficiency].
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Biomedical subjects
Publications and source records attributed to A Creutzig.
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Slow progressive improvement of renal anemia from 21 up to 33% hematocrit by rhEPO treatment results in an increase of tissue oxygenation as indicated by a rise of the transcutaneous oxygen pressure. In normotensive patients this was accompanied by an increase in MAP (delta 6 mm Hg) within the normal range and a significant fall of the regional blood flow. These hemodynamic changes are caused by increases of the regional and presumably also of the total peripheral vascular resistance. Most likely the increase in total peripheral vascular resistance represents an autoregulatory event triggered by the rising tissue oxygenation. From the present data it is difficult to estimate to what extent the observed rise in hematocrit affects peripheral vascular resistance also via an increase of blood viscosity.
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In a randomized prospective double blind study, intraarterial infusion therapy with prostaglandin E1 (PGE) was tested against infusion therapy with energy rich phosphates (ERP) in 40 patients with severe claudication. During the treatment period of three weeks, a significant increase of the painfree (PWD) and maximal walking distance (MWD) was observed. The improvement of PWD was of clinical relevance (PGE: 60----195 m; ERP: 69----170 m; p less than 0.001) and persisted during a 36 week post treatment observation period. The differences between the two drugs were not significant but showed a tendency in favour of the PGE therapy.
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Transcutaneous PO2 (tcPO2) and Laser-Doppler-Flux (LDF) were compared on the dorsum of the foot in 20 healthy probands and 35 patients with peripheral arterial occlusive disease at clinical stage II b or IV. The probes were kept at a temperature of 37 degrees C. Using different procedures, we brought about dynamic changes and compared the reaction of the two signals. Venous occlusion resulted in a decrease of both signals to a similar extent in both groups. During leg dependency both signals decreased in the probands suggesting a normal vasoconstrictor response. In most of the patients an increase was observed, but some showed a decrease even at clinical stage IV. LDF had a stronger tendency towards a decrease. On leg elevation, LDF slightly increased in probands and decreased in patients. Here, the tendency towards a decrease was higher for tcPO2. After arterial occlusion reactive hyperemia was more pronounced in probands. Differences between tcPO2 and LDF seem to be mainly due to the different capillary systems contributing to the signal.
A cumulative dose response to intravenous PGE1 was established in 12 healthy volunteers. Systolic time intervals, including pre-ejection period (PEP), the ventricular ejection time (VET) and the RR-interval, were continuously determined, and transcutaneous oxygen pressure (tcpO2) was recorded. RR-intervals fell in a dose dependent manner, reaching a significantly lower level at 128 ng.kg-1.min-1 of PGE1 (basal value 842 ms falling to 756 ms). PEP decreased from 89 ms to 74 ms and the ratio PEP/VET decreased from 35% to 30%, indicating increased myocardial contractility. The maximal increase in tcpO2 was 125% on the calf and 60% on the foot. The peak tcpO2 was observed at an infusion rate of 16 ng.kg-1.min-1 PGE1. A decline in tcpO2 was seen at infusion rates greater than 64 ng.kg-1.min-1 PGE1 indicating a decrease in skin perfusion. The results indicate that the effects of intravenous PGE1 on skin perfusion occur at a lower threshold than the increase in myocardial contractility. A maximal increase in skin perfusion can be achieved with doses of PGE1 devoid of systemic haemodynamic effects.