[Intermittent intra-arterial infusion treatment of severe intermittent claudication. Results of a prospective double-blind study: prostaglandin El versus energy-rich phosphates].
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Biomedical subjects
Publications and source records attributed to L Caspary.
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Fifteen cases with radial forearm flap harvesting and autologous vein-graft reconstruction of the missing radial artery portion, are reported. Post-repair follow-up examinations, using segment plethysmography, photoplethysmography, and Doppler ultrasound, demonstrated an angiologic donor site morbidity, even when radial artery reconstruction was performed. Typically diminished blood pressure occurred, in comparison with the contralateral healthy extremity. Index shifting of pulse wave peaks, as well as widening of pulse wave bases occurred, especially in the thumb and index finger. These latter findings appear to be discrete indicators of arterial insufficiency.
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.
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Laser Doppler flux (LDF) was determined at the forefoot in 17 healthy volunteers and 16 patients with mild peripheral arterial occlusive disease. LDF was assessed simultaneously by two probes, one was unheated and the other was run with a probe holder temperature of 37 degrees C. During occlusion of the venous circulation a decrease between 43 and 61% was recorded in both groups and at both temperatures. When the leg was elevated there was an increase of about 60% in unheated skin; at 37 degrees C LDF was impaired significantly in patients. During leg dependency LDF decreased in 15 of the volunteers by 44 and 50% which is the result of the physiological vasoconstrictor response. In patients there was a decrease in unheated skin in 12 cases, in heated skin only in 8 cases. When pure oxygen was inhaled, LDF was unchanged in probands, but increased in patients when measured at 37 degrees C. Reactive hyperaemia flow was about three times higher in unheated skin than in heated skin. Reproducibility was best during leg elevation and was more reliable for measurements at 37 degrees C. Rhythmical variations had a frequency of about 4 cycles/min in healthy subjects and 2.6 cycles/min in patients. As a rule, in both groups frequencies at 37 degrees C were higher as compared with unheated skin. Patients had lower frequencies than probands at both temperatures. During intraarterial application of two differently acting drugs quite different reactions of LDF could be recorded. Measurements of LDF at 37 degrees C made differences between patients with PAOD and healthy volunteers more obvious. Moreover, vasomotional changes in skin blood flow could better be studied at this temperature.
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The influence of two different electrode core temperatures on transcutaneous oxygen pressure (tcPO2) was studied in ten probands and 28 patients with peripheral arterial occlusive disease. Hyperaemisation of skin by an electrode core temperature of 44 degrees C reflects local hyperaemia flow and can be reproduced constantly. At 37 degrees C low tcPO2 values are recorded which are in good accordance with mathematically calculated capillary dome PO2. According to great physiological alterations in skin perfusion tcPO2 (37 degrees C) varies in wide ranges. This mode of measurement is well suited to study physiological autoregulation mechanisms or the influence of drugs on skin perfusion. The herein reported results are: forefoot tcPO2 (37 degrees C, 44 degrees C) in volunteers is significantly higher than in patients; forefoot tcPO2 (37 degrees C, 44 degrees C) of patients with diabetes mellitus is significantly higher than in nondiabetics; prestenotic tcPO2 (37 degrees C, 44 degrees C) is about two times higher than poststenotic tcPO2 (37 degrees C, 44 degrees C); tcPO2 (37 degrees C) in probands decreased significantly during occlusion of the venous circulation; tcPO2 (44 degrees C) increased in probands and patients when standing up; however, tcPO2 (37 degrees C) decreased in healthy persons and increased in patients when standing up; after a 5-min suprasystolic cuff occlusion of the arterial circulation there was a four- to six-fold increase of tcPO2 (37 degrees C) which indicates reactive skin capillary flow. In conclusion tcPO2 (37 degrees C) permits measurement of relative changes of skin capillary flow under physiological conditions so that autoregulating mechanisms can be studied.
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