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Congestive heart failure (CHF) is one of the most common medical disorders. The prognosis tends to be unfavorable and the quality of care needs further improvement. The aim of the CorBene project is to improve the health-related quality of life and the prognosis in patients in all stages of CHF and to reduce the hospitalization rate. For this purpose a modern collaborative treatment program involving all relevant health care professionals was developed. The key feature is the close collaboration between family physicians, practicing cardiologists, hospitals and rehabilitation facilities. The CorBene model was launched in Cologne and then spread to North-Rhine/Westphalia and to Saarland. Currently, there is the possibility to offer it in all German states. Preliminary analyses confirm an optimal, guideline-based therapy of CHF.

ZusammenfassungIn dieser Studie sollte bei Patienten mit tiefer Venenthrombose im Verlauf des akuten Ereignisses und bei ambulanter Nachuntersuchung die Beziehung zwischen bekannten hämostaseologischen Risikoindikatoren der Thrombophilie und der Akute-Phase-Reaktion untersucht werden. 73 Patienten mit phlebographisch gesicherter Venenthrombose wurden am Tag der Klinikaufnahme, am zweiten Tag und bei Entlassung aus dem Krankenhaus untersucht, bei 63 Patienten erfolgte eine ambulante Nachuntersuchung nach Abklingen der akuten Symptomatik. Bestimmt wurden die Parameter Plasminogenaktivator-Inhibitor (PAI), Ristocetin-Kofaktor, Plasminogen, Antithrombin III (AT III), Protein C, Protein S, Fibrinogen und C-reaktives Protein (CRP). Es zeigte sich ein deutlicher Abfall der bei 90% der Patienten pathologisch erhöhten CRP-Werte vom Zeitpunkt der Klinikaufnahme bis zur Entlassung aus dem Krankenhaus, 1/3 der Patienten hatte auch zum Zeitpunkt der ambulanten Nachuntersuchung noch erhöhte CRP-Konzehtrationen >0,5 mg/dl. Diese Patienten hatten eine Häufigkeit pathologisch erhöhter Werte von Fibrinogen (84,2%) und Ristocetin-Kofaktor (47,4%) wie zum Zeitpunkt der Akutveränderung bei Klinikaufnahme. Bei 2/3 der Patienten konnte bei der ambulanten Nachuntersuchung anhand unauffälliger CRP-Werte Fibrinogen, Ristocetin-Kofaktor und PAI sind auch als Risikoindikatoren arterieller Thrombosen bekannt. Dies führt zu dem Schluß, daß der Pathomechanismus und die Risikokonstellation bezüglich thromboembolischer Ereignisse zwischen arteriellem und venösem System ähnlicher sind als bisher angenommen.CRP hat sich nach den vorliegenden Ergebnissen als prognostisch wichtiger Risikomarker bei der tiefen Venenthrombose erwiesen. Die vorgelegten Daten können Hinweise darauf geben, daß die Entzündungsreaktion im Pathomechanismus der tiefen Venenthrombose eine kausale und nicht nur sekundäre Rolle spielt. Die prospektive Bedeutung dieser Ergebnisse muß noch durch weitere Untersuchungen geklärt werden.

Congestive heart failure (CHF) is one of the most common medical disorders. The prognosis tends to be unfavorable and the quality of care needs further improvement. The aim of the CorBene project is to improve the health-related quality of life and the prognosis in patients in all stages of CHF and to reduce the hospitalization rate. For this purpose a modern collaborative treatment program involving all relevant health care professionals was developed. The key feature is the close collaboration between family physicians, practicing cardiologists, hospitals and rehabilitation facilities. The CorBene model was launched in Cologne and then spread to North-Rhine/Westphalia and to Saarland. Currently, there is the possibility to offer it in all German states. Preliminary analyses confirm an optimal, guideline-based therapy of CHF.

Die Zielsetzung physiotherapeutischer Masnahmen bei der peripheren arteriellen Verschluskrankheit (pAVK) besteht in der Wiederherstellung der gestorten Funktion durch die Forderung oder Verbesserung der korpereigenen Kompensationsmechanismen des Arterienverschluskranken, einer Verhinderung von Inaktivitatsschaden am Bewegungsapparat sowie einer allgemeinen Mobilisierung und Motivation des Patienten mit allen daraus resultierenden kardiopulmonalen, stoffwechselmasigen und gerinnungsphysiologischen Folgen.

Thrombolytic treatment during cardiopulmonary resuscitation is thought to reverse the cerebral no-reflow phenomenon which is widely considered to limit neurological recovery after prolonged cardio-circulatory arrest. However, the recent multicenter randomized double-blind TROICA (Thrombolysis in Cardiac Arrest) trial revealed that patients with witnessed out-of-hospital cardiac arrest did not experience an improvement of neurological outcome when treated with the throm-bolytic agent tenecteplase [1]. This raises the question of the importance of coagulation disturbances in the pathophysiol-ogy of no-reflow and its reversal by thrombolytic interventions. This article provides an overview of the experimental literature on this subject.

In normothermic anesthetized cats complete cerebral circulatory arrest for one h was produced and followed by blood recirculation of the brain for 30 min to 4 h. Total and local blood flow of the brain, kidney, heart and liver were measured before and after ischemia using radioactive labelled microspheres. Before ischemia blood flow of the brain was 39.1 +/- 2.3 ml/100 g/min, of the kidney 307.2 +/- 28.3 ml/100 g/min, of the heart 241.1 +/- 32.5 ml/100 g/mmin and of the liver 87.8 +/- 25.6 ml/100 g/min (means +/- SEM). Regional flow rates within the brain varied between 35 and 51 ml/100 g/min. Reactive hyperemia was present in the brain 30 min after the beginning of recirculation following ischemia for 1 h. Local cerebral flow rates increased three to five times above the control flow, depending on the respective region. Mean cerebral blood flow returned to or slightly below normal, 2 to 4 h after ischemia, but there was considerable redistribution of flow rates within the brain. The filter capacity of the brain for microspheres of 15 mu and 50 mu diameter did not change after ischemia indicating that postischemic blood recirculation was not accompanied by an opening of arteriovenous shunts.

The dose-dependent inhibition of platelet aggregation by the chemically stable, prostacyclin-mimetic, iloprost, was studied in patients suffering from stage II-III peripheral arterial obliterative disease (PAOD). The study was designed as a randomized placebo-controlled cross-over trial. Iloprost was administered i.v. to six patients at doses of 0.5, 1.0, 2.0 or 3.0 ng/kg X min for 4 h, with an interval of 2-3 days between the infusions. During iloprost infusion, systolic and diastolic arterial blood pressure, heart rate and blood flow in the affected limb remained unchanged. In contrast, there was a considerable, dose-dependent inhibition of ADP- and thrombin-induced platelet aggregation and secretion ex vivo at doses of 0.5-2.0 ng/kg X min iloprost, indicating that iloprost reduced platelet stimulation by 50%-70%. The antiplatelet action of iloprost remained unchanged during infusion but ceased with 2 h after administration had ended. The agent was tolerated by the patients without unacceptable side-effects at doses up to 2 ng/kg X min. It is concluded that iloprost administered i.v. at doses of 1-2 ng/kg X min in patients with stage II-III PAOD does not involve haemodynamic side-effects and might be considered an effective antiplatelet agent.

We investigated the activity of the renin-angiotensin-aldosterone-system, the secretion of catecholamines and the kallikrein-kinin-system in 126 adolescents randomly selected from a large study of 1342 young people examined in an epidemiological survey conducted in Cologne in 1975, 1976 and 1980. 73 of them with arterial blood pressures below 145/90 mm Hg were called "normotensives" (systolic blood pressure 127.2 +/- 1.0 mm Hg, diastolic bp 79.7 +/- 0.8 mm Hg). They were compared with 53 "hypertensives" (systolic blood pressure 147.2 +/- 1.6 mm Hg, diastolic bp 93.7 +/- 1.1 mm Hg). Urinary catecholamines were significantly higher in the hypertensives (155.0 +/- 13.3 micrograms/d) compared to the normotensives (100.7 +/- 5.3 micrograms/d) (p less than 0.001) whereas plasma levels of adrenaline and noradrenaline were similar. Serum aldosterone levels and plasma-renin-concentrations were not different between the two groups. Angiotensin-converting-enzyme-activity was slightly higher in the hypertensive group (107.1 +/- 3.5 U/l versus 98.0 +/- 2.6 U/l, p less than 0.001). Urinary kallikrein excretion was found to be modestly lower in hypertensives compared to normotensives (0.40 +/- 0.05 versus 0.55 +/- 0.06 mU/mg creatinine). Urinary excretion of sodium and potassium, blood levels of glucose, uric acid, cholesterol and triglycerides were similar in both groups. The results of the present study suggest an increased sympathetic activity in the early stage of hypertension in adolescents.

AT III activity and concentration were measured in 36 patients (mean age 65.5 yrs, range 43-77 yrs) with ischaemic stroke within maximally 48 h of the acute event. In 12 patients (= 33%) AT III activity was reduced below 18.4 IU/ml: 50% of these patients showed normal and 50% reduced AT III concentration of less than 22 mg/dl. In 15 patients AT III activity and concentration were measured in the acute phase on admission to hospital and 12 months later. In the acute phase, AT III activity was reduced when compared with AT III concentration (y = 0.19 chi + 15.5) and did not correlate with the latter. 12 months later, however, AT III activity and concentration correlated significantly (r = 0.92; p less than 0.001) and the regression line was steeper (y = 0.8 chi). During the acute phase of ischaemic stroke, intravascular coagulation is evidently increased and inactive AT III-thrombin complexes are formed, whereby the concentration of active AT III decreases. A patient with progressive stroke and reduced AT III activity of 14.2 IU/ml was therefore substituted with AT III concentrate. The further neurological course was favourable.

Inhibition of the ouabain-sensitive Na-K-ATPase by digoxin significantly decreases erythrocyte deformability (5). Since first a decrease in this transport system has been discussed as a pathogenetic factor in the development of essential hypertension and second an increase in blood viscosity, due to an increased hematocrit has been observed in elderly hypertensives, hemorheology and sodium transport systems were examined in adolescent hypertensives and compared with age-matched normotensive controls. 73 normotensives (N; mean blood pressure 127/80 mmHg) and 53 hypertensives (H; mean blood pressure 147/94 mmHg) aged 23-27 yrs were randomly selected from an epidemiological survey, covering 1342 adolescents. While apparent whole blood viscosity at different shear rates, hematocrit, plasma fibrinogen were not significantly different, erythrocyte deformability, measured with a positive pressure filter system (pore phi 5 mu) and expressed as Q = delta P/ery.susp.Hct 10%/delta P/plasma was significantly attenuated with Q = 1.77 +/- 0.05 in H, compared to 1.64 +/- 0.04 in N (p less than 0.05) The decrease in erythrocyte deformability was not accompanied by an inhibition of the Na-K-pump nor of total K+-uptake in erythrocytes, both measured with the 86Rb uptake. There was only a slight increase in Na+-excretion in urine of 184.4 + 12.2 mval in H, compared to 162.0 +/- 10.4 mval in N (n.s.). K-/+-excretion and serum electrolytes did not show any difference. Whether the decrease in erythrocyte deformability may contribute to an increase in peripheral vascular resistance in essential hypertension has to be further clarified.

Thirty-seven patients (15 female, 22 male; aged 46–89 years, mean age 68.8 years) with III or IV grade carotid sinus reflex carotid arteries were investigated by sonography (B-scan and CW-Doppler). It was demonstrated that stenoses or arteriosclerotic plaques, localized in the region of the carotid bulb or bifurcation, were present on both sides in 27 patients and on one side only in four patients. Five patients did not show these changes and four of them had thickening of common carotid artery endothelium. Thus, vascular changes occurred in 35 patients. Occlusions and stenoses >50% were visible in five patients. Primarily bilateral changes were shown as well as unilateral and bilateral pathologic reflex response; main localization was the posterior wall of the carotid bulb. Thus, arteriosclerotic changes seem to be important in the development of pathologic carotid sinus reflex. Cerebral complications (left-sided PRIND) occurred in one patient who did not have high degree carotid stenosis. In comparison to other authors who investigated only with CW-Doppler a much higher rate of arteriosclerotic wall changes and a greater occurrence of bilateral changes could be demonstrated by application of the highly sensitive B-scan sonography.

Reversible complete cerebro-circulatory arrest was produced in normothermic, anesthetized cats for 1 h by clamping the innominate and subclavian arteries, followed by blood recirculation of the brain for 30 min to 4 h. Blood volume of tissue samples was measured by intravenous injection of 125I-albumin and the platelet number by labelling of autologous platelets with 51Cr. The number of platelets trapped in the tissue was determined by subtracting from the total platelet count of the tissue sample those contained in the streaming blood, calculated from the blood volume by 125I-albumin. In sham-operated animals, after recirculation of autologous 51Cr labelled platelets for 60 min, no platelets were entrapped in the brain vasculature and total platelet number and fibrinogen concentration in the venous blood did not change. In animals submitted to complete cerebral ischemia for 1 h the number of trapped platelets increased significantly in the whole brain after 30 min of recirculation, i.e. the period of maximal postischemic vasodilatation and hyperemia, and highest concentrations were found in the border zone with 270 +/- 60 x 10(4) platelets/g tissue and in the brainstem with 240 +/- 70 x 10(4) platelets/g tissue. Blood platelets and fibrinogen concentration in the venous blood decreased significantly from 288 +/- 37 x 10(6)/ml and 299 +/- 50 mg% to 186 +/- 25 x 10(6)/ml platelets and 112 +/- 22 mg+ of fibrinogen, respectively. Platelets were nearly completely washed out of the brain after 4 h of recirculation. The highest increase of platelets was found in the kidney, lung and liver after 30 min of recirculation, indicating that intravascular coagulation following prolonged cerebral ischemia affects the extracerebral organs more than the brain itself.

Complete cerebral ischemia of 30 and 60 min was produced in normothermic cats by arterial clamping and lowering of the blood pressure. The functional impact was monitored by electrophysiological methods. In animals without functional recovery blood flow was not fully restored after ischemia. In the animals in which signs of neuronal function returned, ischemia was followed by a transient phase of hyperemia, the termination of which coincided with the return of spontaneous EEG activity. At this time cerebrovascular autoregulation was present, but CO2 responsiveness was still completely abolished, and vasoactive drugs (papaverine, aminophylline, alpha adrenergic blocking agents, hydergine) failed to increase cerebral blood flow.

Uber die Wirkung von Clonidin bei Hypertonikern mit chronischer Niereninsuffizienz liegen nur wenige klinische Studien vor (siehe Ubersichtsarbeit Itskovitz 1980). Unter einer Dauertherapie mit Clonidin in Dosen bis uber 2,0 mg taglich (Bock et al. 1973) konnten gute antihypertensive Effekte ohne verschlechterung der Nierenfunktion gemessen werden. Allerdings fanden Hoobler et al. (1971) sowie Niarchos et al. (1978), das bei niereninsuffizienten Patienten die Blutdrucksenkung durch Clonidin im vergleich zu nierengesunden Patienten abgeschwacht ist. Da Clonidin zu 40–60% in unveranderter Form renal ausgeschieden wird, nimmt die Plasmahalbwertzeit bei eingeschrankter Nierenfunktion von normalerweise 8–14 Stunden bis zu 53 Stunden bei Hamodialysepatienten zu (Seiler et al. 1978, Hulter et al. 1979). Durch Kumulation werden dementsprechend bei Patienten mit Niereninsuffizienz hohere Plasmaclonidinspiegel erreicht als bei Patienten mit normaler Nierenfunktion und gleicher Dosis. Bei Plasmaclonidinspiegeln oberhalb ca. 2 ng/ml mus allerdings mit einer Abschwachung bzw. sogar Aufhebung der antihypertensiven Wirkung gerechnet werden (Davies et al. 1977, Wing et al. 1977, Frisk-Holmberg et al. 1978). Die Ursache fur diesen nachteiligen Effekt wird in einer peripheren Stimulation der postsynaptischen alpha-Rezeptoren gesehen, durch die eine vasokonstriktion verursacht und damit die zentrale antihypertensive Wirkung uber Senkung des Sympathikotonus und verstarkung des vagotonus antagonisiert wird.

Fifty-three untreated borderline hypertensives and 73 normotensives were randomly selected from 1342 adolescents (age range 23-27 years) who were examined in 1975, 1976 and 1980 in an epidemiological study. Blood pressure was 127.2 +/- 1.0/79.0 +/- 0.8 mmHg in normotensives and 147.2 +/- 1.6/93.7 +/- 1.1 mmHg in hypertensives (P0.001). Erythrocyte deformability was measured with a positive pressure filter system (pore diameter 5 microns) at 37 degrees C. Erythrocyte deformability was significantly increased in hypertensives with a value of 1.77 +/- 0.05, compared with 1.64 +/- 0.04 in normotensives (P0.05). No difference in apparent whole blood viscosity, haematocrit and plasma fibrinogen was measurable between the groups. Although plasma noradrenaline and adrenaline concentration at rest and after 3 min standing were not different, excretion of urinary catecholamines was significantly elevated in hypertensives with 155.0 +/- 3.3 micrograms/24 h (normotensives: 100.7 +/- 5.3 micrograms/24 h; P0.001).

40 patients of the ASA groups I and II in whom intra-operatively an isorhythmic AV dissociation occurred under inhalation narcosis with halothane or enflurane, were examined in a randomized study. Within an observation period of 15 minutes the spontaneous rate of return to the sinus rhythm was 20 per cent (group A, n = 20). Intravenous administration of 0.01 mg/kg atropine sulphate produced a significantly higher rate of return of 80% within the same period. On the whole, no influence on arterial blood pressure was noted. Atropine increases the heart rate by 32%, and this is considered to be an important drawback. The possibility of influencing the AV dissociation via atropine points to the pathogenetic importance of the vagus in so far as it acts as a depressant on the sinus node.

Data on the reversibility of ischemic brain damage are largely based on experiments that lack experimental evidence for a successful restoration of cerebral blood flow. In several communications from this laboratory it has been shown that nerve cells may survive extended periods of ischemia provided cerebral blood flow is efficiently restored and “no-reflow phenomena” (1) can be avoided (5, 6).

Twelve patients (age 33-77 years, mean age 68.4 years) with peripheral vascular disease (PVD) stage III-IV received continuous intravenous infusions of 5 ng prostacyclin (PGI2)/kg/min and physiological saline for 7 days. The administration was randomized and double-blind with an interval of 7 days between the infusions. During PGI2 infusion systolic blood pressure fell significantly from 147.8 +/- 4.8 mm Hg to 140.6 +/- 4.0 mm Hg (P less than 0.01) and returned to 144.5 +/- 4.9 mm Hg post infusion. Transcutaneous pO2 (tcpO2) measured on the instep of the affected limb increased significantly by 8.9 +/- 3.8 Torr during PGI2 infusion and remained elevated during the subsequent week. A significant reduction of pain was observed from the 5th day of PGI2 infusion, lasting for at least the following observation period. Platelet cAMP increased from 18.8 +/- 1.5 pmol/10(8) platelets to 24.7 +/- 1.6 pmol/10(8) platelets on the 3rd day of PGI2 infusion (P less than 0.01). Spontaneous platelet aggregation was also significantly reduced during PGI2 infusion. However, 7 days after the infusion thromboxane B2 (TXB2) in plasma and spontaneous platelet aggregation significantly increased in comparison with the preinfusion values, indicating a rebound phenomenon. The clinical outcome was favorable in 9 of 12 patients, was unchanged in two patients, while progressing to limb amputation in one patient.

In order to investigate the possibility of providing a myocardial protective effect by intracoronary perfusion through the dilatation catheter during the phase of balloon inflation for PTCA, in vitro studies were performed to determine the relationship between proximal perfusion pressure and flow through the catheter. In addition, blood samples obtained proximal and distal to the catheter system were examined to establish whether a change in blood composition across the catheter occurs.

During PTCA, inflation of the catheter balloon to dilate the coronary stenosis produces complete coronary occlusion and results in myocardial ischaemia, thus limiting the duration of inflation. It was the aim of this study to determine if a protective effect can be obtained by blood perfusion through the dilatation catheter during the phase of balloon inflation, which might permit an increase in the duration of inflation. Such a protective effect would reduce the problems of repeated localisation of the catheter if the primary dilatation was unsuccessful, and if PTCA induced a critical phase for the patient requiring surgical intervention, this interval could be bridged by this new method of perfusion.

Bei der pharmakologischen Wirkung von Nitraten steht eine generelle Vasodilatation im Vordergrund, die mit einer Senkung des peripheren arteriellen Widerstandes und einer Kapazitatssteigerung im venosen System einhergeht [3, 5, 6, 9, 11, 14, 15, 17, 22, 23, 25]. Im zentralen Kreislauf kommt es zu einer Druck- und Volumenentlastung des Herzens, indem mittlerer Arteriendruck, Pulmonalarteriendruck und Herzzeitvolumen signifikant abfallen [1, 8, 13, 16, 19, 20, 21, 24].

21 patients (aged 28-81 years) with recent subarachnoid hemorrhage (10 saccular aneurysms, 3 arteriovenous angiomas, 8 normal angiograms) were continuously infused with tranexamic acid at a dosage of 5 g daily for up to 14 days. Therapy was surveyed by daily measurement of the available plasminogen activity (aPl) with the chromogenic substrate S-2251 and by a modified bioassay, whereby the concentration of tranexamic acid was determined thrombelastographically and expressed as antifibrinolytic equivalent. In addition, a battery of blood coagulation tests was performed daily. 5 patients died, 1 after postoperative stroke, 3 as a result of general complications during intensive care treatment, but only 1 due to rebleeding. 4 patients were successfully operated during the first week, 1 patient after 2 weeks. aPl fell from 99.2% (SEM 3.0%, n = 21) before treatment to 72.9% (SEM 3.5%, n = 21) after 24 h and to the therapeutic level between 50 and 60% from day 2 on. The mean steady state of the antifibrinolytic equivalent corresponded to about 150 micrograms/ml of tranexamic acid during infusion. Intra- and interindividual changes were relatively small for aPl, when compared with the antifibrinolytic equivalent measured by the bioassay. In 2 elderly patients tranexamic acid infusion had to be terminated because of clinical and laboratory signs of disseminated intravascular coagulation, whereby aPl fell below the therapeutic range, elucidating that this method is a sensitive indicator for a hypercoagulable state and useful for the surveillance of therapy with antifibrinoltic agents.

Blood coagulation and blood platelets play an important role in the ischemic process. Firstly there is much evidence that both are involved in the development of atherosclerosis (18, 23, 26, 30); and secondly thrombi are usually formed on an atherosclero-tically damaged vessel wall giving rise to severe stenosis or even occlusion of the artery which results finally in infarction (18, 30).

Arterial blood pressure was continuously monitored during rapid atrial pacing in 31 patients with different types of heart disease to determine sinus node recovery time and corrected sinus node recovery time. Pacing was initiated at 70 beats/min and increased stepwise to 160 beats/min. One to one atrioventricular conduction was maintained throughout the one minute stimulation period. Blood pressure fell initially during at least one stimulation period in 21 of our patients and at pacing rates up to 130 beats/min in 18. Once blood pressure had fallen during overdrive pacing maximal sinus node recovery time and maximal corrected sinus node recovery time could not be prolonged by increasing the pacing rate. Sinus node recovery time and corrected sinus node recovery time during the pacing induced fall in blood pressure was significantly shorter than those during stimulation runs with constant blood pressure. No pacing induced fall in blood pressure and no relation between changes in blood pressure and sinus node recovery time were evident in 10 of the 31 patients. Sinus node recovery time is therefore influenced by alterations in autonomic tone due to pacing induced haemodynamic changes.

Twenty patients (67.2 ± 12.3 yrs; aged 39-86 yrs, 10 males, 10 females) with stage IV of peripheral obliterative arterial disease received at random either a) BM 13.177, a thromboxane receptor antagonist, at a dose of 6 g/24 hrs for 7 days i.v., followed by oral treatment of 6.4 g/day in four doses for 2 weeks and a subsequent placebo week, or b) placebo alone with the same protocol. The clinical course was followed by measurement of blood pressure (by Riva-Rocci on the left brachial artery and by Doppler of the ankle artries), blood flow at restand after 3 min of tourniquet ischemia (by venous occlusion plethysmography), TcpCf2 at the wrist of the affected limb, and by subjective estimation of pain with visual analog scale before, at the end of the infusion period, as well as on day 7 and 14 of oral treatment, and 7 days after treatment while patients of both groups were on placebo. In addition spontaneous platelet aggregation by PAT III, induced platelet aggregation in whole blood by collagen and in PRP by ADP at different doses on the same days were measured on the same days as described above.Results: BM 13.177 completely inhibited aggregation in whole blood induced by collagen 0.3 (ig/ml, however one week after treatment a rebound phenomenon was observed with 16.0 ± 3.8 OHM compared to pretreatment value of 11.0 ± 3.8 OHM (p < 0.01). At a higher dose of 1.2 |ig/ml the same inhibiting effect on platelet aggregation was observed. Spontaneous platelet aggregation as measured by PAT III was evident in only 2/10 pat. pre-treatment, was abolished in all patients on i.v. BM 13.177, returned in 1/10 pat. during oral treatment, but in 4/10 pat. on day 7 after treatment, while being on placebo, again indicating a rebound phenomenon (p < 0.03) ADP induced platelet aggregation was not significantly affected by BM 13.177. In the placebo group, too, no significant differences were observable between the different treatment regimens. Clinical data did not show any significant alteration in either verum or placebo group during the six week period, indicating no benificial effect of thromboxane receptor antagonists in advanced stages of peripheral obliterative arterial disease, although platelet inhibiting effects were clearly demonstable.

In twenty-three patients (38-82 yrs, mean age 62.2 yrs) with a history oflight-headedness or syncope sinus node recovery time (SNRT) was measured following atrial stimulation of 85 and 145/min, whereby pulmonary arterial pressure (PAP) and systemic intraarterial pressure (SAP) were continuously recorded, cardiac output (CO) measured by thermodilution and venous blood withdrawn for radioenzymatic determination of plasma norepinephrine (PNE) and epinephrine (PE) after 15 min of rest and at the end of each stimulation period, lasting 3 min. The hemodynamic and electrophysiological measurements were repeated in the same way during volume load (VL) by tilting up the legs and volume depletion (VD) induced by a) venous occlusion of the legs and b) by i.v. injection of 20 mg frusemide. During VL mPAP increased significantly by 2 mmHg from 10.9 ± 0.8 to 12.9 ± 0.9 mmHg at sinus rhythm, SNRT from 1313 ± 58 msec to 1348 ± 57 msec at 85/min, and from 1149 ± 65 msec to 1232 ± 58 msec at 145/min, max. cSNRT from 337 ± 38 msec to 433 ± 37 msec. VD induced by venodilation due to frusemide significantly reduced SNRT to 1056 ± 58 msec at 85/min, 1034 ± 52 msec at 145/min (P < 0.01). CO decreased significantly from 6.0 ± 0.5 I/min to 4.9 I/min at 85/min and from 5.2 I/min to 4.3 I/min at 145/min (p < 0.01), and peripheral vascular resistance significantly increased, as did PNE: from 0.35 ± 0.07 ng/ml to 0.55 ± 0.09 ng/ml (p < 0.05). Baroreceptor mediated adaptation of the autonomic nervous system to volume depletion is evidently responsible for the reduction of SNRT.

Plasma levels of ANP correlate with central hemodynamics and the degree of cardiac dysfunction [1, 2, 4–7, 9]. There is some evidence, that in advanced cardiac failure ANP secretion may be reduced due to a depletion of atrial stores [3, 8]. To determine the diagnostic value of ANP measurements in a clinical routine setting we studied a Short Communications group of unselected patients referred for right heart catheterization during rest and standardized exercise conditions. In addition, we were interested whether stimulation of ANP secretion by exercise is reduced in patients with chronic heart failure.

In einer vorangegangenen Studie konnten wir nachweisen, das Isosorbiddinitrat (ISDN) die Unterschenkel-Durchblutung bei Patienten mit arterieller Verschluskrankheit (AVK) trotz gleichzeitigen Abfalls des systemischen Blutdrucks erhoht [3]. Ein Durchblutungsanstieg ist bei Gefasgesunden durch arteriolare Vasodilatation leicht erklarlich. Bei Patienten mit AVK wird die gunstige Wirkung von Vasodilatatoren auf die Durchblutung der erkrankten Extremitaten jedoch angezweifelt. Wahrend in ausreichend durchbluteten Gefasbezirken die Vasodilatatoren zu einer weiteren Durchblutungssteigerung fuhren, ist in den mangeldurchbluteten Arealen eine weitere Dilatation der poststenotischen Widerstandsgefase nicht mehr moglich, und auf Grund des systemischen Blutdruckabfalls nimmt die Durchblutung sogar druckpassiv ab: sog. Steal-Phanomen. Daher stellte sich die Frage, ob die Durchblutungszunahme nach ISDN z. T. auf hamorheologischen Veranderungen beruht.

A most common complication of acute ischemic stroke is deep vein thrombosis (DVT), preferentially of the paralytic limb. Without prophylactic therapy an incidence of 33%–70% has been reported, according to the method used for detection, i.e., clinical symptomatology, phlebography, or 125I-fibrinogen scanning, the latter being most sensitive [1–4].

Wahrend vor etwa zehn bis funfzehn Jahren die Therapie des Hirninfarktes noch weitgehend in den Handen der Internisten lag, ist durch Einrichtung neurologischer Intensivstationen, verbesserte neurologische Untersuchungsmethoden zur Diagnostik wie z.B. Computertomographie, Positron-Emissionstomographie, Kernspintomographie sowie vertiefte Kenntnisse uber die spezifische Therapie des ischamischen Insultes, diese Aufgabe zunehmend den Neurologen zugewiesen worden. Allerdings sind auch weiterhin einige allgemeininternistische Gesichtspunkte von Bedeutung. So spielen Storungen zweier Systeme bei der Pathogenese und Therapie des Hirninfarktes eine wesentliche Rolle: 1. Storungen der Hamodynamik 2. Storungen des zirkulierenden Blutes; speziell der Blutplattchen, der Blutgerinnung und der Hamorrheologie.