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With a new immunoenzymometric assay we measured human glycogen phosphorylase isoenzyme BB (GPBB) in 116 healthy individuals, 14 patients with stable angina, 107 nontraumatic chest pain patients on admission to the emergency department [45 acute myocardial infarction (AMI), 49 unstable angina, 13 other diseases], and in serial samples from 41 AMI patients. GPBB was compared with creatine kinase (CK), CKMB mass, myoglobin, and cardiac troponin T. Receiver-operating characteristic plots demonstrated the significantly greater (P < or = 0.012) discriminatory power of GPBB to detect acute ischemic coronary syndromes compared with all other tested markers. GPBB was the most sensitive marker for detection of AMI during the first 4 h after onset of chest pain, and only GPBB was increased above the upper reference limit (7 micrograms/L) on admission in patients who had unstable angina at rest and reversible ST-T alterations. This and the high early sensitivity of GPBB are most likely explained by its function as a key enzyme of glycogenolysis.

58,050 patients entering 1086 hospitals up to 24 h (median 8 h) after the onset of suspected acute myocardial infarction (MI) with no clear contraindications to the study treatments (in particular, no cardiogenic shock or persistent severe hypotension) were randomised in a "2 x 2 x 2 factorial" study. The treatment comparisons were: (i) 1 month of oral captopril (6.25 mg initial dose titrated up to 50 mg twice daily) versus matching placebo; (ii) 1 month of oral controlled-release mononitrate (30 mg initial dose titrated up to 60 mg once daily) versus matching placebo; and (iii) 24 h of intravenous magnesium sulphate (8 mmol initial bolus followed by 72 mmol) versus open control. There were no significant "interactions" between the effects of these three treatments, and the results for each are based on the randomised comparison of about 29,000 active versus 29,000 control allocated patients. Captopril There was a significant 7% (SD 3) proportional reduction in 5-week mortality (2088 [7.19%] captopril-allocated deaths vs 2231 [7.69%] placebo; 2p = 0.02), which corresponds to an absolute difference of 4.9 SD 2.2 fewer deaths per 1000 patients treated for 1 month. The absolute benefits appeared to be larger (perhaps about 10 fewer deaths per 1000) in certain higher-risk groups, such as those presenting with a history of previous MI or with heart failure. The survival advantage appeared to be maintained in the longer term (5.4 [SD 2.8] fewer deaths per 1000 at 12 months). Captopril was associated with an increase of 52 (SD 2) patients per 1000 in hypotension considered severe enough to require termination of study treatment, of 5 (SD 2) per 1000 in reported cardiogenic shock, and of 5 (SD 1) per 1000 in some degree of renal dysfunction. It produced no excess of deaths on days 0-1, even among patients with low blood pressure at entry. Mononitrate There was no significant reduction in 5-week mortality, either overall (2129 [7.34%] mononitrate-allocated deaths vs 2190 [7.54%] placebo) or in any subgroup examined (including those receiving short-term non-study intravenous or oral nitrates at entry). Further follow-up did not indicate any later survival advantage. The only significant side-effect of the mononitrate regimen studied was an increase of 15 (SD 2) per 1000 in hypotension. Those allocated active treatment had somewhat fewer deaths on days 0-1, which is reassuring a bout the safety of using nitrates early in acute MI.(ABSTRACT TRUNCATED AT 400 WORDS)

Plasma concentrations of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor type 1 (PAI-1), and D-dimer were investigated in 50 patients treated intravenously for acute myocardial infarction with either streptokinase (n = 23), urokinase (n = 17), or recombinant t-PA (rt-PA, n = 10). The fibrinolytic variables were measured by enzyme immunoassay on admission; 1, 2, 4, 6, 8, 12, and 24 h later; and then daily until day 7 after admission. In each subgroup of patients treated with different thrombolytic agents, PAI-1 increased significantly (P0.01) approximately 3 h after cessation of thrombolytic therapy. PAI-1 peak concentrations did not differ significantly (P = 0.82) among these three subgroups. t-PA and D-dimer did not differ significantly (P0.14) among subgroups except for higher t-PA in the rt-PA group attributable to detection of the therapeutically administered exogenous rt-PA by the t-PA assay. Our findings demonstrate a marked PAI-1 increase after thrombolytic therapy for acute myocardial infarction, which seems to be a common, drug-independent antifibrinolytic rebound phenomenon in response to thrombolytic treatment.

Cardiac troponin I, creatine kinase, and creatine kinase MB activity were tested in serial blood samples from 15 patients with first-time Q wave acute myocardial infarction (2 anterior and 13 inferior wall infarctions). All patients received intravenous thrombolytic therapy. Cardiac troponin I and creatine kinase MB activity were compared with scintigraphic estimates of myocardial scar (single photon emission computed tomography [SPECT] with 99mTechnetium-isonitrile [Tc-sestamibi]) on late images at rest about 5 weeks after myocardial infarction. Scintigraphic defect sizes ranged from 3.2 to 41.2% (median: 27.3%) of left ventricle. Cardiac troponin I increased and peaked in parallel with creatine kinase MB activity, and the peak values correlated with each other (r = 0.76, p = 0.002). Troponin I stayed increased for several days longer than creatine kinase and creatine kinase MB activity. It could be detected at least until the 4th day after admission. Significant correlation coefficients were found between 99mTc-isonitrile defect sizes and areas under cardiac troponin I curves (r = 0.53, p = 0.042) and between 99mTc-isonitrile defect sizes and cumulative creatine kinase MB activity release (r = 0.64, p = 0.01). Animal studies have already shown a very close correlation between histologic infarct size and SPECT 99mTc-isonitrile defect size. Therefore, our results indicate that cardiac troponin I release in patients with acute myocardial infarction is also correlated with infarct size.

Accurate diagnosis of impending acute myocardial infarction (AMI) in patients presenting at an emergency department with acute chest pain is essential for proper triage and treatment. We have developed an algorithm for the early diagnosis of AMI.The diagnostic performances of ECG, creatine kinase (CK) and creatine kinase isoenzyme MB (CKMB) activities, CKMB mass, myoglobin, and cardiac troponin T (cTnT) were compared for early diagnosis of AMI in 60 non-traumatic chest pain patients (22 AMI, 29 unstable angina, nine other diseases) on presentation to an internal medicine emergency department and 1 h thereafter. The classification and regression trees method was used for data analysis and revealed the following results.In patients with electrocardographic signs of acute transmural myocardial ischaemia on admission (mostly regional ST-segment elevations), biochemical markers could not improve the diagnostic accuracy either on admission or 1 h later. By contrast, in patients with non-diagnostic ECG, CKMB mass concentration measured 1h after admission was the best discriminator between AMI and non-AMI patients (discriminator value 5.8 micrograms/l) and was superior to ECG and all other biochemical markers tested. This algorithm for diagnosing AMI is characterized by 96% sensitivity, 90% specificity, 84% positive predictive value, 97% negative predictive value, 92% accuracy, 0.05 negative likelihood ratio, and 9.1 positive likelihood ratio.The classification procedure obtained allows accurate rapid and early diagnosis of AMI and could therefore be a valuable diagnostic aid to physicians of emergency medicine.

It has been shown by a number of authors that early myocardial infarction constitutes a dynamic process of cyclic oscillation between coronary occlusion and spontaneous coronary reopening. Infarct-markers, such as ST-segment elevation, serum-creatine kinase isoenzyme MB, the atrionatriuretic peptide (ANP) and serum-myoglobin (Mb) exhibit cyclic behaviour pattern during early AMI and thus reflect episodes of intermittent, spontaneous reperfusion. The latter have recently been verified by angiography. The mechanism underlying the phenomena seen in early myocardial infarction is likely to be based on a constant vasoconstrictive stimulus, deriving from aggregating platelets. The vasoconstriction subsequent to platelet aggregation produces an initial episode of myocardial ischemia. This episode is followed by a hypoxia of the artery wall. Reactive coronary dilation secondary to ischemia is than promoted by the release of vasoactive by-products of anaerobic glycolysis as well as changes in the open propability of certain transmembrane ion channels. Thereafter, the initial coronary occlusion is interrupted by transient vasodilation. A wave of reperfusion follows and leads to reoxygenation and wash-out of ischemia-induced vasodilative components as well as biochemical markers. The vasoconstrictive forces then take over again. This results in repeated waves of reperfusion. A number of arguments in favour of this concepts are discussed in this paper.

As a result of the limited sensitivity and specificity of creatine kinase and lactate dehydrogenase (LDH) as well as their isoenzymes, there is increasing interest in the use of cardiac contractile proteins for the diagnosis of acute myocardial infarction (AMI) and myocardial damage.This study compared the release of creatine kinase, creatine kinase MB, myoglobin, cardiac troponin I (cTnI), cardiac troponin T (cTnT), cardiac myosin light chain-1 (cMLC-1), and beta-type myosin heavy chains (bMHC) in serial blood samples from 13 patients (10 men, three women; median age 54 years, range 40-74 years) with first-time AMI (11 Q-wave, two non-Q-wave AMI; three anterior and 10 inferior wall AMI). All but one patient received intravenous thrombolytic treatment.Myoglobin was the first marker to increase in blood after AMI and showed the earliest peak levels, whereas bMHC increased latest, showing the latest peak levels. cTnI and cTnT increased significantly earlier than cMLC-1 and bMHC. cTnI and cTnT increased and reached peak levels parallel to each other, but the latter tended to stay increased longer. cTnT time courses were biphasic in the majority of AMI patients, unlike cTnI time courses. cMLC-1 release was mostly biphasic. cMLC-1 allows diagnosis during the acute phase as well as several days after the onset of AMI. The time courses of bMHC were usually monophasic. Its delayed appearance makes it useful for the diagnosis of remote infarction. In contrast to cTnI and cTnT, cMLC-1 and bMHC time courses were not significantly influenced by early reperfusion.Our results demonstrate the impact of the intracellular compartmentation of an intramyocardial protein (cytosolic, structurally bound, or structurally bound with soluble pool) on its concentration time course after AMI, particularly on the rapidity of its release.

Plasma concentrations of polymorphonuclear granulocytes elastase (PMN elastase) in complex with alpha-1 proteinase inhibitor are a marker of neutrophil activation. The latter complex, creatine kinase and cardiac troponin T, were measured in peripheral venous blood samples serially drawn in 39 patients with acute myocardial infarction. Of the total, 29 received intravenous thrombolytic therapy either with streptokinase (n = 15), urokinase (n = 7) or recombinant tissue type plasminogen activator (n = 7). Creatine kinase activities and cardiac troponin T concentrations were used as markers of myocardial tissue injury. In all patients with acute myocardial infarction, PMN elastase was elevated (median 80 micrograms/l, interquartile range 71 to 100 micrograms/l). Peak and cumulative (area under curve) concentrations of PMN elastase did not correlate closely with determinants of myocardial injury (r0.2, n.s.). PMN elastase increased during the first 6 h after starting thrombolytic therapy, whereas it decreased in conventionally treated patients and 12 h later increased. Maximum concentrations of PMN elastase, however, were not significantly higher in patients with thrombolytic therapy than in those without. In acute myocardial infarction patients with complications such as cardiac arrest with subsequent resuscitation (n = 5), cardiac rupture (n = 1) or cardiogenic shock (n = 2), PMN elastase plasma concentrations were significantly higher (p = 0.04) than in uncomplicated infarctions. In the complicated patients, changes in elastase concentrations paralleled or even preceded changes in the clinical presentation. Therefore, thrombolytic treatment seems not to significantly influence the amount of systemic neutrophil activation, but plasma PMN elastase could be a useful marker to monitor and identify complications in acute myocardial infarction.

Der Zweck eines Computermodells ist, bekannte Forschungsergebnisse, die in Form von Mesdaten und Strukturerkenntnissen vorliegen, optimal zu nutzen und ein besseres Verstandnis fur den Ablauf von komplexen Prozessen zu gewinnen.

Endothelin-1 concentrations were measured in peripheral venous blood samples from 42 patients with acute myocardial infarction. In patients with ischemic or hemodynamic complications (n = l1), endothelin-1 concentrations were significantly higher already on admission (P = 0.008) and remained significantly higher until day 6 after admission compared to patients with uncomplicated infarctions (n = 31; P = 0.035). There were no close correlations between peak concentrations of endothelin-1 and creatine kinase or creatine kinase isoenzyme MB mass in either group. Only in complicated patients did left ventricular ejection fraction correlate closely and inversely with peak endothelin-1 concentrations (r = −0.71; P = 0.03). Therefore, plasma endothelin-1 concentrations in patients with acute myocardial infarction patients may reflect states of markedly depressed cardiac performance and recurrent myocardial ischemia.

We investigated atrial natriuretic peptide (ANP) and cyclic guanosine monophosphate (cGMP) in patients undergoing elective direct current cardioversion (CV group) due to atrial fibrillation (n = 9) or atrial flutter (n = 3). Anesthesia for cardioversion (CV) was induced with propofol 1.5 mg/kg. Conversion was achieved in all patients. Before CV all patients had elevated ANP and cGMP plasma levels. After CV the concentrations of ANP and cGMP decreased significantly within 15 and 30 minutes (p less than 0.01), respectively. Only one patient in the CV group showed increasing ANP and cGMP levels although his heart rate had decreased after CV and his blood pressure remained stable. High concentrations of ANP and cGMP might possibly be a compensatory mechanism of cardiac dysfunction. To study the influence the anesthetic agent on plasma levels of ANP and cGMP, we investigated six patients anesthetized with propofol for high-density radiation (HDR group). The data from this control group showed that propofol did not influence the plasma levels of ANP and cGMP. ANP correlated statistically significantly (p less than 0.05) with cGMP in both groups (r = 0.88 and 0.76 in the HDR and CV groups, respectively). In addition, we found a cGMP release of 149.6 +/- 17.6 per mol ANP in the HDR group, in the CV group the release was 109 +/- 54.2 cGMP per mol ANP. This phenomenon could be due to minor response of target cells to ANP stimulation (receptor down-regulation) in patients with heart disease. In conclusion, ANP and cGMP levels decreased after successful cardioversion.(ABSTRACT TRUNCATED AT 250 WORDS)

A computer model of the entire human heart has been developed for simulation of the excitation and repolarization process. Spatial distribution of refractory periods and conduction velocities in the different cardiac tissues, the anisotropy of conduction in the ventricles, and the cycle length dependence of refractory periods and conduction velocities are taken into account. The algorithm calculating the activation process is based on a modified version of Huygen's principle for constructing wavefronts. This study presents simulations concerning the gap phenomenon of the conduction system and the initiation of tachycardias in a heart with Wolff-Parkinson-White syndrome. Results are compared for different basic cycle lengths and for normal and prolonged refractory periods in the His-Purkinje system. The gap phenomenon was found to be present only when using the prolonged refractory periods in the His-Purkinje-system at a cycle length of 700 ms. Induction of tachycardia by a single extrastimulus in the high right atrium in a heart with a bidirectionally conducting accessory pathway is possible by properly timed extrastimuli. The coupling interval of the stimulus for initiating a reentrant tachycardia depends on the cycle length, the conduction velocities and the set of refractory periods used. The same parameters determine whether or not a gap phenomenon in atrioventricular conduction occurs. The model may be useful for investigating similar questions concerning the reentry phenomena of tachycardia.

Antiplatelet therapy to prevent occlusion of coronary bypass grafts is widely used. Though the value of this therapy after bypass surgery is not yet settled, some favourable results have been achieved. Many physicians continue to use the Mayo Clinic recommendations (peri- and postoperative administration of aspirin and dipyridamole) while others used dipyridamole and aspirin after surgery, and others use aspirin alone. It is now well established that pretreatment with platelet inhibitors is effective in lowering the incidence of acute vessel closure after angioplasty: Numerous drugs, including warfarin, aspirin and dipyridamole, aspirin and heparin, nifedipine, diltiazem and the experimental antiplatelet agent ticlopidine have proved ineffective in reducing the rate of restenosis after coronary angioplasty. Only high dose administration of an omega-3 fatty acid dietary supplement for 1 week before angioplasty lowers patients' risk for restenosis, but this therapy does not appear effective if begun the night before the procedure or done with somewhat lower dose. Until additional results are available, clinicians must treat patients on extrapolation from the published trials. Low-dose aspirin should be used for several weeks after the procedure. Careful attention to risk factor modification, especially smoking, lipid profile and diabetes control, seems essential in any long-term plan of management in the patient with coronary disease.

Anaesthesia for elective direct current cardioversion (DCC) was induced with propofol (Diprivan) 1.2 mg/kg in 28 patients and with 0.2 mg/kg etomidate (Hypnomidate) in 20 patients. These mostly high risk patients (NYHA class II to III) were successfully treated with defibrillation. Blood pressure and heart rate were recorded before and after induction and at 2 minutes intervals up to 20 minutes after DCC. Both anaesthetic agents caused mild hypotension. Heart rate did not change significantly after induction but fell significantly after DCC from the mean value of 124 +/- 26 bpm and 122 +/- 37 bpm to 94 +/- 19 bpm and to 91 +/- 19 bpm in propofol and etomidate treated patients respectively. Four patients became apnoeic necessitating assisted ventilation for approximately four minutes. All propofol treated patients had rapid recovery times and opened eyes on command within 5.6 +/- 1.9 minutes after induction, and were fully orientated about 4 minutes later also. Complete amnesia was observed in all patients in this group. In contrast etomidate induced anaesthesia did not cause respiratory depression, but the recovery time was longer. Four patients of this group complained of recall of DCC. In 7 patients due to involuntary movements or myoclonus, after induction with etomidate reliable EKG monitoring appeared to be difficult.

A computer model is presented for simulation of the spread of activation and repolarization in ventricular myocardium. The program calculating the activation sequence is based on an algorithm similar to Huygen's principle of constructing wavefronts. Physiological parameters of the heart, such as areas of early activation on the endocardium, conduction velocity, anisotropy of propagation, duration of action potentials and refractory periods are taken into account. The time-course of ECG and MCG is calculated using the equations of the bidomain model. Simulation of pathologic cases of activation is performed through variation of the physiological heart parameters. The simulations presented here show good agreement of ECG and MCG with measurements in the normal case, the case of bundle branch block and abnormal repolarization. A special feature of the model is the possibility of simulating reentry rhythms following a premature stimulus in ventricular myocardium. Two kinds of reentry are simulated: reentry around an anatomical obstacle and the leading-circle model. The widespread capability for investigating not only ECG but also MCG and various kinds of pathologic activation patterns including reentry rhythms indicates that the model may be useful in studying numerous problems in cardiologic research.

Summary. Acute myocardial infarction (AMI) can no longer be considered as a single event, but as a series of episodes. In most of the cases, the initial event may be the induction of a severe spasm of the coronary artery by vasoconstrictive substance released from aggregated platelets. These spasms are followed by dilatation, which is caused by substances set free from the ischemic tissue. Dilatation then results in a washing-out of vasoactive mediators (as well as myoglobin) and platelets, which is reflected as a peak in the blood myoglobin concentration—time curve. The local depletion of vasodilative metabolites allows a further contraction of the coronary vessel. A new accumulation of platelets then stimulates another spasm. This vicious circle (thrombo-ischemic re-entry-mechanism) is repeated several times and can be interrupted by the systemic administration of thrombolytic drugs (streptokinase).

Das Auftreten von unreifzelligen LeukAmien wAhrend der Schwangerschaft ist Au\erst selten. Auf der mutterlichen Seite bedarf die unbe-handelt rasch zum Tode fuhrende Erkrankung meist der sofortigen, aggressiven Chemotherapie. Diese ist jedoch insbesondere wAhrend der Fruhschwangerschaft durch die Moglichkeit irreversibler SchAdigungen der Leibesfrucht belastet. Die Problematik dieser Konstellation soll hier am Beispiel einer erfolgversprechenden Remissionsinduktion ohne derzeit fa\bare SchAdigung des Kindes bei akuter, kompliziert verlaufender PromyleozytenleukAmie diskutiert werden.

This paper describes an ECG analysing system, which simultaneously analyses six different ECG leads of patients with acute myocardial infarction (tissue which is dying because the blood supply has been cut off). Three characteristic ECG features (height of the R-spike, existence of a Q-spike and the ST-segment elevation) are measured, and their means over time intervals, the length of which can be chosen at the beginning of the measurement, are computed and printed. The analyser works online, therefore the measuring period is not limited.

In a multicenter, parallel, double-blind study, lisinopril was compared with atenolol in the treatment of mild to moderate essential hypertension. Four hundred ninety patients were randomized to a once-a-day treatment with lisinopril 20 mg or atenolol 50 mg for 4 weeks, and the doses of lisinopril or atenolol were increased up to 80 mg or 200 mg, respectively, at 4-week intervals if sitting diastolic blood pressure (SDBP) was not well controlled. Hydrochlorothiazide (HCTZ) 12.5 or 25 mg was added after 12 weeks, if necessary, and titrated upward after 4 weeks to a maximum dose of 25 or 50 mg/day. Lisinopril and atenolol reduced SDBP to a similar extent. All reductions from baseline in sitting diastolic and systolic blood pressure were significant (less than 0.01). Lisinopril produced a significant (less than 0.01) greater reduction in sitting systolic blood pressure (SSBP) than atenolol. Addition of HCTZ caused further blood pressure reductions (p less than 0.01). Five patients (1.7%) on lisinopril and four (2.0%) on atenolol developed skin rashes during weeks 1-12. Two patients (0.7%) on lisinopril 80 mg developed proteinuria (greater than 1 g/day). Cough occurred more often with lisinopril (4.5%), and elevated triglycerides occurred more often with atenolol (2.0%).

Myoglobinemia in acute myocardial infarction (AMI) shows atypical profile in its time course. Multiple peaks are noted during the early phase of AMI, which is called ‘staccato phenomenon’. We observed that this phenomenon changed under thrombolytic treatment (streptokinase, 500 000 to 1000 000 IU as a single dose i.v.) within the first 4 h after onset of symptoms. Out of a group of 22 patients (8 control subjects), 14 received intravenous short term infusion of streptokinase. Six of them showed 1 peak (298.33 ± 23.58 min after onset of symptoms), six showed 2 peaks (after 192 ± 17.72 and 220.2 ± 63.84 min), one streptokinase patient died during the investigation, one showed 4 peaks in the myoglobin curve and, remarkably, also 3 peaks in the CK-time course. In the control group we observed 3–4 peaks in the myoglobin curve. Myoglobin was assessed by use of radioimmunoassay. Our findings indicate a possible relation between the presence of a thrombus and the discontinuity of myoglobin release. Successful reperfusion is reflected in the disappearance of the typical staccato phenomenon.

1. Die Wirkung von Propranolol (eine adrenergischeβ-Receptoren blockierende Substanz) und einer intravenosen Adrenalininfusion vor und nach Propranolol wurde an funf kreislaufgesunden Personen untersucht. Blutdruck, Herzfrequenz und Mechanokardiogramm wurden registriert.

Durch die Infusion von Propranolol kommt es beim Menschen zu einer Senkung der Konzentration der freien Fettsauren, zu einer signifikanten Erniedrigung der Umsatzrate der freien Fettsauren und einer signifikanten Erniedrigung der „Fractional turnover rate“ der freien Fettsauren im Plasma. Die Bildung der endogenen Plasmatriglyceride aus freien Fettsauren wird signifikant erniedrigt.

A method is described for the quantitative determination of alkaline lipase activity of blood cells. The pH optimum of the enzyme in macrophages and lymphocytes from patients with chronic lymph-leukemia is 9.2, the optimum substrate (triglyceride) concentration is 7 x 10-2 M, and the Michaelis constant approximately 4.3 x 10-2 M. Macrophages from guinea pigs exhibit a lipase activity approximately 10 times that of granulocytes and lymphocytes. In granulocytosis an acid lipase could also be demonstrated. The physiologic importance of this finding is discussed.

1. Die Spaltung vonl-Leucyl-β-naphthylamid-HCl durch Cytolysate von weisen Blutzellen wird biochemisch gemessen. Normale Granulocyten, Zellen von chronischen Myelosen und Meerschweinchen-Makrophagen weisen einen etwa dreifach hoheren Enzymgehalt als Lymphocyten von chronischen Lymphadenosen auf. 2. Das pH-Optimum betragt 7,1, Mangan-Ionen (5×10−5 Mol/l, pH 7,1) bewirken keine Aktivierung, im alkalischen Bereich und in hoherer Konzentration wird eine Hemmung beobachtet. Unter den gegebenen Versuchsbedingungen folgt die LNA-Spaltung einer Reaktion nullter Ordnung. Das Substrat-Optimum liegt bei 5×10−4 Mol/l. Die Michaelis-Konstante betragt 5×10−5 Mol/l. 3. Das untersuchte Enzym weist dieselben Eigenschaften auf, wie sie fur LNA spaltende Enzyme anderer Gewebe beschrieben wurden, unterscheidet sich jedoch von der Leucinaminopeptidase.

1. Bei 16 stoffwechselgesunden Personen wurden die Umsatzrate der freien Fettsauren im Plasma und die Einbaurate von freien Fettsauren in Plasmatriglyceride unter gleichzeitiger Infusion von Noradrenalin (0,25γ/min/kg) bestimmt. 2. Die Infusion von Noradrenalin in der angegebenen Dosierung bewirkte einen Anstieg der Konzentration der freien Fettsauren im Mittel um 100,6% ± 49,35 des Ausgangswertes sowie eine Erhohung des Blutzuckerspiegels im Mittel um 11,38 mg-% ± 4,18. Die Umsatzrate der freien Fettsauren war unter der Wirkung von Noradrenalin im Mittel signifikant hoher als bei einer Kontrollgruppe von elf Normalpersonen ohne Noradrenalin. Die „Fractional turnover rate“ war unter Noradrenalin gegenuber der Kontrollgruppe signifikant erniedrigt. 3. Die Infusion von Adrenalin (0,25, 0,125 bzw. 0,063γ/min/kg) bewirkte in jeder der drei Dosierungen einen wesentlich starkeren Anstieg der Blutzuckerkonzentration als Noradrenalin; die Konzentration der freien Fettsauren im Plasma nahm nach Beginn der Adrenalininfusion deutlich zu, begann aber bereits wahrend der ersten Stunde der Infusion wieder deutlich abzusinken. Da somit hinsichtlich des Fettsaureumsatzes kein „steady state“ bestand, konnten der Fettsaureumsatz und die Einbaurate von freien Fettsauren in Plasmatriglyceride mit den angegebenen Formeln nicht exakt berechnet werden. 4. Unter der Wirkung von Noradrenalin lies sich eine positive Korrelation zwischen Umsatzrate der freien Fettsauren und Konzentration der freien Fettsauren im arteriellen Plasma nachweisen. 5. Die Einbaurate von freien Fettsauren in Plasmatriglyceride war unter der Wirkung von Noradrenalin gegenuber der Kontrollgruppe im Mittel zwar erhoht, der Unterschied lies sich aber statistisch nicht sichern. 6. Im Gegensatz zur Kontrollgruppe lies sich wahrend der Infusion von Noradrenalin keine Beziehung zwischen Umsatzrate der freien Fettsauren und Einbaurate von freien Fettsauren in Plasmatriglyceride nachweisen. Im allgemeinen reagieren nur Personen mit einem hoheren Plasmatriglyceridspiegel auf Noradrenalin mit einer der hohen Fettsaureumsatzrate entsprechenden Steigerung der Plasmatriglyceridsynthese. Es besteht demnach wahrscheinlich auch gegenuber endogenem Noradrenalin eine individuelle Empfindlichkeit. 7. Bei stoffwechselgesunden Personen lies sich eine positive Korrelation zwischen Logarithmus des Plasmatriglyceridspiegels im Nuchternzustand und Plasmatriglyceridbildung unter Noradrenalin nachweisen. Es konnte weiters gezeigt werden, das bei denselben Personen unter Noradrenalin ein umso hoherer Anteil der umgesetzten freien Fettsauren in Plasmatriglyceride eingebaut wird, je hoher die Plasmatriglyceridkonzentration vor der Verabreichung von Noradrenalin war.

Lymphoide Zellen aus Lymphknoten von Patienten mit primar chronischer Polyarthritis aggregieren um menschliche Amnionzellen in Zellkultur und zerstoren sie zum Teil. Lymphoidzellen von Normalpersonen zeigen keine derartige Wirkung. Die Beziehung dieser Erscheinung mit der Allergie vom verzogerten Typ und dem Rundzellinfiltrat wird kurz besprochen.

Es wird uber 8 Patientinnen mit verschiedenen hamatologischen Erkrankungen (primare und sekundare Thrombopenic, Thrombasthenie) berichtet, bei denen schwere Meno- und Metrorrhagien durch Ovulationshemmer (Kombinationspraparate Anovlar oder Lyndiol) unterdruckt werden konnten. Die Behandlung kann ohne Schaden fur die Patienten uber einen langen Zeitraum fortgesetzt werden. Die Wirkung der Praparate ist prompt reversibel.

An drei kreislaufgesunden Mannern wurde die Wirkung einer Adrenalininfusion nach Ausschaltung derβ-Receptoren durch Propranolol auf Blutdruck und Mechanokardiogramm vor und nach intravenoser Gabe von Atropin gepruft.