[Maturwissenschaften und Medizin in Deutschland. Biomedizinische Technik].
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Biomedical subjects
Publications and source records attributed to H Buss.
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In animal experiments the ligation of the left renal vein after nephrectomy on the right side and the ligation of the suprarenal inferior vena cava is explored by four different methods. Degree and length of postoperative renal dysfunction depend on the preliminary ligation or the narrowing of the suprarenal inferior vena cava. The period of adaptation is correlated to the development of a collateral circulation of the left renal vein.
In 50 patients with proven acute myocardial infarction (AMI), left ventricular hemodynamics (pulmonary end-diastolic pressure [PAEDP]; cardiac index [CI]; stroke volume index [SVI]; and SVI/PAEDP were related to the size of the acute infarct. Acute infarct mass was calculated from serial determinations of serum creatine phosphokinase (CPK) every two hours, using a computer program. In 15 cases postmortem measurement of acute infarct size after staining with Nitro-BT was made and correlated with calculated infarct size. Correlation in this limited number of cases was good with a mean difference of 7 g. Acute infarct mass in 38 survivors was 46 +/- 5 g and was significantly smaller (P less than 0.05) than in the 12 nonsurvivors (76 +/- 12 g.) PAEDP in surviving patients was significantly lower (17 +/- 1 mm Hg) and SVI (36 ml/m2) and SVI/PAEDP (2.4 ml/m2/mm Hg) significantly higher than in the nonsurvivors (PAEDP: 24 mm Hg; SVI: 23 ml/m2; SVI/PAEDP: 0.86 ml/m2/mm Hg) (P less than 0.001 for all differences). Similar significant differences were observed between patients not in shock and those in cardiogenic shock. Although in 39 patients, in whom the infarction was their first, infarct mass was larger (58 +/- 6 g) than in 11 patients with repeat infarctions (37 +/- 8 g), left ventricular hemodynamics were slightly more impaired in reinfarctions (PAEDP: 21 +/- 3 mm Hg; CI:2.60 L/min/m2) than in first infarctions (PAEDP: 18 +/- 1 mm Hg; CI:2.82 L/min/m2). The occurrence of cardiogenic shock was a strong predictor of death; however, the wide scatter of the data for the parameters cardiac index, PAEDP, and acute acute infarct mass precluded their usefulness, when taken individually, in predicting survival. When a relationship between hemodynamics and infarct size was looked for, four constellations of individual patients were identified. These groups were defined by PAEDPs of above or below 18 mm Hg and infarct sizes above or below 65 g. Class A patients (N = 22) had a small infarct (29 +/- 4 g) and good pump function (PAEDP: 13 mm Hg; SVI: 40 ml/m2; SVI/PAEDP: 3.27 ml/m2/mm Hg); prognosis was good for these patients. In class B (N = 13) the infarct was large (96 +/- 8 g) and pump function markedly impaired (PAEDP: 26 mm Hg; SVI: 24 ml/m2; SVI/PAEDP: 0.98 ml/m2/mm Hg); 54% of these patients died. Five patients in class C had, in the presence of a large infarct (84 g), only a slightly elevated PAEDP of 17 mm Hg and an almost normal SVI of 37 ml/m2. In contrast, the ten class D patients had an infarct size (34 g) similar to that in class A, but high PAEDP (23 mm Hg) and moderately reduced SVI (31 ml/m2). In this group a high incidence of reinfarctions (six out of ten) occurred. It is concluded that infarct mass calculated from serial CPK analysis, as a single parameter, cannot be used to predict mortality or development of cardiogenic shock in an individual patient.
Acute infarct size was estimated from serial determinations of creatine-kinase (CK) activity. In 15 patients the infarct size was obtained post-mortem, using nitro-blue-tetrazolium stain. There was good correlation between the two measurements (r = 0.98). The relationship between the calculated infarct size and haemodynamic values was obtained in 50 patients (end-diastolic pulmonary arterial pressure [PAEDP], cardiac output, stroke volume, stroke volume/filling pressure of left ventricle [SVI/PAEDP]). On average there was a tendency towards impaired left ventricular haemodynamics with increasing infarct size. Among the survivors the infarct size (51 g) was significantly less (P less than 0.05) than that of those who had died (83 g). PAEDP at 24 mm Hg was significantly higher in those who died than in the survivors (17 mm Hg), cardiac index was 2.95 l/min-m2 in the survivors compared with 2.14 l/min-m2, while SVI/PAEDP was 2.4 ml/m2-mm Hg in the former and 0.9 ml/m2-mm Hg in the latter. However, in individual cases the infarct size sometimes did not correlate with haemodynamic values. Taking into account infarct size and haemodynamics, four classes could be distinguished: (a) infarct size less than 65 g with good haemodynamics (PAEDP less than 18 mm Hg, normal cardiac index); (b) infarct size greater than 65 g with PAEDP greater than 18 mm Hg and markedly reduced cardiac index). Only 10% of those a to c had previously had infarcts, compared with 60% of those in class d (infarct less than 65 g, PAEDP above 18 mm Hg). Small infarcts with markedly impaired haemodynamics thus indicate that there has been previous damage to remaining myocardium.
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In two Turkish female patients, aged 14 and 29 years, with familial mediterranean fever amyloidosis of the perireticular type was found. The disease was characterized by feverish bouts, abdominal colics, and joint involvements. The younger patient had the diagnosis confirmed at an early stage by renal biopsy, and under heparin and azathioprine the clinical signs, especially the nephrotic syndrome, regressed over a period of seven months. The second patient died of treatment-resistant shock in acute renal failure, due to rapidly progressing renal amyloidosis.
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Rats with a nephrotoxic serum nephritis reveal changes of proteinuria and content of serum proteins as well as serum cholesterol in the direction of a nephrotic syndrome as is seen after Daunomycin. Nevertheless, the morphological findings with TEM and especially with SEM are quite different. A striking feature of the nephritis is the rather good preservation of cell processes through all the time of experiment in spite of the elevated proteinuria. Moreover, podocytes with furrowed or ribbed surfaces originate and are most numerous when the signs of inflammation are most pronounced. These furrowed podocytes are interpreted as representing a special reactive, perhaps mobilized form. With SEM it is evident that the glomeruli are altered focally and segmentally in the nephrotoxic serum nephritis.
Creatine kinase (CK) release curves were analysed in 40 patients with acute myocardial infarction. Three groups could be identified. Group A (duration of CK release less than 30 hours) comprised 15 patients whose CK release was completed within 22.8 hours. In these patients chest pain was noted on the first hospital day and necropsy in three showed a homogeneous myocardial infarction. Group B (duration of CK release greater then 30 hours) comprised 16 patients who had a significantly longer CK release time of 42.2 hours (P less than or equal to 0.05). Their chest pain persisted for two to three days and pathological examination in five patients showed a heterogeneous composition of the infarcted myocardium. Group C comprised nine patients who had a second rise of serum CK. This was always associated with chest pain. It reflected an extension of the infarct which accounted on average for 24 per cent of the size of the final infarct. We concluded that a CK release of short duration indicated infarction without extension, CK release of longer duration indicated a gradual extension of infarction, and a repeated CK release resulted from a sudden extension of an infarct. According to these criteria an extension of the infarct occurred in 62 per cent of our patients.
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