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Biomedical subjects

C Müller

Publications and source records attributed to C Müller.

At least 505 records · Page 28Linked to original sources
PubMed1991

Cardiac left ventricular function before and during early thyroxine treatment in severe hypothyroidism.

In some patients with severe hypothyroidism, thyroxine replacement therapy precipitates or aggravates angina pectoris, whereas in other patients angina pectoris is ameliorated or even cured. Cardiac function in eight severely hypothyroid patients was studied by means of radionuclide ventriculography (RNV) at rest and during supine bicycle exercise before thyroxine treatment, and repeated during treatment before and after administration of 160 mg of oral verapamil. There was an exercise-induced fall in left ventricular ejection fraction (LVEF) in two patients before therapy, and in two additional subjects after 17 d on suboptimal doses of thyroxine. Verapamil attenuated the fall and induced a significant increase in LVEF during exercise (P less than 0.014). No abnormal regional cardiac wall movement (RWM) was observed. After 2 months of thyroxine treatment, LVEF increased significantly during exercise both before and after verapamil (P less than 0.012 and P less than 0.005). These findings are indicative of reversible coronary artery dysfunction. We recommend that, if feasible, thyroxine should be supplemented with verapamil during the early phase of treatment.

Adult↗
PubMed1991

Phenotypes of peripheral blood lymphocytes during acute hepatitis A.

We investigated peripheral blood lymphocyte phenotypes of 74 patients at weekly intervals during the course of acute hepatitis A. In the second week after onset of jaundice, a significant elevation of total lymphocytes was observed (4,096 X 10(6) +/- 1,003 X 10(6)/l vs. controls 3,038 X 10(6) +/- 1,208 X 10(6)/l, p less than 0.005). However, no change in the relative percentage of B-cells (CD20+), T-cells (CD3+ or CD2+), or T-cell subpopulations (CD4+ helper cells and CD8+ suppressor cells) could be demonstrated during the course of the disease. Activated T-cells (CD3+ DR+) were elevated during the first week (204 X 10(6) +/- 134 X 10(6)l vs. normal 91 X 10(6) +/- 54 X 10(6)/l, p less than 0.005) and during the second week (202 X 10(6) +/- 82 X 10(6)/l, p less than 0.0005) after onset of disease and returned to normal values until the third week. Cells expressing phenotypes of lymphocytes capable of exerting non-MHC-restricted cellular cytotoxicity, i.e. Natural Killer cell activity (CD57+, CD16+, and CD56+) were significantly elevated in percentage in the first week of disease, as compared to controls (CD57: 14.5 +/- 7.0% vs. 9.3 +/- 5.8%, p less than 0.05; CD16: 13.4 +/- 7.3 vs. 9.5 +/- 5.1%, p less than 0.05; CD56: 10.5 +/- 3.5% vs. 8.0 +/- 1.5%, p less than 0.005). Also the absolute numbers of these lymphocyte subpopulations were found to be elevated during the first and second week. The increase in NK cells in the initial phase of acute hepatitis A suggests an important role of these cells in the first line of defence in this disease.

Acute Disease↗
PubMed1991

Expression of T-cell-associated serine proteinase 1 during murine Leishmania major infection correlates with susceptibility to disease.

The expression of T-cell-associated serine proteinase 1 (MTSP-1) in vivo during Leishmania major infection was analyzed in genetically resistant C57BL/6 mice and in genetically susceptible BALB/c mice. Using a monoclonal antibody as well as an RNA probe specific for MTSP-1 to stain tissue sections, we found T cells expressing MTSP-1 in skin lesions and spleens of mice of both strains. In skin lesions, MTSP-1-positive T cells could be detected as early as 3 days after infection. Most importantly, the frequency of T cells expressing MTSP-1 was significantly higher in susceptible BALB/c mice than in resistant C57BL/6 mice. These findings suggest that MTSP-1 is associated with disease-promoting T cells and that it may be an effector molecule involved in the pathogenesis of cutaneous leishmaniasis.

Animals↗
PubMed1991

Model for skeletal muscle ischemia in rat hindlimb: evaluation of reperfusion and necrosis.

In this study we describe a technique for complete arrest of blood flow in rat hindlimbs. After graded periods of ischemia, immediate reperfusion in the leg was demonstrated by direct microscopy and scintigraphy. Laser Doppler flowmetry indicated microvascular hypoperfusion in the anterior tibial muscle during the first 2 h of reperfusion. The extent and distribution of necrosis in the middle part of the anterior tibial muscle of the legs were determined histologically 3 days after the ischemic insult. We found a reproducible degree of necrosis under constant experimental conditions. The necrosis was most pronounced in the central part of the muscle, leaving the subfascial fibers undamaged. After 4.0 h of ischemia, 46% of the cross-section area was necrotic. After 4.5 h, the necrosis increased to 70%. This difference was significant. Two types of necrotic zones were detected. One type was characterized by numerous macrophages and partial resorption of the muscle fibers, the other by a lack of macrophages and no resorption. Most cases with little damage had only the first type of necrosis, while most cases with extensive damage had both types. The areas that had no signs of resorption and therefore had been without circulation during most of the postischemic period, measured 8% after 4.0 h of ischemia and 22% after 4.5 h.

Animals↗
PubMed1991

Increased Fc-receptor-mediated clearance via reticuloendothelial system in patients with nephrotic syndrome.

Reticuloendothelial phagocytic cell function, which is an important participant in host defense, was investigated by studying the Fc-receptor-mediated clearance of IgG-anti-RhD-sensitized radiolabelled autologous erythrocytes in patients with nephrotic syndrome known to have an increased risk of infectious complications due to hypogammaglobulinemia. Patients with serum IgG concentrations less than 500 mg/dl had a significantly accelerated Fc-receptor-mediated clearance (t1/2 = 52 +/- 3.6 min) compared to patients with IgG levels greater than 500 mg/dl (t1/2 = 93 +/- 17 min) or healthy controls (t1/2 = 100 +/- 7.5 min). Serum IgG concentrations correlated significantly with Fc-receptor-mediated clearance (t1/2: r = 0.70; p = 0.035) in patients with nephrotic syndrome. These results indicate that Fc-receptor-mediated clearance by the reticuloendothelial system is enhanced in patients with nephrotic syndrome with low serum IgG concentrations and may, at least in part, compensate for reduced opsonic antibody concentration.

Adult↗
PubMed1991

Leukotriene B4 and tumor necrosis factor release from leukocytes: effect of peritoneal dialysate.

The effect of peritoneal dialysate on the capacity of peripheral blood polymorphonuclear (PMNL) and mononuclear leukocytes (MNC) to release leukotriene B4 (LTB4) and tumor necrosis factor alpha (TNF alpha) was investigated in vitro. Following density gradient separation, aliquots of 5 x 10(6) PMNL or MNC were incubated in peritoneal dialysis fluid containing 1.5% glucose or Hanks' buffer (= control) for 1-2 h at 37 degrees C. TNF alpha and LTB4 production was stimulated with Escherichia coli lipopolysaccharide (LPS) and calcium ionophore A23187, respectively. MNC incubated in buffer and LPS produced (mean +/- SD) 1,006 +/- 522 pg TNF alpha/5 x 10(6) cells; no significant amounts of TNF alpha were detectable in the presence of dialysate. An inhibition of TNF alpha release was also observed in MNC exposed to bicarbonate-buffered dialysates (pH 7.40) and 4.25% and 1.5% glucose solution with physiologic osmolality. Incubation of PMNL in Hanks' buffer followed by A23187 stimulation led to production of 29.1 +/- 19.2 ng LTB4/5 x 10(6) cells, whereas glucose-incubated cells were refractory to ionophore stimulation (less than 0.1 ng LTB4/5 x 10(6) cells). The failure of dialysate-exposed leukocytes to release inflammatory mediators in response to adequate stimuli may contribute to the impairment of cellular host defense in the setting of continuous ambulatory peritoneal dialysis.

Calcimycin↗
PubMed1991

Helper-inducer and suppressor-inducer lymphocyte subsets in alcoholic cirrhosis.

Peripheral blood lymphocytes from patients with alcoholic cirrhosis, alcohol-induced fatty liver, and healthy controls were analyzed for helper-inducer (CD4+CD29w+) and suppressor-inducer (CD4+CD45R+) T lymphocytes. In confirmation of earlier reports, patients with alcoholic cirrhosis were found to have a significantly reduced absolute number of peripheral lymphocytes (p = 0.03), an elevated relative percentage of CD3+ cells (median, 76% versus 68%; p = 0.0004) and CD4+ T cells (median, 56% versus 51%; p = 0.0011), and a reduced percentage of CD8+ T lymphocytes (median, 11% versus 20%; p = 0.0007) as compared with the control group. No difference in lymphocyte subsets was observed between controls and patients with alcohol-induced fatty liver. Within the CD4+ T-cell population a change in the relative proportion of two complementary lymphocyte subsets (CD4+CD29+ helper-inducer and CD4+CD45R+ suppressor-inducer T cells) was observed in patients with alcoholic cirrhosis: a higher percentage of CD4+CD29w+ helper-inducer T cells were circulating in their peripheral blood than in healthy controls (median, 33% versus 28%; p = 0.0036), whereas the CD4+CD45R+ suppressor-inducer T-cell subset did not differ (median, 21% versus 21%) between the two groups. Owing to the reduction of lymphocyte counts in cirrhotic patients the absolute number of CD4+CD29w+ cells was not different from that of control individuals; however, CD4+CD45R+ T cells in peripheral blood (p = 0.0063) were absolutely reduced. More CD4+ cells were simultaneously CD29w+ in cirrhotic patients (61%) than in controls (52%), whereas a lower percentage of CD4+ lymphocytes was also CD45R+ in these patients (33%) as compared with controls (40%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Quantification of human hepatic binding protein (HBP) via 99mTc-galactosyl-neoglycoalbumin (NGA) liver scintigraphy.

99mTc-galactosyl-neoglycoalbumin (99mTc-NGA) was synthesized by covalent coupling of 2-imino-2-methoxyethyl-1-thio-beta-D-galactopyranoside to the primary amino groups of human serum albumin. Injection of 99mTc-NGA (150 MBq; 3.5 mg (= 50 nmol)/ml demonstrated the liver to be the exclusive site of tracer-uptake. Simulation of 99mTc-NGA-kinetics allowed quantification of binding to the hepatic binding protein (HBP). Using this model we studied 250 patients with various liver disease. In alcoholic liver cirrhosis such patients with Child B and Child C stage cirrhosis had a lower HBP-concentration in the liver compared to control individuals (0.85-1.2 mumol/l). The group with the most advanced cirrhosis (Child C stage) had a significantly lower HBP-concentration (0.20-0.45 mumol/l) than Child A patients (0.60-0.85 mumol/l; p less than 0.01) and Child B patients (0.45-0.60 mumol/l; p less than 0.05). In patients with biopsy proven liver fibrosis (0.80-1.22 mumol/l) no difference in receptor concentration to normal individuals was estimated. Patients with recently diagnosed acute viral hepatitis underwent repeated 99mTc-galactosyl-neoglycoalbumin (NGA) scanning of the liver during the course of the disease. Return of liver function tests to normal values was associated with an increased hepatic imaging size as well as increase in HBP-concentration (up to a 3-fold of initial concentration). In patients exhibiting a prolonged course of the disease changes in NGA-kinetic data were borderline and the hepatic image size unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗
PubMed1991

["Routine" versus "on demand" ultrasonography in the surgical intensive care patient. A prospective randomized study].

Between May 1988 und March 1989 all patients who underwent elective or emergency surgery followed by intensive care were randomly assigned to group A (n = 149): routine sonography at the postoperative day 1, 3, 7 and 9, group B (n = 151): sonography on demand. In these two groups, the following parameters were compared: number of relaparotomies, lethality of relaparotomies, total lethality, moment of relaparotomy, period of hospitalisation, time spent with sonography. In the analyzed parameters, our examination showed no difference between the two groups. For this we state that the routine sonographical control of the surgical patient with intensive care being opposed to the sonography on demand shows no significant advantage. The demand for a routine sonography as a postoperative control can not be generally supported.

Adult↗
PubMed1990

[Postoperative supraventricular arrhythmias in atrial septal defects].

Before operation as well as over a mean postoperative period of 8.9 years 222 adults with atrial septal defects underwent a follow-up examination concerning frequency and clinical significance of supraventricular dysrhythmias. Thereby disturbances of the formation of stimuli were found before the operative procedure in 60 patients and after the correction in 115 patients. Disturbances of the sinoatrial and atrioventricular conduction were registered preoperatively in 53 cases and postoperatively in 81 cases. Within these statistically significant increases in particular the significant forms of dysrhythmia elevated after the atrial septal defect closure. Thus the tachycardiac atrial dysrhythmias increased from 7 to 28%, complex arrhythmias even from 2 to 16%. Of dysrhythmias to be taken seriously patients with IAVC and supraventricular defect are significantly more frequently affected than those with interatrial septal defects. Size of the defect, shunt volume and pressure of the pulmonary artery did not show any connections with the frequency of dysrhythmia. On the other hand, when accompanying cardiac anomalies, symptoms of a manifest heart insufficiency were present and at an operation age over 40 years arrhythmias were proved more frequently. The complaints of the patients did not correlate with the endangering, but are imprinted by the haemodynamics and its postoperative normalization. By the established profile of complaints and a decrease of frequency from 76% pre- to only 40% postoperative the patient with atrial septal defect cannot estimate his individual risk and needs an adapted long-term concept for his cardiological care.

Adolescent↗
PubMed1990

Impaired lipopolysaccharide-inducible tumor necrosis factor production in vitro by peripheral blood monocytes of patients with viral hepatitis.

We investigated lipopolysaccharide-induced tumor necrosis factor production in vitro by peripheral blood monocytes from patients with various liver diseases. Tumor necrosis factor production was found to be significantly reduced in patients with chronic hepatitis B (n = 17; 135 +/- 30 pg tumor necrosis factor/ml; mean +/- S.E.M.) and patients with chronic non-A, non-B hepatitis (n = 15; 212 +/- 22 pg tumor necrosis factor/ml) compared with healthy control individuals (n = 47; 411 +/- 40 pg tumor necrosis factor/ml; p less than 0.0005 and p less than 0.01, respectively). This reduced tumor necrosis factor production was not only seen with an optimal stimulating concentration of lipopolysaccharide (100 ng/ml) but also with suboptimal concentrations (0.1 ng/ml). In contrast to patients with chronic viral hepatitis, monocytes from patients with alcohol-induced cirrhosis (n = 26; 444 +/- 49 pg tumor necrosis factor/ml), primary biliary cirrhosis (n = 7; 412 +/- 81 pg tumor necrosis factor/ml) and alcohol-induced fatty liver changes (n = 5; 401 +/- 62 pg tumor necrosis factor/ml) produced normal amounts of tumor necrosis factor when stimulated with an optimal concentration of lipopolysaccharide. Lipopolysaccharide (0.1 ng lipopolysaccharide/ml)-stimulated peripheral blood monocytes of patients with chronic hepatitis B (n = 15; 102 +/- 32 pg/ml) or non-A, non-B hepatitis (n = 13; 97+/- 16 pg/ml) could not be induced to produce more tumor necrosis factor either when prestimulated with gamma-interferon (170 +/- 45 pg/ml and 149 +/- 32 pg/ml, respectively), a lymphokine known to activate monocytes, or with the cyclooxygenase inhibitor indomethacin to reduce the suppressive effect of prostaglandin E2 (148 +/- 40 pg/ml and 153 +/- 45 pg/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗