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Biomedical subjects

J Fuchs

Publications and source records attributed to J Fuchs.

At least 91 records · Page 5Linked to original sources
PubMed1987

Plasma viscosity and haematocrit in the course of acute myocardial infarction.

Plasma viscosity and haematocrit were determined in 44 patients with acute myocardial infarction on the 1st, 2nd, 3rd and 10th day of hospitalization. The highest haematocrit value for the entire group was found on the 1st day of acute myocardial infarction--43.3 SD +/- 4.6% declining progressively to 38.8 SD +/- 3.5% on the 10th day (P less than 0.001). Plasma viscosity for the entire group was normal on the first day of acute myocardial infarction (1.44 SD +/- 0.10 cp) and started to increase on the second day (1.51 SD +/- 0.16 cp, P less than 0.001). A relationship was found between reinfarction or death (17 patients) occurring during hospitalization and changes in haematocrit and plasma viscosity. In this group plasma viscosity rose to 1.63 SD +/- 0.19 cp on the second day of acute myocardial infarction (P less than 0.001 vs plasma viscosity value on the first day). This elevation persisted on the third day. Haematocrit values in this group were 47.9 SD +/- 3.6% on the first day of acute myocardial infarction declining progressively and significantly afterwards. In the remaining patients both plasma viscosity and haematocrit were normal and did not change. No correlation of plasma viscosity and haematocrit were found when tested for other clinical complications, sex, age, maximal creatine phosphokinase values and coronary risk factors. We suggest that variations in haematocrit and plasma viscosity during acute myocardial infarction exist in a group of patients in whom reinfarction or death occurs. The changes in haematocrit and plasma viscosity precede the complications by 4-8 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Room temperature ADP induced first stage hyperaggregation of human blood platelets: a previously undescribed phenomenon and its relationship to spontaneous cold induced platelet aggregation.

ADP induced human platelet aggregation was shown to be accentuated when tested at 20-30 degrees C as increased sensitivity and as a greater change of optical density although second stage aggregation and the release reaction did not occur. This previously undescribed phenomenon is defined as room temperature ADP induced first stage hyperaggregation. Aggregation, which occurs under the above mentioned conditions with a quantity of ADP insufficient to maintain the aggregation (usually less than 1.5 micron), is reversible when the temperature is raised to 37 degrees C. After rewarming to these temperatures, second stage aggregation appeared in the presence of larger quantities of ADP (usually more than 2 microns) and could be blocked by aspirin. The absence of the release reaction was demonstrated with a lumi-aggregometer. Spontaneous cold induced platelet aggregation seen after chilling platelets to 0-4 degrees C is shown to be a distinct phenomenon.

Adenosine Diphosphate↗
PubMed1987

Acute transmural myocardial infarction in elderly patients hospitalized in the coronary care unit versus the general medical ward.

The hospital records of 126 patients over 75 years of age with transmural myocardial infarction initially treated in the coronary care unit were compared with a concurrent similar group of 94 patients admitted directly to the general medical wards. The in-hospital mortality rate for both groups together was 40%. The mortality rate within the coronary care unit was 24% as compared with 46% in the ward group (P less than 0.005). However, the mortality rate for the coronary care unit group as a whole (including those patients later transferred to the general ward) was 35 versus 46% in the ward group. Congestive heart failure and cardiogenic shock were the most frequent complications in both groups (47 and 30%, respectively), and they were the main cause of death. Patients with these complications were less likely to be successfully resuscitated, even in the coronary care unit. The overall incidence of serious ventricular arrhythmias and complete heart block was similar to that reported for younger patients. Eleven patients in the coronary care unit group were successfully resuscitated from these arrhythmias and eight survived to be discharged from hospital. In contrast, only two patients in the ward group were successfully resuscitated and eight (9%) patients died suddenly and the fatal event could not be diagnosed. We concluded that elderly patients with an acute myocardial infarction can benefit from early admission to a coronary care unit.

Aged↗
PubMed1987

Prosthetic valve endocarditis caused by Acinetobacter calcoaceticus subsp. lwoffi.

Acinetobacter spp. are uncommon etiologic agents of prosthetic valve endocarditis. Two patients with Acinetobacter calcoaceticus subsp. lwoffi prosthetic valve endocarditis are described. The patients were successfully treated with antibiotics (cefotaxime sodium and gentamicin sulfate); thus, we suggest medical treatment rather than early valve replacement in this particular type of infection.

Acinetobacter Infections↗
PubMed1987

Improvement of myocardial function after global hypoxia by protection of the inner mitochondrial membrane.

In the present study the hypothesis is tested that hypoxia causes morphological damage to the inner mitochondrial membrane and that this damage can be reversed by modification of the reoxygenated perfusate. Using the working rat heart model, hearts in group I (n = 40) were subjected to a 30 min normothermic, normoxic phase and a 90 min hypoxic phase, followed by 60 min reoxygenation. Hearts in group II (n = 32) were also subjected to a 30 min normoxic and a 90 min hypoxic phase. However, after 30 min of reoxygenation 1.5 mmol/l 2-mercaptopropionylglycine (MPG) was injected in the reoxygenated solution in order to test its ability to improve mitochondrial function. Mitochondrial function was assessed by measuring oxygen uptake (ST3), ST4, respiratory control index (RCI), ADP/O and oxidative phosphorylation rate (OPR). In addition mechanical function (heart rate, aortic and coronary flow, cardiac output, stroke volume) was monitored along with ultrastructural parameters. 90 min of hypoxia caused a deterioration of all parameters with persistent impairment in hemodynamic, morphologic and biochemical functions after 60 min of reoxygenation (group I). The role of the ATP-synthetases in the pathogenesis of oxygen-paradox is discussed. In contrast, the MPG-enriched reoxygenated solution (group II) improved hemodynamics, ultrastructure and mitochondrial function significantly (alpha = 0.05). It is concluded from these data that the ATP-synthetases are damaged during oxygen-deficiency and that MPG may be a useful drug for protecting the inner mitochondrial membranes during reoxygenation.

Adenosine Diphosphate↗
PubMed1987

A novel cardioprotective regimen for improvement of inner mitochondrial membrane function after ischemic stress.

Treatment of the normoxic working rat heart with 1 mmol/l 2-mercaptopropionylglycine (MPG) results in a significant increase of postischemic aortic flow. Measurement of N,N-dimethylaminostyrylmethylpyridinium iodide (DASPMI) fluorescence on the surface of the heart preparation gives semiquantitative information on mitochondrial energization in situ. No differences in fluorescence have been found between therapy and control groups. This finding is confirmed by fluorescence studies on isolated mitochondria. Investigations on postischemic mitochondrial oxygen consumption and ATPase clearly reveal ameliorated function of oxidative phosphorylation and reduced ATP splitting activity by MPG treatment. Mitochondrial energization (i.e. membrane potential) thus does not run strictly parallel with oxidative and phosphorylative capabilities.

Adenosine Triphosphatases↗
PubMed1987

Whole gut lavage for colonoscopy. A comparison between preparation at home or at the hospital.

The clinical efficiency and patient acceptability of peroral colonic lavage with a 3 liters balanced electrolyte solution (BES), when performed either at the hospital on the day of colonoscopy or during the preceding evening in the patient's home, was evaluated in 62 consecutive outpatients. No significant difference was found between adequacy of bowel preparation, when the lavage was performed in the patient's home or at the hospital. The bowel preparation was found to be satisfactory in 61% and 77% of the patients. The percentage of sufficient preparation was 60% of the patients, who were not able to drink 3 litres of BES within the 2-hours period. This study demonstrated that colonic lavage with BES could be performed equally well at home the day before colonoscopy as at the hospital on the day of colonoscopy. The relatively low rate of sufficient preparation was related to the fixed and small volume of BES ingested. To improve the adequacy of bowel preparation a graded intake of BES is suggested.

Administration, Oral↗
PubMed1987

Lactate dehydrogenase isoenzymes in serum during recent acute myocardial infarction.

Lactate dehydrogenase (LD, EC 1.1.1.27) isoenzymes 1 and 2 and the LD 1:2 ratio were determined in 62 patients with recent myocardial infarction 24, 48, and 72 h after total serum LD activity had returned to normal values. From the results we could define two groups of patients. The first, 40 patients in whom proportions of LD-1 and LD-2 isoenzymes in serum and the LD 1:2 ratio were all within the normal reference interval, all had an uncomplicated course of recovery from myocardial infarction. In the remaining 22 patients, LD-1 still exceeded LD-2 24 to 72 h after total LD activity returned to normal values; i.e., the ratio was similar to that in patients with myocardial infarction. Seven of these 22 patients (32%) had a complicated course, with re-infarction in all seven. Thus, even in the presence of normal total LD activity, a high LD 1:2 ratio may reflect a consistent focal myocardial necrosis in some patients with recent myocardial infarction and may serve as an early marker for further re-infarction.

Adult↗
PubMed1987

Amiodarone-induced thrombocytopenia.

Amiodarone hydrochloride-induced thrombocytopenia seems to be an additional side effect in the course of amiodarone treatment. Two patients with thrombocytopenia during amiodarone treatment are described, in whom the diagnosis of amiodarone-induced thrombocytopenia was made by the fact that thrombocytopenia developed during amiodarone treatment and by rechallenge with the drug. Amiodarone-induced thrombocytopenia is probably due to delayed hypersensitivity reaction as indicated by the strongly positive lymphocyte stimulation test results using amiodarone. According to our results, platelet counts should be included in the routine follow-up of patients within the first two weeks after initiation of amiodarone treatment.

Aged↗
PubMed1986

31P-NMR spectroscopic investigations and mitochondrial studies on the cardioprotective efficiency of 2-mercaptopropionylglycine.

Contents of high energy phosphates in the isolated perfused rat heart were followed during ischemia and reperfusion using 31P NMR spectroscopy. Application of 2-mercaptopropionylglycine resulted in significantly higher content of ATP in the reperfusion phase whereas during ischemia no differences between control and therapy hearts were found. Analysis of postischemic mitochondrial function reveals that improved ATP level is paralleled by an increased respiratory control index and a reduced ATPase activity. It is suggested that 2-mercaptopropionylglycine may cause increase of high energy phosphates during reperfusion by improving mitochondrial oxidative phosphorylation.

Adenosine Triphosphatases↗
PubMed1986

The acute effect of sublingual nifedipine and isosorbide dinitrate on plasma viscosity in patients with acute myocardial infarction.

The effect of sublingual nifedipine 10 mg (pierced capsule) and isosorbide dinitrate (ISDN) 5 mg on plasma viscosity (Pl.V) was investigated in 60 consecutive patients 7-10 days after hospitalization for acute myocardial infarction (AMI), who were randomized for either nifedipine (30 patients) or ISDN (30 patients). Pl.V, hematocrit (Htc), and erythrocyte sedimentation rate (ESR) were measured 20 minutes before and thereafter at 5, 10, and 30 min after drug administration while in the recumbent position. Blood pressure (BP) and heart rate (HR) were determined before each blood sample. In 18 patients (60%) Pl.V decreased by greater than 0.05 centipoise (Cp) after nifedipine (0.0953 +/- 0.033 Cp p less than 0.001 vs. initial values). After ISDN, Pl.V decreased by greater than 0.05 Cp (0.0933 +/- 0.036 Cp) in only 7 patients (23%). Systolic blood pressure (SBP) fell by 11.7 +/- 14.6 mmHg after nifedipine and by 16 +/- 14 mmHg after ISDN (nifedipine vs. ISDN = NS). Diastolic blood pressure (DBP) fell by 8 +/- 9.6 mmHg after ISDN and by 6.6 +/- 19.3 mmHg after nifedipine (nifedipine vs ISDN = NS). HR, ESR, and Htc did not change after drug administration. It is thus concluded from our study that nifedipine 10 mg sublingual has a significant Pl.V-lowering activity compared to sublingual ISDN 5 mg in patients with AMI.

Adult↗
PubMed1986

"Flipped" lactic dehydrogenase pattern in acute coronary insufficiency.

Serum lactic dehydrogenase (LDH) isoenzymes were measured 24, 48, and 72 hours after administration in 85 patients with acute coronary insufficiency (ACI) and 10 patients with stable angina pectoris who served as controls. The above patients did not develop myocardial infarction according to the criteria of development of new Q waves or elevation of cardiac enzymes. In 15 patients with ACI a "flipped" LDH pattern (LDH1 greater than LDH2) was found in the presence of normal total LDH activity and normal creatine kinase-MB. The values of LDH 1:2 ratio ranged between 1.02 and 1.13 (normal values 0.45-0.75). In the 10 control patients, normal levels of total LDH and normal LDH enzyme distribution and creatine kinase-MB were found. A possible explanation for the flipped LDH pattern in the ACI patients (indicating some myocardial damage) could be myocytolysis and coagulation necrosis found on postmortem examinations. The conclusion of our study is that LDH isoenzymes should be measured in patients with ACI to determine the LDH 1:2 ratio. The finding of a "flipped" LDH pattern demonstrating myocardial damage, lacking in stable angina, may also be helpful in patients who developed the clinical picture of ACI more than 24 hours before arrival at the hospital, since by that time the creatine kinase-MB may have already returned to normal. An additional advantage of measuring LDH isoenzymes in these patients may be that patients with "flipped" LDH pattern may need a longer rest and earlier coronary angiographic evaluation.

Acute Disease↗
PubMed1986

On the interaction between anthralin and mitochondria: a revision.

Anthralin is an inhibitor of oxidative phosphorylation at concentrations found in vivo. ADP-stimulated oxygen consumption is diminished. Consequently, the rate of ATP synthesis is reduced and mitochondrial ATP content declines. Neither the isolated ATPase (F1F0-ATPase), nor the mitochondrial membrane-bound ATPase are influenced by the drug. Respiration under resting conditions is not affected. The experimental data unequivocally indicate that anthralin is not an uncoupler of oxidative phosphorylation, as previously stated. Furthermore, the interpretation that respiratory deficiency induced in yeast strains by anthralin is a consequence of petite mutations has to be reconsidered. Under in vivo conditions, anthralin inhibits respiration per se. Our experiments, including the electron spin resonance spectroscopy, reveal that anthralin alters mitochondrial membrane structure and function simultaneously. A redox or free-radical mediated step may be involved. In consequence, inhibition of ATP production occurs which may become the limiting factor for increased cellular metabolism in psoriasis.

Adenine Nucleotides↗
PubMed1986

Circulating platelet aggregate size in ischemic heart disease.

Platelet aggregate size was measured in 178 patients with ischemic heart disease, among whom 56 had stable angina, 42 suffered from unstable angina, and 80 had had uncomplicated acute myocardial infarction. A group of 50 healthy volunteers and 20 hospitalized noncardiac patients served as controls. Venous blood (0.5 cc) was introduced into a solution containing 11.7 mM EDTA and 1.0 g formaldehyde. Platelet aggregate size was determined by microscopic reading as the number of platelets forming aggregates (per 1000 counted platelets) divided by the number of aggregates. Mean aggregate size was found not significantly different in both control groups, as well as in patients with stable angina and acute myocardial infarction (2.21 +/- 0.36 platelets, 2.20 +/- 0.58 platelets, 2.28 +/- 0.19 platelets, 2.76 +/- 1.07 platelets, respectively, p = NS). The highest value was found in the unstable angina group: 4.00 +/- 1.40 platelets (p less than 0.001 vs other studied groups). Platelet aggregate size was found not to be related to sex, age, medication, or coronary risk factors. Unstable angina may thus be a unique entity in ischemic heart disease concerning its platelet behavior, demonstrated in this study by the increased size of peripheral platelet aggregates, which may have pathogenetic, diagnostic, and eventual therapeutic implications.

Adult↗
PubMed1986

Cushing's disease coexisting with a single macronodule simulating adenoma of the adrenal cortex.

A rare case of Cushing's disease coexisting with a single macronodule simulating adenoma of the adrenal cortex is presented. The basal and dynamic tests supported the diagnosis of Cushing's disease, whereas the CT-scan, ultrasound and iodocholesterol uptake were suggestive of a left adrenal adenoma. Treatment consisted of extirpation of the nodular gland followed by pituitary irradiation. The examination revealed a single macronodule with no histological membrane, surrounded by hyperplastic adrenocortex. Together with the three similar ones reported in the literature this case suggests that nodular hyperplasia may be an intermediary stage between diffuse hyperplasia and the appearance of an autonomous adenoma after long-term stimulation of the hyperplastic gland.

Adenoma↗
PubMed1986

Effects of bepridil on heart mitochondrial membrane and the isolated rat heart preparation.

Bepridil (Cordium) was found to activate rat heart mitochondrial membrane-bound ATPase at concentrations of 10 nmol/l-10 mumol/l. By contrast, oligomycin-sensitive ATPase from beef heart mitochondria was inhibited at concentrations of 1-10 mumol/l. In both systems sensitivity toward the inhibitor oligomycin was reduced. Under the influence of the drug, RCR (coupling degree of electron transport to ATP synthesis), ST3 (oxygen uptake in presence of substrate and ADP) and OPR (oxidative phosphorylation rate, amount of ATP synthesized in mitochondrial metabolic state ST3) values are reduced, indicating partial inhibition of oxidative phosphorylation. At 0.25 mumol/l concentration of bepridil, in the isolated normoxic working rat heart preparation aortic flow was reduced to zero. No changes in oxidative phosphorylation parameters were found in mitochondria isolated from these preparations. In the isolated, working rat heart preparation bepridil at a concentration of 0.05 mumol/l reduced aortic flow to about 75% of its original value. In this preparation, no cardioprotective effects (neither on aortic flow nor on mitochondrial function) could be demonstrated during postischemic reperfusion. It is suggested, that in vitro mitochondrial activities of bepridil are not related to in vivo action of the drug.

Adenosine Triphosphatases↗