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Biomedical subjects

F Saborowski

Publications and source records attributed to F Saborowski.

At least 19 recordsLinked to original sources

[Hypercalcemia in florid pulmonary and cervical lymph node tuberculosis].

A 57-year-old man with a history of tuberculosis (TB of the knee-joint 44 years ago and open pulmonary TB six months ago with poor patient drug compliance) had lost 10 kg in weight during the preceding six months. In addition, firm lymph-node swellings with redness of the overlying skin and a skin fistula developed on the right side of the neck. There was mild hypercalcaemia (albumin-corrected serum calcium concentration 2.59 mmol/l) and hyperphosphataemia (2.0 mmol/l) with low-normal serum concentrations of parathormone and of 25-hydroxy-vitamin D3 (14 ng/ml). Serum 1,25-dihydroxy-vitamin D3 concentration was reduced (16 ng/l). The activity of osseous isoenzyme of alkaline phosphatase was normal (19 U/l) and skeletal scintigraphy revealed no abnormality. The cervical lymph-nodes were excised (histology: active caseous lymph-node TB). Tuberculostatic treatment was begun with daily doses of 0.3 g isoniazid, 0.45 g rifampicin, 1.2 g ethambutol and 1.5 g pyrazinamide. Serum calcium concentration rose to 3.22 mmol/l (albumin-corrected) in the first two weeks, even though the patient was on a low-calcium diet. The various concentrations subsequently decreased, but remained slightly elevated throughout the period of observation (11 weeks). This is thus a case of TB-associated hypercalcaemia which was not caused by 1,25-dihydroxy-vitamin D3 or bone destruction.

Alcoholism

[Silent myocardial ischemia in long-term ECG with various mani festations of coronary heart disease].

Silent myocardial ischaemia seems to be of prognostic value in coronary artery disease. We examined 47 patients with coronary artery disease: 1. 20 patients with a history of myocardial infarction (MI), 2. 15 patients with chronic stable angina pectoris without a history of myocardial infarction (sAP), and 3. twelve patients with unstable angina with or without a history of myocardial infarction (uAP). Horizontal and downsloping ST-segment-depressions greater than or equal to 1 min and greater than or equal to 0.1 mV were defined as significant. There were 132 ST-segment-depressions, the relation between symptomatic and asymptomatic being 1:7.3, in MI 1:6.2, in sAP 1:5.3, in uAP 1:14. Heart rate increased before beginning of ST-segment-depression in 74% in MI, in 86% in sAP, but only in 38% in uAP. In sAP ST-segment-depressions were smaller (14% greater than 0.2 mV, none greater than 0.3 mV) than in patients with MI (42% greater than 0.2 mV, 12% greater than 0.3 mV) and uAP (25% greater than 0.2 mV, 9% greater than 0.3 mV). Mean duration of ST-segment-depression was 15.3 +/- 11.7 min in sAP (2 to 49 min), 28.5 +/- 35.6 min in MI (2 to 168 min), and 41.2 +/- 40 min in iAP (2 to 140 min). ST-segment-depressions in MI and sAP showed a circadian rhythm with a peak at midday and in the early evening and a small amount of ST-segment-depressions at night. In uAP ST-segment-depressions did not show that circadian variation. The number of ST-segment-depressions was higher in uAP than in MI and sAP.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged

[The hemodynamic profile of amrinone and enoximone in patients with severe heart failure].

Hemodynamic measurements were done in 42 patients with congestive heart failure of NYHA classes III and IV after administration of the phosphodiesterase inhibitors amrinone und enoximone. Amrinone decreases mean arterial pressure (-4%), right atrial pressure (-39%), and systemic vascular resistance (-23%), while cardiac index and stroke volume index increase to 27% and 26%, respectively; heart rate is nearly unchanged. Enoximone administration in a dose of 1 mg/kg bw produces an increase in cardiac index of 13%, an increase in heart rate of 12%, and a decrease of systemic vascular resistance of 13%, whereas stroke volume index is unchanged. Enoximone in a dose of 1.5 mg/kg bw increases heart rate (+ 9%), cardiac index (+ 33%), and stroke volume index (+ 21%), and decreases systemic vascular resistance (-26%). The hemodynamic profile of amrinone and enoximone in an equal dose shows only slight differences. Furthermore, phosphodiesterase inhibitors produce an increase of cardiac index (+ 19%) and stroke volume index (+ 17%) in patients with pump failure having already received dopamine and dobutamine.

Aged

Determination of mean whole body intracellular pH in unanesthetized dogs.

In order to determine mean whole body pHi in unanesthetized dogs, assumptions on the urinary and intestinal excretion of DMO, the total loss of an injected single dose of [14C] DMO, and the distribution kinetics of DMO were tested experimentally. Urinary excretion of DMO was almost negligible. The best assumption on the total loss of DMO was based on the exponential decay observed over a period of 1 to 4 weeks. The biological half-life of DMO was 5 days, the time constant being --0.14 d-1. The extracellular distribution of DMO was considered to equal that of [3H] inulin. Between 1 and 7 hours after an injection of inulin in nephrectomized dogs the distribution volume increased linearly from 16% of the body weight after 2 hours to 21% after 6 hours. Based on these experimental results, pHi was determined in 16 unanesthetized dogs. 120 min after the injection of DMO pHi was 7.05 and 430 min after the injection pHi was 7.11. It is concluded that the assumption made allow the estimation of pHi in unanesthetized dogs over a period of 1 to 7 hours.

Acid-Base Equilibrium

The effect of temperature and mechanical work load on the intracellular pH and buffer capacity of cardiac muscle in rats.

The effect of temperature on hydrogen ions and buffer capacity in extracellular fluid differs from the effects in intracellular fluid. In our experiments cardiac hypertrophy was achieved by increasing the mechanical work load. It could be demonstrated that there is a certain correlation between buffering of hydrogen ions and mechanical activity of heart muscle.

Animals

[Intracellular pH of cardiac muscle after administration of potassium-magnesium-aspartate (author's transl)].

27 Sprague-Dawley rats were anesthetized with pentobarbital. Artificial ventilation was given by a Starling pump respirator via a tracheal tube. Intracellular pH of cardiac muscle was determined by means of the indirect procedure of measuring the distribution of 5,5-dimethyl-2,4-oxazolidinedione (DMO) in intra- and extracellular spaces (DMO-method). 12 rats were injected i.p. with 0.33 mval potassium-magnesium-aspartate/100 g body weight and 15 rats served as controls. Using a regression analysis, the following relationships were obtained: 1. animals injected with potassium-magnesium-aspartate pHa = --0.75 log PaCO2 + 8.535, PHi = --0.30 log PaCO2 + 7.509, pHi = 0.41 pHa + 4.036; 2. control animals pHa = --0.59 log PaCO2 + 8.308, pHi = --0.27 log PaCO2 + 7.381, pHi = 0.47 pHa + 3.503. At a pCO2 of 40 torr a pHa of 7.33 (7.36) and a pHi of 7.03 (6.95) was obtained. At an arterial pH of 7.40 the pHi was 7.07 (6.98). The results of the control group are written in brackets. -- The experiments demonstrate an increase in the intracellular buffer bases after administration of potassium-magnesium-aspartate. This effect can be recognized by a concomitant increase in the intracellular pH of 0.09 compared to the control group.

Animals