[Determination of sinuatrial conduction time in hospital].
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Biomedical subjects
Publications and source records attributed to F Saborowski.
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In 10 patients (age: 31--72 years) oxygen supply of skeletal muscle was measured by pO2-multiwire technique. All patients suffered from chronic renal failure of differing etiologies and from chronic renal anemia. In muscle tissue 1,128 different O2-tensions were registered and the results were expressed as pO2-histograms. Seven of these pO2-histograms show a normal distribution, three are shifted to the left to lower O2-tensions. Therefore the microcirculation in the skeletal muscle of patients with chronic reduced O2-carrying capacity is largely undisturbed. The microcirculation is able to increase with exercise as shown by a shift to the right in the PO2-histogram. The use of the pO2-multiwire electrode is largely devoid of risk to the patient. Important pathological features may be demonstrated.
In 36 patients sinoatrial conduction time (SACT) was calculated by the continuous-atrial-pacing technique, first described by Narula et al. (9). Using three different stimulation frequencies, it could be shown that the return cycles A2A3 and the postreturn cycles A3A4 both were linearly correlated with rising stimulation frequency. Thus, if the formula given by Narula et al. was used [SACT = (A2A3 - A1A1) : 2] the calculated SACT-values linearly rose, too, which was caused by a stimulation frequency dependent progressive depression of the sinus nodal automaticity. This interfering influence of sinus nodal depression could be corrected by applying a modified formula for calculation of the SACT, i.e. SACTM = (A2A3 - A3A4) : 2. Thus calculation of sinuatrial conduction time by the modified continuous-atrial-pacing technique represents a method widely applicable in routine electrophysiological testing.
In 25 patients the systolic time intervals were simultaneously measured by echocardiography and by the conventional method using the ECG, phonocardiogram and indirect carotid pulse tracing. Beat-to-beat-analysis showed no significant difference for QS2 (367.1 +/- 26.7 ms vs. 367.9 +/- 26.5 ms). In contrast, the LVET measured by echocardiography was significantly longer than the LVET taken from the indirect carotid pulse tracing (275.3 +/- 26.3 ms vs. 266.2 +/- 25.9 ms, p less than 0.001). As a consequence, the echocardiographic PEP was significantly shorter than the conventionally measured PEP (91.3 +/- 18.0 ms vs 100.9 +/- 22.7 ms, p less than 0.001). Furthermore, both methods showed the weakest correlation for the ratio PEP/LVET. We conclude that STI can be reproducibly measured by echocardiography, which will lead to significantly different values for the STI compared to those measured by the conventional method.
The clinical picture of the panarteritis nodosa is characterized by vague early symptoms, manifestations in various organs and a changing prognosis. In seven patients with histologically proven panarteritis nodosa the clinical course was followed up over a long period. The commonest early symptoms were fever of unknown origin and a considerable loss of weight. Three out of seven patients showed in the initial phase a hypertension, in two other patients the blood pressure rose as the disease progressed. Those patients, whose renal function was impaired when the diagnosis was established, had a poor prognosis in spite of immunosuppressive therapy and dialysis. The life expectancy of these patients was between two and 16 months (in average 6,4 months). On the other side the clinical course in two patients without renal failure was more favourable; they are alive eight months and 15 years respectively after the diagnosis was confirmed.
The importance of synchronized atrial and ventricular action is well known. Especially in elderly patients the circulation of the brain, the kidneys and the coronary arteries may be diminished by ventricular stimulation. Permanent atrial, atrial triggered ventricular, and bifocal stimulation increases cardiac output by 20-30 percent. From the hemodynamic data the best results during atrial stimulation are obtained at a frequency of 80 to 85 bpm.
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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.
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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.
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.
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