Biomedical subjects
Publications and source records attributed to S Krause.
The calcium determination by atomic absorption spectroscopy is impaired in samples which contain 1-hydroxyethylidene-1,1-bisphosphonate. We describe possibilities to avoid these bisphosphonate-mediated interferences of calcium measurement.
Treatment of polymorphonuclear leukocytes with the soluble and cell penetrating thiol N-(2-mercaptopropionyl)-glycine (2-MPG) inhibits luminol-enhanced chemiluminescence induced by opsonized zymosan, which is believed to be a measure for the generation of reactive oxygen species, and accelerates the rate of phagocytosis measured as ingestion of zymosan particles. It is discussed that 2-MPG protects the phagocyting cells from oxidative damage by reactive oxygen species that are formed during particle ingestion.
Demineralization of hydroxyapatite (HAP) columns by acidic acetate buffer proceeds in two phases. In an initial phase which is characterized by the formation of pH gradient within the HAP sediment, calcium but no phosphate ions are eluted from the column. In the second phase when a low pH value has been established in the pellet calcium and phosphate are eluted in a ratio identical to that of the original HAP. The binding of human blood plasma proteins and saliva proteins to the HAP as well as the effect of the protein binding on HAP demineralization was investigated. The maximum binding capacity of HAP for the proteins of unstimulated mixed saliva is about four times lower than the binding of human serum albumin or blood plasma proteins. However, saliva proteins affect HAP demineralization more markedly than the other proteins. Whereas the pretreatment of HAP with human serum albumin does not alter the the demineralization process. binding of blood plasma proteins inhibits the initial phase of demineralization. Both phases of HAP demineralization are strongly inhibited when saliva proteins are bound to HAP. It is also shown that demineralization modifies the protein binding to HAP.
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It has been suggested that feverfew extracts (FE) inhibit platelet behaviour via effects on platelet sulphydryl (SH) groups. In the present study we found evidence that FE inhibits uptake as well as liberation of arachidonic acid (AA) into/from platelet membrane phospholipids (PL).
Kallikrein excretion and renal function were studied on 37 one-day-old newborn infants (14 fullterm and 23 preterm infants). Preterm infants excreted less kallikrein (p less than 0.001), had lower creatinine clearance (p less than 0.02) and urinary osmolality (p less than 0.01). They had higher values on urinary volume (p less than 0.001), FENa (p less than 0.001), FEK (p less than 0.02), and free water clearance (p less than 0.01) than fullterm infants. The excretion of kallikrein correlated directly with gestational age (p less than 0.01) and body weight (p less than 0.01). No correlations were found with FENa, urinary volume, FEK or free water clearance. The values of kallikrein excretion were very low when compared with a young adult population. As kallikrein is synthesized in the distal nephron we advance as an hypothesis that the low levels of kallikrein excretion observed in newborns could be a reflection of immature distal tubular mass, and to the relative unresponsiveness of the distal nephron to hormones known to stimulate renal kallikrein such as aldosterone and antidiuretic hormone.
A prospective study of full-term infants with neonatal asphyxia was performed to evaluate possible alterations in renal function. Twenty-one newborns with an Apgar score less than or equal to 3 at 1 minute after birth and a control group of 20 normal infants were included. Oliguria of 12 hours or more (less than 1 ml/Kg/h) during the first 24 hours after birth was considered indication for a volume challenge test and use of diuretic. The study of renal function was effected between 24 and 48 hours after birth for asphyxiated and control infants (Period I), and was repeated between 48 and 72 hours (Period II) for the asphyxiated group only. Intrinsic acute renal failure was diagnosed in two patients, one of whom died. In 10 cases, prerenal oliguria responded promptly to volume expansion with improvement of biochemical indices in Period II. In nine cases, urine volume was not altered, and all functional parameters were comparable with those of control.
Urologic surgery was necessitated by complications following radiotherapy for gynecologic cancer in 17 patients. Four had recurrent malignant disease and 13 were without evidence of malignancy. The median interval to onset of the urologic complications was 18 (range 0-144) months. Ileal substitution was performed because of bilateral ureteral obstruction in two cases, and transureteroureterostomy for unilateral obstruction in one case. Vesicovaginal fistula was present in 14 patients, who underwent urinary diversion--cutaneous ureterostomy and ligation of the other ureter (6 cases), cutaneous ureterostomy and transureteroureterostomy (3) and ileal conduit diversion (5). The immediate morbidity and mortality were determined by the patients' general state of health rather than by presence or absence of recurrent malignant disease. The choice of diversion procedure should be guided by the patient's fitness, the status regarding recurrence of malignancy and the distribution of function between the two kidneys.
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The effect of glucagon administered as a bolus (1 mg) followed by a continuous infusion (2 mg/h) for 8 h and a placebo was compared in 37 adults with urographically demonstrated ureteral calculi less than 6 mm. The bolus injection was given 20 min after start of intravenous urography, and the infusion was initiated immediately afterwards. No effect on pain relief or passage of calculi was found. Nausea and/or vomiting were recorded significantly more frequently in patients who had glucagon than in patients who had the placebo. It is concluded that glucagon is of no value in acute ureteral colic.
Acetate buffers were passed through small hydroxyapatite columns and the column effluents were analysed for calcium and phosphate. Changes in the pH of the column effluents were also measured. As long as the pH of the column effluent was higher than about 5.5, only calcium was eluted from the column. However, when the pH fell below 5.5, the rate of calcium elution decreased and phosphate elution increased until calcium and phosphate elution reached constant values. Pretreating the hydroxyapatite with sodium fluoride or 1-hydroxyethylidene-1,1-bisphosphonate accelerated the drop of the pH and reduced the initial Ca/P ratio in the column effluent. We suggest that these results are due to the formation of a pH gradient along the progressing buffer fron with calcium and phosphate liberated from the hydroxyapatite reprecipitating to form calcium-poor minerals.
We investigated an outbreak of nosocomial pneumonia due to gentamicin, methicillin-resistant Staphylococcus aureus (GMRSA). We compared the predisposing factors for pneumonia due to GMRSA to those for pneumonia due to gentamicin, methicillin-sensitive Staphylococcus aureus (GMSSA). Seventeen of 29 patients with staphylococcal pneumonia were infected with GMRSA. Risk factors and associated diseases which selected for infection with GMRSA as opposed to GMSSA included prior antibiotic therapy for a prolonged period of time (p = 0.0001), number of risk factors per patient (p = 0.0001), days hospitalized prior to diagnosis of pneumonia (p = 0.002) and number of associated diseases per patient (p = 0.002). Despite the epidemiologic differences between GMSSA and GMRSA pneumonia, there were no differences in the clinical presentation, course of illness, complications, response to appropriate therapy or outcome between the two groups. Survival was adversely affected by age only among the GMSSA patients (p = 0.02) and by the number of associated diseases (p = 0.005).
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Gastric rupture following ventilation during cardiopulmonary resuscitation is a rare occurrence. We report two cases of documented gastric rupture plus two additional cases in which the clinical diagnosis of pneumoperitoneum was made and gastric rupture was assumed to be the mechanism. Review of the literature reveals the lesser curvature of the stomach to be the common site of rupture. This complication emphasizes the necessities of correct positioning of the jaw with mouth-to-mouth ventilation and careful assessment of air entry and chest movement following endotracheal intubation.
It has been proposed that breakdown of the excitation-contraction coupling system plays a pivotal role in myocardial dysfunction during the course of acute ischemia. We tested this hypothesis by characterizing the function of the sarcoplasmic reticulum at pH 7.1 and 6.4 after 7.5, 15, and 30 minutes of canine normothermic global ischemia. At pH 7.1, whole heart homogenate sarcoplasmic reticulum demonstrated a 49% depression of oxalate-supported calcium uptake at 7.5 minutes of ischemia, which progressed to 85% at 30 minutes of ischemia. At pH 6.4, control homogenate calcium uptake rates were significantly depressed, accompanied by a further depression in the ischemic groups. Isolated sarcoplasmic reticulum calcium uptake mirrored the effects of the whole heart homogenate. Calcium-stimulated magnesium-dependent ATPase (calcium-ATPase) activity was significantly depressed by both ischemia and acidosis, with a decrease in the coupling ratio (mumol calcium/mumol ATP) at 15 and 30 minutes of ischemia. Acidosis (pH 6.4) significantly shifted the sarcoplasmic reticulum pCalcium-ATPase curve to the right, increasing 50% activation from pCalcium 6.0 to 5.5 and depressing the maximum velocity (pH 7.1 = 2.06 +/- 0.14; pH 6.4 = 1.41 +/- 0.05 mumol Pi/mg per min; P less than 0.01). With ischemia, there was a progressive decrease in maximal activation of the calcium-ATPase enzyme and a progressive shift in calcium sensitivity to a higher concentration. Steady state calcium uptake, in the absence of oxalate, demonstrated a similar depression after 7.5 and 15 minutes of ischemia at pH 7.1 and 6.4, associated with a significant increase in the passive permeability coefficient for calcium.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute myocardial ischemia results in a decrease in developed tension and an increase in resting tension. A breakdown of the excitation-contraction coupling system can explain the behavior of the ischemic muscle at a subcellular level. We have identified a specific defect in the sarcoplasmic reticulum (SR) from the ischemic myocardium; i.e., the uncoupling of calcium transport from ATP hydrolysis. The mediators of this excitation-contraction uncoupling process have not been identified. It is now established that the intracellular pH of the ischemic myocardium is in the range of 6.4 but the role of protons and potential role of free radicals have not been identified. We have hypothesized that protons and free radicals may interact to produce the excitation-contraction uncoupling of the ischemic myocardium. Cardiac SR was isolated from the wall of canine left ventricle and calcium uptake velocity and Ca2+ stimulated-Mg2+ dependent ATPase activity determined. Increasing proton concentration between pH 7.0 and 6.4 significantly reduced calcium uptake rates (pH 7.0 = 0.95 +/- 0.02; 6.4 = 0.50 +/- 0.02 mumoles Ca2+/mg-min; p less than 0.01) with no effect on ATPase activity. Calculated coupling ratios (mumoles Ca2+/mumoles Pi) decreased from 0.87 +/- 0.06 at pH 7.0 to 0.51 +/- 0.05 at pH 6.4. At pH 7.0, the generation of exogenous free radicals from the xanthine-xanthine oxidase system significantly depressed both calcium uptake rates (Control = 0.95 +/- 0.02; X+XO = 0.15 +/- 0.02) and ATPase activity (Control = 1.05 +/- 0.02; X+XO + 0.30 +/- 0.01 mumoles Pi/mg-min; p less than 0.01). The decreases in calcium uptake and in ATPase activity were completely reversible with superoxide dismutase (SOD). At pH 6.4 in the presence of xanthine and xanthine oxidase, there is a further depression of calcium uptake rates (Control = 0.50 +/- 0.02; X+XO = 0.11 +/- 0.01; p less than 0.05) but there is no SOD reversible component. The addition of SOD + 20mM mannitol normalized calcium transport at pH 6.4. The calculated coupling ratio at pH 6.4 in the presence of free radicals was 0.13. In contrast sarcoplasmic reticulum isolated from ischemic myocardium demonstrated a significant depression of calcium uptake rates at pH 7.1 which was further accentuated at pH 6.4. Ca2+-ATPase was significantly depressed at pH 7.1 but there was no accentuation at pH 6.4. It is concluded that no single species of free radical can explain the intracellular excitation-contraction uncoupling of the ischemic myocardium. The system can be explained by the interaction of hydrogen ions and superoxide anions producing both injury to the sarcoplasmic reticulum and the formation of lipid free radicals with hydroxyl-like activity.