[Rupture of the bladder in blunt abdominal injuries].
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Abdominal Injuries↗
Biomedical subjects
A Heinz
Publications and source records attributed to A Heinz.
The transport and accumulation of oxyvanadium compounds in human erythrocytes in vitro.
Metavanadate, at physiologic pH the oxyanion form of pentavalent vanadium, is a potent reversible inhibitor of the sodium pump. Vanadium must enter cells to inhibit the sodium pump, and metavanadate may be converted to an inactive form inside of cells. Because of these factors and the complex inorganic chemistry of vanadium, we examined the kinetics of vanadium uptake and accumulation in normal erythrocytes in vitro at 37 degrees C. The kinetics of vanadium influx, efflux, and accumulation in erythrocytes in Tris-buffered, isotonic salt medium were fit closely by a model with vanadium in two possible oxidation states and with the vanadium permeating between two compartments. The equation for this model is: (formula: see text) in which subscripts i and o signify "inside" and "outside" the cells, respectively, and k1, k-1, and k2 are rate constants. 48V or EPR of vanadium(IV) gave similar estimates of the concentrations of the components. The k1 was 0.37 +/- 0.06 (S.E.M.) min-1 and k2 was 0.04 +/- 0.01 min-1. In control Tris-medium, k1 exceeded k-1 by a factor of 1.8. After 120 min of incubation in media with initial concentrations of 1, 10, or 100 microM vanadium(V), the total intracellular vanadium concentration exceeded that in the bath 4.5 to 18-fold. Vanadium influx was not appreciably changed by variations of external sodium or glucose levels. The k1 and k-1 were inversely related to external pH over the range 6.5 to 8.2. High O2 tension (95% to 100% O2) caused a decrease in k2, and the lipophilic oxidant, cumene hydroperoxide, accelerated the loss of accumulated vanadium from the cells, indicating that the k2 step represents reduction of vanadium(V) to vanadium(V) within the cells. On the basis of these studies we suggest that the intracellular concentration of vanadium(V), the inhibitor of the sodium pump, is determined by the combined effects of the rate of vanadium influx (dependent on the extracellular concentration of free metavanadate), the rate of vanadium efflux, and the rate of conversion of vanadium(V) to vanadium(IV).
Biological Transport↗
[Honvan-high-dose therapy of prostatic carcinoma with metastases: early complications and value of prophylaxis against thrombosis].
Since 1972 in the Urology Department at Darmstadt Hospital the Honvan-high-dose-therapy of 130 patients with metastatic prostatic carcinoma has been carried out under standardizing condition. The analysis shows that there is no significant difference between the patients with prophylaxis against thrombosis (Macrodex and Dihydergot-Heparin) and without prophylaxis. The patients with anti-thrombotic prophylaxis demonstrated significantly higher incidence of reversible elevation of transaminases. The effect of Heparin is probably responsible for this.
Aged↗
Amino Acid Transport and stimulation by substrates in the absence of a Na2+ electrochemical potential gradient.
Uptake of alpha-aminoisobutyric acid (AIB) was examined in Ehrlich ascites tumor cells treated with the cation-exchange ionophore nigericin (20 microgram/ml). Membrane voltages were measured using the voltage-sensitive dye diethyloxadicarbocyanine (DOCC). In normal phosphate-buffered media, nigericin changed the distribution ratios of Na+ and K+ (the ratio of intra- to extracellular concentrations) nearly to unity, but AIB was still accumulated to a distribution ratio of approximately 9.0. When all but 40 mM Na+ in the medium was replaced by choline, nigericin resulted in K+ loss and Na+ gain and both cation distribution ratios approached 2.8-3.4, as would be expected if both ions were distributing near electrochemical equilibrium with a membrane voltage in the range of -28 to -33 mV. This conclusion was supported by the observation that the addition of 5 X 10(-7) M valinomycin to the nigericin-treated cell suspension produced no change in DOCC absorbance. In spite of the apparent zero electrochemical potential gradients for Na+ and K+, AIB was accumulated to a distribution ratio of 5.4 in the low-Na+ medium. Addition of 0.1 mM oubain or 50 microM vanadate did not alter the extent of AIB accumulation as would have been expected if a large component of the membrane voltage were due to electrogenic operation of the (Na+ + K+)-ATPase. Addition of lactate, pyruvate or glucose increased the AIB distribution ratios to 11.9, 9.4 and 15.3, respectively. The effect of glucose could be explained, at least in part, by an enhanced Na+ electrochemical potential gradient. However, neither lactate nor pyruvate produced any change either in membrane voltage or the intracellular Na+ concentration. Therefore, these results confirm the existence of a metabolic energy source which is coupled to AIB accumulation and operates in addition to the Na+ co-transport mechanism, and which is augmented by metabolic substrates such as lactate and pyruvate.
Amino Acids↗
Evidence for activation of an active electrogenic proton pump in Ehrlich ascites tumor cells during glycolysis.
The addition of glucose to a suspension of Ehrlich ascites tumor cells results in rapid acidification of the extracellular medium due to lactic acid production. The nature of the H+ efflux mechanism has been studied by measuring the time course of the acidification, the rate of proton efflux, the direction and relative magnitude of the H+ concentration gradient, and the voltage across the membrane. Using the pH-sensitive dye acridine orange, we have established that after addition of 10 mM glucose an outward-directed H+ concentration gradient develops. As the rate of glycolysis slows, the continued extrusion of H+ reverses the direction of the H+ concentration gradient. Changes in absorbance of the voltage-sensitive dye diethyloxadicarbocyanine iodide (DOCC), and changes in the distribution of the lipid permeant cation tetraphenyl phosphonium, showed a dramatic and persistent hyperpolarization of the membrane voltage after glucose addition. The hyperpolarization was prevented by the protonophore tetrachlorosalicylanalide (TCS) and by valinomycin, but not by the neutral-exchange ionophore nigericin. Inhibitors of lactate efflux were found to reduce the rate of acidification after glucose addition but they had no effect on the magnitude of the resulting hyperpolarization. On the basis of these and other data we suggest that an active electrogenic pump mechanism for H+ efflux may be activated by glucose and that this mechanism operates independently of the lactate carrier system.
Acridine Orange↗
Role of external potassium in the calcium-induced potassium efflux from human red blood cell ghosts.
The exposure of red cell ghosts to external Ca++ and K+ leads to a rapid net K+ efflux. Preincubation of the ghosts for various lengths of time in the absence of K+ in the external medium prior to a challenge with maximally effective concentrations of Ca++ and K+ renders the ghosts unresponsive to that challenge with a half-time of about 7-10 min. Preincubation at a range of K+ concentrations for a fixed length of time (60 min) prior to the challenge revealed that K+ concentrations of about 500 microM or more suffice to maintain the K+ channel in a maximally responsive state for at least 60 min. These K+ concentrations are considerably lower than the K+ concentrations required to make the responsive channel respond with a maximal rat of K+ efflux. Thus external K+ is not only necessary to induce the permeability change but also to maintain the transport system in a functional state. The presence of Mg++ or ethylenediamine-tetraacetic acid (EDTA) in the K+-free preincubation media preserves the responsiveness to a challenge with Ca++ plus K+. In contrast to external K+, the presence of external Ca++ does not reduce but rather enhances the loss of responsiveness. An excess of EDTA prevents the effects of Ca++ while washes with EDTA after exposure to Ca++ do not reverse them. In red cell ghosts that contain Ca++ buffers, the transition from a responsive to a nonresponsive state incubation in the absence of external K+ is enhanced. The effects of incubation in the presence of Ca++ in K+-free media are reversed; external Ca++ now reduces the rate at which the responsiveness is lost. The loss of responsiveness after incubation in K+-free media prior to a challenge with external K+ and internal Ca++ does also take place when K+-efflux from red cell ghosts is measured by means of 42K+ into media that have the same K+ concentrations as the ghost interior. This confirms that the effects of K+-free incubation are due to the modification of the K+-selective channel rather than to an inhibition of diffusive Cl--efflux.
Calcium↗
The renal response to intravenous vanadate in rats.
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Animals↗
[Diagnosis of neurologic and motor development in pre-school age children with minimal cerebral dysfunction].
An investigation on neurologic development of pre-school children does not yet clearly differentiate between children with minimal neuromotor disturbances and healthy ones. This is due to the lack of knowledge on brain function in normal children. Diagnostic problems on Minimal Brain Dysfunction are demonstrated by neurologic and motor examinations of 4 to 6 years old children.
Attention Deficit Disorder with Hyperactivity↗
Quantitative evaluation of Epstein-Barr-virus-infected mononuclear peripheral blood leukocytes in infectious mononucleosis.
We devised a quantitative assay for Epstein-Barr-virus-infected mononuclear leukocytes (virocytes) to determine their prevalence in the blood of patients with acute-phase and convalescent-phase infectious mononucleosis and in healthy Epstein-Barr-virus-seropositive controls. Mononuclear peripheral blood leukocyte suspensions were tested for virus-determined cytoproliferative activity by cocultivation with human cord-cell indicator cultures. The highest levels of virocytes among circulating mononuclear leukocytes were found in the early acute phase of infectious mononucleosis (up to 0.05 per cent). Virocytemia decreased to levels comparable with those of healthy controls (less than 0.00001 per cent) by the third month after onset of infectious mononucleosis. These findings provide a quantitative profile of the course of the infection at cellular level and support existing evidence of the efficiency of immune control mechanisms in limiting Epstein-Barr-virus infection during the course of infectious mononucleosis.
Acute Disease↗
Intensity of the normal second heart sound components in their traditional auscultatory areas.
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Adolescent↗
Genotype effects on neurodegeneration and neuroadaptation in monoaminergic neurotransmitter systems.
Neuroadaptation and neurodegeneration in central dopaminergic and serotonergic systems are central to vulnerability, process and consequences of addictive behavior. Serotonergic dysfunction has been associated with behavior disinhibition and negative mood states that may predispose to excessive alcohol intake, while alcohol-induced stimulation of dopaminergic neurotransmission may encode the reinforcing properties of alcohol consumption. Chronic alcohol intake induces neuroadaptive reductions in striatal dopamine transporter (DAT) and D2 receptor availability, which were reversible during early abstinence. A polymorphism of the DAT gene (SLC6A3) was associated with the in vivo transporter availability in the putamen of abstinent alcoholics and control subjects. The same genotype was associated with severity of alcohol withdrawal symptoms, hypothetically due to interactions of genotype and alcohol-induced neuroadaptation. Reduction in raphe serotonin transporter (5-HTT) availability was observed in abstinent male alcoholics and it may be the result of neurodegeneration rather than reversible neuroadaptation. Neurotoxic reduction in 5-HTT protein expression seems to be limited to homozygous carriers of a long, more transcriptionally active allele of a promoter repeat polymorphism of the 5-HTT gene (SCL6A4). This genotype was also associated with a low level of acute unpleasant effects of alcohol consumption, a factor predisposing to excessive alcohol intake. The time course of neuroadaptation and recovery of monoaminergic neurotransmission in alcohol intake and withdrawal imply that monoamine transporter genotype could profoundly influence alcohol-induced reinforcement and, perhaps, contribute to neurochemical changes which are long lasting or permanent.
Adaptation, Physiological↗