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Biomedical subjects

G Schwarz

Publications and source records attributed to G Schwarz.

At least 109 records · Page 6Linked to original sources
PubMed1995

[Cerebral monitoring in anesthesia and intensive care].

To ensure efficient computer-based cerebral monitoring in the ICU and during anaesthesia, sophisticated and sometimes expensive equipment is needed. It is thus all the more important that the clinician should have a good understanding and knowledge of the various methods involved, the origins of the different signals and their relationships, and of the possibilities of artefacts occurring, if the information that this equipment is capable of providing is to be fully and properly utilized. The present paper describes a number of new techniques of cerebral monitoring, and their successful application in the intensive care unit and the operating theatre.

Adult↗
PubMed1994

Cytoskeletal modulation of the response to mechanical stimulation in human vascular endothelial cells.

Possible interactions of cytoskeletal elements with mechanically induced membrane currents and Ca2+ signals were studied in human endothelial cells by using a combined patch-clamp and Fura II technique. For mechanical stimulation, cells were exposed to hypotonic solution (HTS). The concomitant cell swelling activates a Cl- current, releases Ca2+ from intracellular stores and activates Ca2+ influx. To interfere with the cytoskeleton, cells were loaded either with the F-actin-stabilizing agent phalloidin (10 mumol/l), or the F-actin-depolymerizing substance cytochalasin B (50 mumol/l). These were administered either in the bath or the pipette solutions. The tubulin structure of the endothelial cells was modulated by taxol (50 mumol/l), which supports polymerization of tubulin, or by the depolymerizing agent colcemid (10 mumol/l) both applied to the bath. Immunofluorescence experiments show that under the chosen experimental conditions the cytoskeletal modifiers employed disintegrate the F-actin and microtubuli cytoskeleton. Neither of these cytoskeletal modifiers influenced the HTS-induced Cl- current. Ca2+ release was not affected by cytochalasin B, taxol or colcemid, but was suppressed if the cells were loaded with phalloidin. Depletion of intracellular Ca2+ stores by thapsigargin renders the intracellular [Ca2+] sensitive to the extracellular [Ca2+], which is indicative of a Ca2+ entry pathway activated by store depletion. Neither cytochalasin B nor phalloidin affected this Ca2+ entry. We conclude that F-actin turnover or depolymerization is necessary for Ca2+ release by mechanical activation. The tubulin network is not involved. The Ca2+ release- activated Ca2+ entry is not modulated by the F-actin cytoskeleton.

Actins↗
PubMed1994

Multiple effects of SK&F 96365 on ionic currents and intracellular calcium in human endothelial cells.

1. Multiple effects of the imidazole compound SK&F 96365 have been evaluated on endothelial cells from human umbilical vein using a combined patch clamp and Ca(2+)-microfluorimetric technique (Fura-2). 2. At concentrations of 100 mumol/l or higher of SK&F 96365, the block of the receptor-mediated Ca2+ entry overlaps with the activation of another Ca(2+)-entry mechanism, which is associated with a non selective cationic current. 3. This rise in [Ca2+]i depends on the extracellular Ca(2+)-concentration, and the entry pathway is in contrast with the receptor-mediated Ca(2+)-entry pathway permeable to Ni2+, as shown by quenching of the Fura-2 fluorescence signal. 4. The concentration of SK&F 96365 for half maximal increase in [Ca2+]i was 141 +/- 19 mumol/l (n = 16). 5. SK&F 96365 activated a current that reversed at +11.8 +/- 2.1 mV (n = 21) when measured using nystatin-perforated patches with either Cs+ or K+ in the pipette and 140 Na+, 1.5 Ca2+ in the bath (chloride equilibrium potential ECl = -36 mV). 6. SK&F 96365 (200 mumol/l) blocked an inwardly rectifying K+ current in endothelial cells independently of [Ca2+]i. This block caused depolarization of the endothelial cells from -55.3 +/- 2.57 mV (n = 33) to -10 +/- 5.5 mV (n = 6). This block was concentration-dependent, half maximal block occurred at a concentration of about 40 mumol/l SK&F 96365. 7. In cells which showed an outwardly rectifying current, this outward component was also completely blocked by 200 mumol/l SK&F 96365. 8. It is concluded that SK&F 96365 reversibly activates a non-selective cation channel at concentrations higher than 100 mumol/l, but also blocks K+ currents in endothelial cells independently of [Ca2+]i. These multiple effects overlap with the proposed block of receptor-mediated Ca2+ entry. The block of K(+)-channels may in unclamped cells reduce the driving force for Ca2+, and thereby interfere with the Ca(2+)-influx.

Calcium↗
PubMed1994

Sitting position for neurosurgery: experience with preoperative contrast echocardiography in 301 patients.

A persisting foramen ovale (PFO) is the most common cause of paradoxical air embolism. To detect right-to-left shunting, transthoracic contrast echocardiography was performed preoperatively in 301 patients scheduled for neurosurgical procedures in the sitting position. Echocardiography yielded evaluable results in 285 patients (94.7%). In 72 of 285 patients (25.2%), a PFO was diagnosed on the basis of contrast echo signals appearing in the left atrium or ventricle within 5 heart cycles after application of contrast medium via a peripheral vein. If echo signals appeared in the left heart after more than 5 heart cycles, an intrapulmonary right-to-left shunt was considered (11 patients, 3.9%). Venous air embolism (VAE) occurred in 27.4% of 226 patients operated on in the sitting position and in none of the 59 patients operated on in a nonsitting position. We conclude that the sitting position during neurosurgery should be avoided in patients with preoperative evidence of a right-to-left shunt at contrast echocardiography to reduce the risk of paradoxical air embolism (PAE).

Adolescent↗
PubMed1994

Computer-assisted neurovegetative monitoring in patients after heart transplantation.

The effects of orthotopic heart transplantation on spontaneous fluctuations of the respiration rate and heart rate were studied with a computer-assisted system for neurovegetative monitoring in 22 patients (mean age +/- SD: 48.7 +/- 9.4 years) 19.5 +/- 14.4 months after transplantation. The control group consisted of 12 healthy volunteers (mean age +/- SD: 38.7 +/- 6.6 years). The mean (+/- SE) respiratory rate was higher in the transplantation group than in the control group (17.7 +/- 0.8/min vs. 14.6 +/- 1.1 breaths/min, P < 0.2). The mean variability of the respiratory rate was smaller in the transplant patients than in the controls (3.7 +/- 0.3 vs. 2.8 +/- 0.4, P < 0.2). The heart rate variability coefficient in the patients after transplantation was lower than that in the controls (1.3 +/- 0.1% vs. 6.9 +/- 0.5%, P < 0.001). Spectral analysis of heart rate variability showed a smaller decrease of variability of respiration (P < 0.05) than of blood pressure regulation (P < 0.001) or of the angiotensin-renin system (P < 0.001). A separate group of 7 transplant patients (mean age 51.0 +/- 7.7 years) had activated cardiac pacemakers and thus no spontaneous physiologic heart rate oscillations. The variability of the respiratory rate in these patients was lower than in the other 22 transplant patients (1.8 +/- 0.2 vs. 3.7 +/- 0.3, P < 0.001). The data provided by multiparametric neurovegetative monitoring support the evaluation of complex regulatory mechanisms of respiratory and cardiovascular function and their adaptability after orthotopic heart transplantation.

Adult↗
PubMed1993

Association of the wasp venom peptide mastoparan with electrically neutral lipid vesicles. Salt effects on partitioning and conformational state.

We have measured circular dichroism signals of aqueous mastoparan and mastoparan-X when titrated with electrically neutral phospholipid unilamellar vesicles. The data could be converted into association isotherms (binding curves) under various conditions of salt content. In spite of the absence of a net charge in the lipid moiety, substantial salt effects have been observed regarding the partition coefficient of the peptide and its conformation in the associated state. These results are discussed on the basis of a general thermodynamic approach for peptide association with lipid bilayers.

Amino Acid Sequence↗
PubMed1993

Impairment of retinal increment thresholds in Huntington's disease.

We have investigated detection thresholds for a foveal blue test light using a Maxwellian view system in 61 normal subjects, 19 patients with Huntington's chorea, 14 patients with Tourette's syndrome, and 20 patients with schizophrenia. Ten measurements were made: The blue test light (1 degree diameter, 500 msec duration) was presented either superimposed on a yellow adaptation field (5 degree diameter) or 500 msec after switching off this field (transient tritanopia effect). In both cases five different background intensities were presented. The only abnormality found was in patients with Huntington's chorea. During adaptation these patients' thresholds are significantly higher than normal (p < 0.005). No change was found in the transient tritanopia effect. Huntington's disease causes degeneration of several different transmitter systems in the brain. Increment threshold testing allows for noninvasive investigation of patients and confirms the involvement of the retina in the degenerative process in Huntington's chorea.

Adaptation, Ocular↗
PubMed1993

Nonselective ion pathways in human endothelial cells.

Four probably different transmembrane pathways are described in human endothelial (EN) cells that are all nonselective for cations. i) A nonselective cation channel that is more permeable for Na+ and K+ than for Ca2+ can be gated by agonists such as histamine. This channel provides an agonist-gated entry route for Ca2+ into EN cells with a single-channel conductance of 25 pS for Na+, K+, and approximately 4 pS for Ca2+ (110 mM). ii) Another Ca(2+)-permeable pathway can be activated by shear stress. This supposedly mechanically activated channel is more permeable for divalent than for monovalent cations and provides mechano-sensing properties to EN cells. iii) A third ionic current, activated by the selective Ca(2+)-ATPase blocker thapsigargin, seems to be related to Ca(2+)-release from Ca(2+)-stores in the endoplasmic reticulum. In EN cells, this Ca(2+)-entry route is cation selective, but cannot differentiate between Na+ and K+. Activation of this nonselective current is associated with an increase in intracellular Ca2+. We therefore assume a Ca(2+)-entry through this thapsigargin-activated pathway. iv) A nickel-blockable, Ca(2+)-permeable, nonselective leak is described that is present in nonstimulated EN cells. It will be discussed whether agonist-gated channels and leak channels might be related to the Ca(2+)-release activated Ca(2+)-entry mechanism.

Animals↗
PubMed1993

Modulation by histamine of an inwardly rectifying potassium channel in human endothelial cells.

1. Whole-cell and single-channel currents were recorded together with intracellular Ca2+ in voltage clamped, single endothelial cells isolated from human umbilical vein. 2. The major current component under resting conditions in the whole-cell configuration was a strongly inwardly rectifying potassium current. 3. This current is due to activation of a K+ channel with an inward conductance of 29 +/- 3 pS (n = 7) with symmetrical 140 mM K+ on both sides of the membrane. This channel could be measured both in the cell-attached and in the inside-out configuration. At potentials below -110 mV both whole-cell and averaged single-channel currents showed a fast inactivation. 4. During stimulation of endothelial cells with histamine, whole-cell K+ currents initially increased but then substantially declined, despite the sustained increase in intracellular Ca2+ concentration ([Ca2+]i). 5. The blockade of the inwardly rectifying K+ channel by histamine could not be observed in cell-attached patches if histamine was added to the bath. 6. It is concluded that endothelial cells possess K+ channels that are directly inhibited by agonists, such as histamine. Blocking these channels may depolarize the cell membrane and thereby reduce the driving force for Ca2+ influx.

Calcium↗
PubMed1993

Control of intracellular calcium by membrane potential in human melanoma cells.

The modulation of intracellular calcium ([Ca2+]i) by the membrane potential was investigated in human melanoma cells by combining the nystatin-perforated patch-clamp technique with Ca2+ measurements. Voltage steps to -100 mV induced a rise in [Ca2+]i and a creeping inward current. These effects were absent in Ca(2+)-free solution and could be blocked by Ni2+ or La3+. Voltage ramps revealed a close correlation between [Ca2+]i and voltage, with the strongest voltage dependence around the resting potential. Long-lasting tail currents, closely correlated with the rise in [Ca2+]i and a reversal potential close to the K+ equilibrium potential, occurred if the membrane potential was clamped back to 0 mV. They were absent if intracellular K+ was replaced by Cs+ and blocked by extracellular tetraethylammonium (5 mM), Ba2+ (1 mM), or a membrane-permeable adenosine 3',5'-cyclic monophosphate analogue. These observations are discussed in relation to cell proliferation. The enhanced expression of K+ channels during cell proliferation provides a positive-feedback mechanism resulting in long-term changes in [Ca2+]i required for the G1-S transition in the cell cycle.

Barium↗
PubMed1993

Microbial metabolism of quinoline and related compounds. XVII. Degradation of 3-methylquinoline by Comamonas testosteroni 63.

A bacterial strain which utilizes 3-methylquinoline as sole source of carbon, nitrogen and energy was isolated from activated sludge. On the basis of its morphological and physiological characteristics, this isolate was classified as Comamonas testosteroni. Four metabolites of 3-methylquinoline degradation were isolated from the culture supernatant and identified as 3-methyl-2-oxo-1,2-dihydroquinoline, 6-hydroxy-3-methyl-2-oxo-1,2-dihydroquinoline, 5,6-dihydroxy-3-methyl-2-oxo-1,2-dihydroquinoline and 2,5,6-trihydroxy-3-methylpyridine. Based on these results, a degradation pathway for 3-methylquinoline is proposed.

Culture Media↗
PubMed1993

Microbial metabolism of quinoline and related compounds. XIX. Degradation of 4-methylquinoline and quinoline by Pseudomonas putida K1.

A bacterial strain, designated K1, which utilizes 4-methylquinoline and quinoline as sole source of carbon, nitrogen and energy was isolated from soil. Based on its morphological and physiological characteristics, it was classified as Pseudomonas putida biovar B. Four metabolites of 4-methylquinoline degradation were isolated from the culture supernatant and identified as 4-methyl-2-oxo-1,2-dihydroquinoline, 8-hydroxy-4-methyl-2-oxo-1,2-dihydroquinoline, 7,8-dihydroxy-4-methyl-2-oxo-1,2-dihydroquinoline and 6-hydroxy-5-(2-carboxyethenyl)-4-methyl-1H-2-pyridone. Formation of the latter compound is suggested to proceed by decarbonylation of a putative meta-cleavage product of the 7,8-dihydroxy derivative. During growth on quinoline four compounds were released into the culture fluid, too. Upon isolation they were identified as 2-oxo-1,2-dihydroquinoline, 6-hydroxy-2-oxo-1,2-dihydroquinoline, 5-hydroxy-6-(3-carboxy-3-oxopropenyl)-1H-2-pyridone and 2H-pyran-2-on-[3,2b]-5H-6-pyridone. Thus it is proved, that Pseudomonas putida possesses two different catabolic pathways for various quinoline derivatives, which are induced selectively depending on the growth substrate.

Biotransformation↗
PubMed1993

Computer-based analysis of continuous non-invasive blood pressure and heart rate variability-methodology and normal values during wakefulness and sleep.

Polysomnographic recordings were made in 10 healthy male adult subjects (mean age 25.1 +/- 2.8 years). Parameters were obtained from continuous non-invasive measurement of blood pressure and from heart rate spectra analysed both in the waking state and during sleep (stage 4). The total heart rate variability (mean +/- SE) was not significantly diminished (p < 0.2; paired t-test) during stage 4 sleep (6.2 +/- 0.5%) as compared with the waking state (7.1 +/- 0.5%). The relative heart rate variability coefficient within the frequency band HRV-II ((3-9)/min) was, however, significantly higher (p < 0.001) during slow-wave sleep (0.55 +/- 0.04) than during wakefulness (0.34 +/- 0.04). This fact is in accordance with results concerning an estimated value of the baroreflex sensitivity, which was also significantly higher (p < 0.001) during sleep stage 4 (7.0 +/- 0.8 ms/mmHg vs. 10.4 +/- 1.4 mmHg).

Adult↗
PubMed1993

[Computer controlled brain death documentation in the intensive care unit].

An interactive, knowledge-based computer system for brain death documentation is presented. The specific exponents BRAINDEX R and G were realised by the software tool Personal Consultant Plus and the programming language Clipper, respectively. The strategies of conclusion were forward chaining for approximate evaluation of coma stages and backward chaining for analysing the brain death syndrome. BRAINDEX was developed for use with an IBM personal computer or compatible equipment. Systemic analyses were compared retrospectively with the data from clinical brain death protocols (n = 132) of 128 comatose patients (mean age 35.1 +/- 15.8 years) with a Glasgow Coma Score of 3. Identical classifications (system vs physician) were found in all patients without diagnosis of brain death (n = 35). Differences related to the findings of the physician were evaluated in lower numbers of the systemic positive diagnosis of brain death (82 vs 89) and higher numbers of impossibility of systemic evaluation (11 vs 2). These results were obtained by conclusions of the computer system drawn by restrictive systemic mechanisms to avoid false-negative diagnoses. The system therefore seems to be useful for documentation, consultation, and as a teaching instrument and data bank in brain death.

Adult↗
PubMed1992

Kinetics of melittin induced pore formation in the membrane of lipid vesicles.

We have investigated the permeabilization of POPC unilamellar vesicle bilayers upon the addition of melittin. This process was measured in an early time range of a few minutes by means of monitoring the release of an entrapped marker, the self-quenching fluorescent dye carboxyfluorescein. Pore formation is indicated by an apparent 'all-or-none' efflux out of individual vesicles and a higher than linear dependence on melittin concentration. Applying a recently developed evaluation procedure, the data are readily converted into the gross number of pores per vesicle formed within the elapsed measuring time t. The results can be generally described in terms of a fast initial rate of pore formation that slows down to a much lower value after a period of about 1 to 2 minutes, following a single exponential time course. The three rate parameters involved are shown to be power functions of the concentration of melittin that is actually associated with the vesicle membrane. These findings are in excellent quantitative agreement with a proposed scheme of reaction steps where the formation of lipid associated peptide dimers becomes rate determining once an initial fast deposit is exhausted.

Ion Channel Gating↗
PubMed1992

Shear stress induced membrane currents and calcium transients in human vascular endothelial cells.

We have measured membrane currents induced by shear stress together with intracellular calcium signals in endothelial cells from human umbilical cord veins. In the presence of extracellular calcium (Ca2+]o), shear stress induced an inward current at a holding potential of 0 mV which is accompanied by a rise in intracellular Ca2+ ([Ca2+]i). In the absence of extracellular calcium shear stress was unable to evoke a calcium signal but still induced a membrane current. The voltage dependence of the shear stress induced current was obtained from difference currents evoked by linear voltage ramps before and during application of shear stress. Its reversal potential Erev shifted from -2.3 +/- 0.8 mV (n = 4) in a nominally Ca2+ free solution to +1.5 +/- 1.6 mV at 1.5 mM [Ca2+]o (n = 4) and to +21.9 +/- 4.4 mV (n = 7) at 10 mM [Ca2+]o. From our data we conclude that shear stress opens an ion channel that is 12.5 +/- 2.9 (n = 7) times more permeable for calcium than for sodium or cesium.

Calcium↗
PubMed1992

Brain death: timing of apnea testing in primary brain stem lesion.

In a 73-year-old patient complete areflexia of the cerebral and peripheral nerves following the rupture of an aneurysm of the basilar artery was diagnosed. During apnea testing the spectral analysis of electroencephalography (EEG) revealed an irreversible shift of peak from 6 to 3 Hz within the low-frequency bands. These findings suggest that apnea testing in patients with primary lesion of the brain stem should be carried out only after an isoelectric EEG.

Aged↗