Biomedical subjects

J Kehr

Publications and source records attributed to J Kehr.

47 records · Page 3Linked to original sources

PubMed1995

[Changes in protein repletion markers in undernourished patients receiving enteral nutrition and its relation with energy and nitrogen balance].

AIM: To study the relationship between the changes in protein repletion indicators and calorie and nitrogen balance in undernourished patients receiving enteral nutrition. PATIENTS AND METHODS: Fourteen patients (11 female, age range 55-85 years old) with an initial serum albumin below 3.5 g/dl or serum transferrin below 200 mg/dl, which received enteral nutrition, were studied. On days one and ten of nutritional support, indirect calorimetry, nitrogen balance and serum levels of albumin, transferrin, pre-albumin and total lymphocyte count were measured. RESULTS: Initial resting energy expenditure was 25.1 +/- 5 Kcal/kg/day (115.4 +/- 20% of that predicted by Harris Benedict equations) and urinary urea nitrogen 5.4 +/- 3.7 g/day. Initial and final nitrogen balances were 66.9 +/- 71 and 81.4 +/- 105.9 mg N/kg/day and mean energy balance throughout the study was +9.0 +/- 7.2 Kcal/kg/day. During the ten days of nutritional support, albumin improved significantly in 0.35 +/- 0.43 g/dl (15.2 +/- 19.8%). Transferrin, pre-albumin and total lymphocyte count did not change significantly. The changes in these last parameters did not correlate with nitrogen or calorie balance. CONCLUSIONS: Probably other factors, besides nutritional balances, influence serum protein levels and these may not change despite an adequate nutritional repletion.

Aged↗

PubMed1993

A survey on quantitative microdialysis: theoretical models and practical implications.

The existing methods of quantitative microdialysis are reviewed. The methods are divided into 8 groups, depending on the mathematical models and theoretical principles used to describe convective diffusion in the extracellular space of the brain. Special emphasis is made to describe each method from a historical perspective, showing its main contribution to recent knowledge, as well as its limitations and drawbacks. It is concluded that those methods based on explicitly derived equations for in vivo recovery are still too approximative and not suitable for routine application. Therefore, empirical models based on varying perfusion flow rates or concentrations of substances in the perfusion solution, found several practical implications. Methods using a reference substance as a marker of in vivo recovery are also discussed. The paper stresses the increasing importance of methods allowing the quantitative evaluation of microdialysis data whenever measuring neurotransmitter release, drug concentrations or pharmacokinetic variables.

Animals↗

PubMed1991

In vivo characterisation of extracellular dopamine, GABA and acetylcholine from the dorsolateral striatum of awake freely moving rats by chronic microdialysis.

Basal extracellular (EC) DA, 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), gamma aminobutyric acid (GABA) and acetylcholine (ACh) were measured in dialysates from the dorsolateral striatum (DLS) of awake rats, every 30 min for 4.5 h each day over a 4-day period. The responsiveness of basal EC DA, DOPAC, HVA and GABA to local perfusion with tetrodotoxin (1 micron) was measured 1 and 4 days after implantation. In addition EC ACh was also measured 4 days after probe implantation. The results of this study indicate that EC levels of DA, DOPAC, HVA, GABA and ACh can be reliably monitored for up to 4 days after probe implantation. In addition, we show that striatal EC levels of DA, GABA and ACh may be regarded as a reflection of ongoing neuronal activity for up to 4 days after implantation of a microdialysis probe.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1990

Regional specific effects of clozapine and haloperidol on GABA and dopamine release in rat basal ganglia.

gamma-Aminobutyric acid (GABA) and dopamine release were measured concomitantly in rat dorsolateral striatum, fundus striati (a ventral region of striatum) and globus pallidus following s.c. administration of haloperidol or clozapine. Release was measured by microdialysis in halothane-anesthetized rats. Clozapine (5.0 mg/kg) increased GABA release in the fundus striati and haloperidol (0.5 mg/kg) increased GABA release in the globus pallidus. In contrast, clozapine (2.5-40 mg/kg) failed to increase GABA release in the globus pallidus and haloperidol (0.1-2.0 mg/kg) failed to increase GABA release in the fundus. Thus, haloperidol and clozapine are clearly distinguished by their effects on GABA release in the fundus striati and globus pallidus (both drugs increased GABA release in the dorsolateral striatum). Dopamine release was increased by haloperidol and clozapine in the two regions of the striatum. However, except in the fundus striati where clozapine-induced increases in dopamine and GABA occurred in parallel, both drugs were more potent in releasing dopamine than GABA. Drug-induced increases in GABA and dopamine release were reversed by addition of 1 microM tetrodotoxin to the perfusion medium. These data suggest that (1) regional differences in the effects of haloperidol and clozapine on GABA release in the basal ganglia may parallel the unique clinical profiles of these drugs; and (2) increases in dopamine release may occur independently of a GABAergic component in the dorsolateral striatum following low doses of haloperidol and clozapine and in the fundus striati following all effective doses of haloperidol.

Animals↗

PubMed1990

Striatal dopamine and glutamate release: effects of intranigral injections of substance P.

The levels of extracellular striatal dopamine and glutamate were measured simultaneously in halothane-anaesthetized rats using microdialysis. Unilateral injections of substance P (0.07 nmol) into the substantia nigra, pars reticulata enhanced the levels of dopamine and glutamate in the ipsilateral striatum. Intranigral injections of neurokinin A (0.09 nmol) enhanced the levels of striatal dopamine, and intranigral injections of gamma-aminobutyric acid (300 nmol) or dynorphin A (0.5 nmol) decreased the levels of striatal dopamine, but none of these had any effect on the levels of striatal glutamate. Local perfusion with the dopamine agonists apomorphine (D1/D2), SKF 38393 (D1) or pergolide (D2) (each at 10(5) M) decreased the levels of striatal dopamine and enhanced the levels of striatal glutamate. In unilateral 6-hydroxydopamine-lesioned rats, basal striatal glutamate levels were decreased bilaterally. Furthermore, on the denervated side intranigral substance P stimulation of striatal glutamate levels was enhanced, while on the intact side intranigral substance P stimulation of striatal dopamine and glutamate levels was similar to that seen in normal rats. These findings suggest that striatonigral substance P provides a stimulatory regulation of ipsilateral striatal glutamate release. Furthermore, it is indicated that striatal glutamate release can also be regulated by dopamine terminals.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1989

Characterization of gamma-aminobutyric acid and dopamine overflow following acute implantation of a microdialysis probe.

The present study characterized the voltage and calcium dependence of gamma-aminobutyric acid and dopamine overflow after the acute implantation of a microdialysis probe. Probes were implanted in dorsolateral striatum and globus pallidus. Experiments were performed under light halothane anesthesia. Basal, extracellular levels of GABA were not affected by tetrodotoxin (TTX) and were increased to 140 percent of basal values by calcium free Ringer. Basal, extracellular levels of dopamine were reduced to 14 percent of basal values by the addition of TTX and to 30 percent of basal values by the removal of calcium from the Ringer solution. The results suggest that in this in vivo preparation basal extracellular dopamine is largely of vesicular origin while GABA is not.

Animals↗

PubMed1989

[Levels of homovanillic acid and 5-hydroxyindoleacetic acid in the cerebrospinal fluid in patients with focal cerebral ischemia].

The investigated group comprised 35 patients where clinical examination revealed focal cerebral ischaemia in the area of the a. cerebri media. In the group of elderly patients above 60 years, as compared with controls, the homovanillic acid (HVA) and 5-hydroxyindolacetic acid (5-HIAA) concentration in cerebrospinal fluid was elevated. In the group of patients under 60 years no changes in the concentration of these metabolites were found. In older patients the increased level of metabolites in cerebrospinal fluid persisted also after three days following the attack, while in younger patients the elevated HVA and 5-HIAA levels were found only in specimens collected up to three days.

Adult↗

PubMed1988

Fast HPLC estimation of gamma-aminobutyric acid in microdialysis perfusates: effect of nipecotic and 3-mercaptopropionic acids.

A method for rapid, automated (less than 5 min), and sensitive (detection limit 50 fmol/10 microliter) determination of gamma-aminobutyric acid (GABA) is described. The method is based on precolumn derivatization with o-phthaldialdehyde/t-butylthiol reagent and separation by reverse-phase HPLC with electrochemical detection under isocratic conditions. A 100 X 4 mm Nucleosil 3 C18 column was used; the mobile phase consisted of 0.15 M sodium acetate, 1 mM EDTA (pH 5.4), and 50% acetonitrile; the flow rate was 0.8 ml/min. The potential of the glassy carbon working electrode was +0.75 V. The method allows for the monitoring of GABA levels in the extracellular fluid sampled by microdialysis as documented in the present study when 0.5 mM nipecotic acid is infused via the probe, or 3-mercaptopropionic acid is injected at a dose of 100 mg/kg i.p. There was a 15-fold increase of extracellular GABA after nipecotic acid, whereas in the second case the inhibition of GABA synthesis was followed by a 74% decrease of GABA as compared to basal levels.

3-Mercaptopropionic Acid↗

PubMed1988

In vivo microdialysis as a technique to monitor drug transport: correlation of extracellular cocaine levels and dopamine overflow in the rat brain.

A sensitive and rapid HPLC-UV method for in vivo determinations of cocaine levels in extracellular fluid of specific brain regions and plasma is described. Free drug levels resulting from intravenous administration of cocaine were sampled using in vivo microdialysis probes simultaneously located in the jugular vein, nucleus accumbens, and anteromedial caudate-putamen of halothane-anesthetized rats. In a separate group of animals, the influence of cocaine on extracellular dopamine concentrations in the anteromedial caudate-putamen was also assessed. The time dependences of changes in cocaine concentration in each of the above regions were congruent, and peak concentrations were reached 10 min after the drug was administered. The half-lives of cocaine in the blood, nucleus accumbens, and anteromedial caudate-putamen were estimated to be 31.5, 29.1, and 21.4 min, respectively. A repeated injection of cocaine, given 90 min later, produced a maximal cocaine level and pharmacokinetic profile that were indistinguishable from those of the initial infusion. Cocaine was concentrated to a greater extent in brain than in blood, a feature consistent with the action of a lipophilic drug. In addition, extracellular dopamine levels measured in the anteromedial caudate-putamen following cocaine infusions closely mirrored those of cocaine itself. The ability to measure the free concentration of drugs by microdialysis should be applicable to a wide range of in vivo pharmacological studies.

Animals↗

PubMed1987

Adenine nucleotide levels and regional distribution of ATP in rabbit spinal cord after ischemia and recirculation.

Rabbit spinal cords were subjected to 10 to 40 minutes of ischemia with and without 4 days of recirculation and L-4 segment was analyzed for adenylates and ATP-induced bioluminiscence. ATP level and energy charge was progressively reduced by increasing durations of ischemia. Regional evaluation of ATP-induced bioluminiscence after 10 and 20 minutes of ischemia revealed ATP depletion mainly in the gray matter of spinal cord. Forty minutes of ischemia resulted in complete reduction of ATP bioluminiscence in both gray and white matter. Within 4 days of recirculation following all periods of ischemia studied, only partial metabolic recovery occurred. Restitution of ATP-induced bioluminiscence was regionally heterogeneous, reduced predominantly in the anterior horns of gray matter.

Adenine Nucleotides↗

PubMed1985

Rapid determination of adenine nucleotides in brain tissue by ion-paired reversed-phase column liquid chromatography under isocratic conditions.

A rapid method for analysis of adenine nucleotides (AMP, ADP and ATP) in nervous tissue based on ion-paired reversed-phase column liquid chromatography under isocratic conditions is described. An optimal composition of elution buffer was 25 mM potassium phosphate and 4% triethylamine adjusted to pH 6.5 with phosphoric acid. Typical separation time did not exceed 10 min with a 10-cm long compact glass cartridge packed with 5-microns silica C18. The method was employed to determine ATP, ADP and AMP concentrations in rat brain extracts and values thus obtained were compared with those published elsewhere.

Adenine Nucleotides↗