Biomedical subjects

L Barth

Publications and source records attributed to L Barth.

At least 19 recordsLinked to original sources

PubMed2005

Circadian variation of the cell proliferation in the jejunal epithelium of rats at weaning phase.

Circadian variation in cell proliferation of the jejunal epithelium of 18-day-old rats was studied using the 2-h arrested metaphase score and crypt isolation method. A continuous decrease in the arrested metaphases occurred from 07.00 h to 13.00 h. From 17.00 h arrested metaphase values increased and were maintained at the higher level during the dark period as showed by Cosinor analyses (P < 0.05). These results indicate that in the young rat there is already a circadian variation in jejunal epithelial cell proliferation as early as 18 days. We can even suggest that the presence of a circadian rhythm at weaning contributes to the steady state of cell proliferation in the intestinal epithelium observed in adult life.

Animals↗

PubMed2004

Glycine-induced neurotoxicity in organotypic hippocampal slice cultures.

The role of the neutral amino acid glycine in excitotoxic neuronal injury is unclear. Glycine coactivates glutamate N-methyl-D-aspartate (NMDA) receptors by binding to a distinct recognition site on the NR1 subunit. Purely excitatory glycine receptors composed of NR1 and NR3/NR4 NMDA receptor subunits have recently been described, raising the possibility of excitotoxic effects mediated by glycine alone. We have previously shown that exposure to high concentrations of glycine causes extensive neurotoxicity in organotypic hippocampal slice cultures by activation of NMDA receptors. In the present study, we investigated further properties of in vitro glycine-mediated toxicity. Agonists of the glycine recognition site of NMDA receptors (D-serine and D-alanine) did not have any toxic effect in hippocampal cultures, whereas competitive blockade of the glycine site by 7-chlorokynurenic acid was neuroprotective. Stimulation (taurine, beta-alanine) or inhibition (strychnine) of the inhibitory strychnine-sensitive glycine receptors did not produce any neurotoxicity. The toxic effects of high-dose glycine were comparable in extent to those produced by the excitatory amino acid glutamate in our model. When combined with sublethal hypoxia/hypoglycemia, the threshold of glycine toxicity was decreased to less than 1 mM, which corresponds to the range of concentrations of excitatory amino acids measured during in vivo cerebral ischemia. Taken together, these results further support the assumption of an active role of glycine in excitotoxic neuronal injury.

Alanine↗

PubMed1996

bFGF enhances the protective effects of MK-801 against ischemic neuronal injury in vitro.

The neuroprotective activity of basic fibroblast growth factor (bFGF) in combination with the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 was evaluated in organotypic hippocampal slice cultures. Oxygen/glucose deprivation produced neuronal damage which was assessed using propidium iodide fluorescence. Treatment with increasing doses of bFGF demonstrated significant neuroprotection that was optimal at 10 ng ml-t. This effect was diminished at higher concentrations. MK-801, at the optimal concentration of 30 microM, demonstrated greater neuroprotective efficacy than bFGF. However, bFGF significantly enhanced the protection conferred by MK-801 alone. These results suggest that neurotrophic factors such as bFGF may augment the neuroprotective effects of NMDA antagonists against ischemic neuronal injury.

Animals↗

PubMed1996

Combination therapy with MK-801 and alpha-phenyl-tert-butyl-nitrone enhances protection against ischemic neuronal damage in organotypic hippocampal slice cultures.

In vitro combinations of MK-801, an NMDA receptor antagonist, and alpha-phenyl-tert-butyl-nitrone (PBN), a free radical scavenger, have been tested for possible additive neuroprotective effects against anoxia/hypoglycemia (Ax/Hg)-induced neuronal damage. Rat organotypic hippocampal slice cultures were exposed to Ax/Hg for different lengths of time to vary the severity of the insult. Cell death (CD) was assessed using propidium iodide fluorescence and expressed as a percentage of the total neuronal cells present. Pretreatment with PBN alone (500 microM) provided significant protection against moderate ischemic injury and reduced CD from 65% in controls to 2% in the treated group (P < 0.003). A longer ischemic exposure time caused more neuronal damage, which was only slightly reduced by PBN, but significantly reduced by MK-801 (30 microM) (4% CD with MK-801 vs 75% CD in controls; P < 0.0003). With a further increase in the time of ischemic exposure, MK-801 was still protective (33% CD with MK-801 vs 90% CD in controls; P < 0.002), although the combination MK-801 + PBN was more efficient (7% CD with combination, P < 0.01 compared to MK-801 alone). With yet a further increase in the ischemic exposure, PBN or MK-801 alone was not protective; however, a combination of the two still provided significant protection (64% CD with combination vs 100% CD with MK-801 alone; P < 0.01). PBN was protective when administered up to 2 h after Ax/Hg (66% CD in controls vs 36% CD with PBN 500 microM; P < 0.007). The combination MK-801 + PBN was able to increase the therapeutic window up to 3 h (61% CD in controls vs 41% with PBN alone vs 7% with MK-801 + PBN; P < 0.002 compared to PBN alone). In conclusion, the combination of MK-801 and PBN increases both the efficacy and the time window of protection against ischemia.

Animals↗

PubMed1979

[Tetanus-Myomechanographic measurement of receptor liberation by pyridostigmine in neuromuscular block produced by d-tubocurarine, gallamine, pancuronium or alcuronium (author's transl)].

In 48 patients anaesthetized with nitrous oxide-oxygen and hexobarbitone the neuromuscular (n-m) block (greater than or equal to 95% depression) produced by roughly equipotent doses of d-tubocurarine (dTC), gallamine (GALL), pancuronium (PANC) or alcuronium (ALC), respectively, was antagonized by 10 mg of pyridostigmine (P) applied intravenously 35-460 min after the relaxant at variable levels of spontaneous recovery from n-m block. Muscular reactions to tetanic stimulation (30 to 400 Hz, 4-5 s each) of the ulnar nerve transmitted by a force-displacement system served as a measure for calculating the relative amount of n-m receptors liberated from relaxant molecules. Within 3-10 min after its injection P increased the number of relaxant-free n-m receptors by 16 +/- 6% (M +/- SD). Thereafter recovery progressed at similar speed as before. Reinjections of 5-10 mg P were comparably as effective as the first injection. No correlations were to be found between the effectiveness of P and the dose of relaxant applied (r = 0,12 to 0,27), the level of recovery reached before P (r = 0,32), or the time at which P was injected after the relaxant (r = -0,39), respectively. However, the amount of receptors liberated by P decreased with increasing recovery from n-m block and with increasing time interval between the relaxant and the antidote injection. P was significantly more effective (P less than 0,01), when applied within 150 min after the relaxant than at applications after that time. The relative number of receptors liberated by this drug was insignificantly larger in the PANC-and GALL-block than in the ALC-and dTC-block.

Alcuronium↗

PubMed1977

[Control of muscle relaxant effect].

Explore the source record for details and available documents.

Muscle Relaxants, Central↗

PubMed1977

[Long-lasting neuromuscular effects of non-depolarizing muscle relaxants, as measured by tetanic stimulation (author's transl)].

Spontaneous decurarization after single doses of tubocurarine (d-Tc) 0.44+/-0.04 mg/kg, pancuronium (PANC) 0.093+/-0.013 mg/kg, gallamine (GALL) 1.69+/-0.31 mg/kg and alcuronium (ALC) 0.193+/-0.02 mg/kg b.w. was investigated by means of tetanic stimulation of the ulnar nerve in 37 routinely anaesthesized adults of either sex. Tetani of 4-5 s and 30-400 Hz were sustained prior to muscle relaxation during light anaesthesia. After the injection of muscle relaxants the frequency of incomplete myographic black-out revealed slight underestimation of the doses of both GALL and ALC. However, no significant differences could be found between the drugs investigated, as far as latency of recovery is concerned. Recovery time to 30 Hz (=75-80% receptor occlusion) was 110+/-37, 109+/-66, 92+/-25 and 90+/-35 minutes for d-Tc, GALL, PANC and ALC, respectively. Up to 100 Hz (=50% receptor occlusion) it was 328+/-69, 327+/-83, 282+/-88 and 218+/-66 minutes for d-Tc, ALC, GALL and PANC, respectively. Myographic recurarization rather frequently occurred with ALC, GALL and d-Tc. The use of antidotes seems urgently to be indicated whenever non-depolarizing muscle relaxants have been applied in the above mentioned range of dosage.

Adolescent↗

PubMed1975

[Clinical studies on the narcotic effects of nitrous oxide (author's transl)].

In 340 male and 450 female patients of various age the depth of anaesthesia acquired during induction with nitrous oxide (75%) and oxygen (25%) was investigated by means of clinical methods. Premedication consisted of atropine (0,1 mg/1o kg body weight) in 26% and atropine plus pethidine (or morphine) in 74% of the patients, respectively of the total, 2.4% of the patients failed to enter the analgesic-amnestic level, determined as I-3, while 97.6% occupied and more than 50% of the patients surpassed it. Thus the MAC of nitrous oxide in man seems to be 75 volume per cent or less. The depth of anaesthesia varied significantly with duration of inhalation (p smaller than 0.001). Up to five minutes of inhalation 5% of the patients failed to arrive at I-3, while 95% reached this plane and 46% surpassed it. After more than five minutes of inhalation the corresponding values were 1%, 99% and 56%, respectively. Significantly deeper levels of anaesthesia were acquired by females than by males (p smaller than 0.001) during the initial 10 minutes of inhalation. After that time sexual differences disappeared. Patients of good physical condition reached deeper planes of anaesthesia than bad risk cases (p smaller than 0.001). The use of analgesics as premedicants reduced the effectiveness of nitrous oxide, as compared to premedicated patients with atropine alone (p smaller than 0.01 in men and p smaller than 0.05 in women). Adults below 30 years of age entered the stages II and III-1 significantly less frequently than older patients (p smaller than 0.01), whereas children (up to 14 years of age) reached those stages significantly more frequently than adult patients in general (p smaller than 0.01).

Adolescent↗

PubMed1973