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Biomedical subjects

W Vogel

Publications and source records attributed to W Vogel.

At least 469 records · Page 26Linked to original sources

[Intensive care in chest trauma (author's transl)].

A statistical analysis of the case material at the Intensive Care Unit, Freiburg, for the years 1975 and 1976 established that 40% and 39% respectively of patients with multiple injuries had also suffered a chest trauma and that the latter was the direct cause of respiratory insufficiency in 61% (1975) and 57% (1976) of patients in need of controlled respiration, i.e. respiratory insufficiency dominated the clinical and pathophysiological picture. The causes were: restricted respiratory movements due to pain, compression of the lungs or pathological changes in the injured lung, and they affected the normal gaseous exchange in a variety of ways. Alveolar hypoventilation with disturbance of ventilation-perfusion, increase in the functional shunt volume, rise in the functional dead space combined with reduced functional residual capacity and compliance result, if left uncorrected, in a drastic increase of resistance on the part of the pulmonary vessels and finally in, often fatal, hyoxaemia and hypercapnia. Regular estimations of the arterial blood gases in air and pure oxygen, of the arterio-alveolar difference in oxygen pressure, shunt volume, dead space and effective compliance of the chest wall and lungs are, therefore, essential. Treatment in an intensive care unit comprises the relief of any acute condition, such as tension pneumothorax, haemothorax, and general measures. Means to relieve pain in patients whose chest injuries are not sufficiently severe to require artificial ventilation are: intercostal blocking, acupuncture or peridural analgesia; efficient breathing exercises are important. The indications for artificial ventilation should be interpreted generously and the decision to perform it should be made at an early stage. The technique is determined by the type of pathological changes in the gaseous exchange and should aim at restoring normal conditions as far as possible.

Blood Gas Analysis↗

Comparison of thymidine, fluorodeoxyuridine, hydroxyurea, and methotrexate blocking at the G1/S phase transition of the cell cycle, studied by replication patterns.

Cultures of human amniotic fluid cells and fibroblasts were temporarily blocked by the replication inhibitors thymidine (dT) surplus, fluorodeoxyuridine (FdU), hydroxyurea (HU), or methotrexate uridine (MU). The respective arresting point at G1-S transition and the homogeneity of the blocked cell population were determined by means of BrdU replication patterns. Most variation of patterns were found after HU. After MU, cells were arrested before the onset of replication, while with dT surplus of FdU an arresting point in early S seemed more likely.

Amniotic Fluid↗

Decrease of DNA synthesis in amniotic fluid cells during the middle part of S-phase revealed by differential chromosome staining after incorporation of BrdU.

The time sequence of DNA replication in partially synchronized human amniotic fluid cells has been analysed, employing BrdU incorporation techniques.--Regardless of the interval between removal of the methotrexate/uridine block and addition of BrdU during S-phase, the treatment results in an R-type replication pattern. Conversely, replacement of BrdU containing medium by another one with thymidine yields G-type replication patterns. A thymidine pulse during the first 4 h of S-phase results in R-type replication patterns; from 7--10 h after block removal it produces G-type pattern. In between, only faint red staining dots can be found indicating a marked decrease of replicational activity during the middle part of the S-phase.

Amniotic Fluid↗

Effects of caffeine on sister chromatid exchange (SCE) after exposure to UV light or triaziquone studied with a fluorescence plus giemsa (FPG) technique.

Studies are reported that are designed to analyze the mechanism by which caffeine reduces the induction of SCE by UV light or alkylating agents. The substantial points are (1) caffeine does not inhibit SCE formation, and (2) the caffeine-mediated apparent decrease of SCE induction after UV or triaziquone exposure is due to a selective destruction of those metaphases otherwise exhibiting a high number of SCE. These findings and their relevance to the ascertainment of the SCE-forming process are discussed.

Animals↗

Silver-staining specificity in metaphases after incorporation of 5-bromodeoxyuridine (BUDR).

Silver staining is reported to be reduced in chromatin substituted by BUDR. This quenching effect allows for the demonstration of replication patterns and differential chromatid staining. Though the differentiation, as compared to other staining techniques, is of inferior quality, it is of theoretical importance concerning the effect of BUDR incorporation into chromatin.

Bromodeoxyuridine↗

[The effect of tramadol, a new analgesic, on respiration and cardiovascular function (author's transl)].

1. The effect of 1-(m-methoxyphenyl)-2-(dimethylaminomethyl)-cyclohexan-1-ol (tramadol; Tramal), a new i.v. administered analgesic, on respiration and cardiovascular function was investigated in 15 patients in a clinic of general surgery. 2. Blood gas analysis revealed that tramadol, unlike morphine-like analgesics, does not depress respiration. 3. The drug did not affect blood pressure, and the observed slight increase in heart rate was transient and statistically not significant.

Analgesics↗

Comparative in vivo mutagenicity testing by SCE and micronucleus induction in mouse bone marrow.

The treatment of mice with repeated injections of BUdR and FUdR allows for the demonstration of differentially stained metaphases from bone marrow after FPG (fluorescence plus Giemsa; Perry and Wolff, 1974) treatment. Thus, it is possible to determine the number of SCE's under in vivo conditions, which appears as a very promising system for mutagenicity testing. We studied the response of this system in comparison to the micronucleus test using six mutagenic agents: triaziquone, cyclophosphamide (CP), dimethylphenyltriazene (PDMT), methylnitronitrosoguandine (MNNG), dimethylnitrosamine (DMNA), and diethylnitrosamine (DENA). With the exception of MNNG and DENA, all these agents induce both, SCE and micronuclei, MNNG and and DENA being ineffective in both systems. The most potent SCE-inducing agent was triaziquone, followed by PDMT, CP, and DMNA. The quantitative comparison indicates that SCE are induced at 1/10-1/100 of the concentrations which are required for the detection of micronuclei.

Animals↗