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Biomedical subjects

B Kohler

Publications and source records attributed to B Kohler.

At least 109 records · Page 6Linked to original sources
PubMed1986

Control of end-tidal halothane concentration. Part A: Anaesthesia breathing system and feedback control of gas delivery.

Conventional anaesthetic breathing systems are not designed to control end-tidal gas concentrations, nor can they be used to measure accurately the uptake of oxygen or of anaesthetic agent. We built and tested a leak-tight closed-loop anaesthetic breathing system with low solubility to volatile anaesthetic agents and with efficient gas mixing. The system included a water-sealed spirometer, a small carbon dioxide absorber, a coaxial tube to the patient, a circulating pump and feedback controllers for system volume and anaesthetic concentration. Feedback control was implemented to adjust and control automatically the end-tidal anaesthetic concentration and the volume of the system with oxygen supplied through a mass flow controller and with halothane supplied by a titrating syringe. Controller gains, as a function of body weight, were found using a nine-compartment tissue uptake model. Stability was maintained with +/- 50% changes in alveolar ventilation and cardiac output. During subsequent investigations in an animal model, arterial, mixed venous and cerebral venous blood halothane concentrations were measured to show that the feedback-controlled halothane induction was optimized. We conclude that feedback control appears to be clinically applicable for adjusting the end-tidal halothane concentration and system volume to provide a rapid and optimized induction of anaesthesia.

Anesthesia, Inhalation↗
PubMed1985

Pharmacokinetics of amiodarone, desethylamiodarone and other iodine-containing amiodarone metabolites.

In 23 patients treated with the iodine-containing antiarrhythmic drug amiodarone, the plasma concentrations of amiodarone, desethylamiodarone and iodine have been studied. Besides amiodarone and desethylamiodarone, a pool of iodine-containing substances, NANDAI (non-amiodarone-, non-desethylamiodarone-iodine), was present. At steady state the iodine content of NANDAI amounted to 64% and the iodine content of amiodarone plus desethylamiodarone to 36% of total serum iodine. At steady state 26% of the NANDAI fraction was made up of inorganic iodide, the average plasma concentration of which was at least 40 times above the upper limit of the normal range. The serum elimination half-life of NANDAI of 57-160 days exceeded that of amiodarone (35-68 days) and of desethylamiodarone (31-110 days). At steady state the serum concentration of desethylamiodarone appears to be related to the concentration of amiodarone by a Michaelis-Menten type function, yielding a Km of amiodarone of 2.45 mumol/l and a maximal desethylamiodarone concentration of 3.61 mumol/l.

Adolescent↗
PubMed1984

6-Fluoro-vitamin D3: a new antagonist of the biological actions of vitamin D3 and its metabolites which interacts with the intestinal receptor for 1 alpha,25(OH)2-vitamin D3.

The biological activity and the binding affinity for the 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] intestinal receptor of a new fluorine-containing vitamin D compound, namely 6-fluoro-vitamin D3 (6-F-D3), is reported. A significant interaction of 6-F-D3 with the 1,25(OH)2D3 receptor was found, with a relative competitive index (RCI) of 0.26 +/- 0.04, which is intermediate between 25-hydroxyvitamin D3 (0.14 +/- 0.01) and 1 alpha-hydroxyvitamin D3 (0.46 +/- 0.08), where the RCI of 1,25(OH)2D3 is defined to be 100. In contrast, vitamin D3 was unable to interact with the 1,25(OH)2D3 receptor. Also, the biological activity of 6-F-D3 was assessed in vivo in the vitamin D-deficient chick. 6-F-D3 at doses up to 130 nmol displayed no biological action on either intestinal calcium absorption (ICA) or bone calcium mobilization (BCM) over the time interval of 14-48 h after dosing. However, when 130 nmol 6-F-D3 was given 2 h before and 6 h after vitamin D3 (1.62 nmol), a significant inhibition of vitamin D-mediated ICA was noted. Also, a dose of 130 nmol 6-F-D3 given 2 h before and 6 h after 1,25(OH)2D3 (0.26 nmol) significantly inhibited ICA, as measured at 12 h. 6-F-D3 is the first vitamin D analog found which has an ability to both bind to the 1,25(OH)2D3 receptor and to antagonize the production of biological responses by 1,25(OH)2D3.

Animals↗
PubMed1981

Biochemical changes in a 100 km run: carbohydrates, lipids, and hormones in serum.

During the 100 km race in Biel, Switzerland, seven-well trained men (age 33.3 +/- 3.5 years; V02 max. 59.9 +/- ml/kg) have been investigated. Their mean running time over the 100 km distance averaged 10.41 +/- 1.25 h. In contrast to almost unchanged blood glucose and lactate concentrations, blood lipids showed significant changes. Triglycerides decreased about two-fold, whereas glycerol and free fatty acids increased to extremely high concentrations (0.628 and 2.44 mmol/l respectively). Plasma insulin after the run was unaffected, whereas growth hormone, aldosterone and cortisol concentrations were significantly increased. With the exceptions of a still significantly elevated aldosterone and lactate concentration as well as a decreased triglyceride concentration all other values in the blood are restored to normal 24 h after completion of the run.

Adult↗
PubMed1978

[Experimental coronary ligation in swine: reduction of myocardial infarct and hemodynamic and metabolic changes by means of the calcium antagonist RO 11-1781].

In a comparative study the effect of the new calcium antagonist Ro 11-1781 on experimental infarct size and left ventricular function in the pig has been investigated. The calcium antagonist was administered 30 min prior to ligation of the left anterior descending coronary artery and twice daily on the following 4 days. For morphometric assessment of infarct size the ventricular myocardium was cut into slices and stained with nitro-benztoluene. There was a significant reduction in infarct size of about 25% in the calcium antagonist-treated group in comparison with the control group. After coronary occlusion left ventricular function is equally depressed in both groups, as is myocardial lactate extraction, which becomes negative.

Animals↗
PubMed1977

[Effect of pindolol (Visken) on the size and hemodynamics of the exerimental myocardial infarct in the pig].

In a comparative study the effect of pindolol (Visken, Sandoz) on experimental infarct size and left ventricular function in the pig has been investigated. Pindolol was given 30 min prior to the ligation of the left anterior descending coronary artery and on the following 5 days twice daily in a dosage of 0.05 mg/kg body weight. For morphometric assessment of infarct size the ventricular myocardium was cut into slices and stained with nitro-benztoluene. There is a significant reduction of infarct size (by one third) in the pindolol-treated group as compared to the controls. In addition, deterioration of left ventricular function is less marked in the pindolol-treated group.

Animals↗
PubMed1976

The development of a reliable and sensitive bioassay for gastrin in body fluids.

The sensitivity and reliability of the Ghosh and Schild rat stomach preparation was improved by implantation of bulky intragastric cannulae, recirculation of the perfusate and measurement of conductivity instead of pH. With these procedures, the threshold values for gastrin I were in the range of 1-2 ng. In attempts to increase the sensitivity further it was shown that neither vagotomy nor antrectomy influenced the sensitivity of the method. The threshold values were not lowered by attempts to reduce gastrin metabolism through nephroligature or small bowel resection. Although rats fitted with portacaval shunts did raise the threshold, the limited increase in sensitivity was also achieved by selecting the rats that gave an initially high response to a test dose of gastrin thus avoiding the complicated shunt operation. The assay procedure enabled statistically valid measurements of gastrin in plasma and from tumour extracts from patients suffering from the Zollinger-Ellison Syndrome to be assayed using a 2 + 2 block design.

Analysis of Variance↗
PubMed1975

Secretin snuff: evaluation of the action on pentagastrin-stimulated gastric acid secretion and on pancreatic bicarbonate production.

In an informative qualitative study 75 U (near the range of 1 U/kg) secretin given as a snuff resulted in a weak but significant stimulation of pancreatic bicarbonate output in 8 volunteers studied. The result further indicated that this dose would slightly inhibit pentagastrin-stimulated gastric acid secretion. This was confirmed in a quantitative study at the dose of 150 U (similar to 2 U/kg), and the mean amount of inhibition of MAO was 30% in the 10 subjects studied. A supramaximal dose of 1 mg (approximatively 54 U/kg) of synthetic secretin given to one volunteer resulted in a transient block of near maximally pentagastrin-stimulated gastric acid secretion. The amount of acid inhibition as compared to a control experiment was 45% in the first and 52% in the two post-secretin hours. These results indicate that secretin given as a snuff at dose levels that would induce maximal pancreatic secretion when given as an i.v. injection results only in a weak inhibition of stimulated gastric acid secretion and evokes only a little stimulation of pancreatic bicarbonate secretion. Supramaximal secretin snuff doses have, however, a potent effect on both gastric and pancreatic secretion that is of similar order to that achieved by intravenous secretin. Owing to the obviously incomplete absorption of secretin through the nasal mucosa, secretin snuff is unlikely to solve the therapeutic problem of duodenal ulcer disease. If, however, an active fragment of the peptide could be synthetized at a reasonable price, the greater convenience of pernasal application might compensate for the partial loss of action.

Adult↗