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Biomedical subjects

K D Höhle

Publications and source records attributed to K D Höhle.

At least 19 recordsLinked to original sources
PubMed2000

Muscarinic control of histamine release from airways. Inhibitory M1-receptors in human bronchi but absence in rat trachea.

Isolated human bronchi and rat tracheae were incubated in organ baths to measure histamine release. The calcium ionophore A23187, 3 micromol/L in rat trachea and 10 micromol/L in human bronchi, stimulated histamine release by 145 +/- 50% (n = 6) and 270 +/- 48% (n = 7) above the prestimulation level, respectively. Acetylcholine (100 pmol/L; human bronchi) or oxotremorine (1, 100, 10,000 nmol/L; rat trachea) did not affect the spontaneous histamine release. In rat tracheae neither acetylcholine nor oxotremorine inhibited A23187-evoked histamine release, whereas 100 pmol/L acetylcholine significantly suppressed the evoked histamine release in human bronchi by 86%. For receptor characterization the following subtype-specific muscarinic receptor antagonists were applied: pirenzepine (M1 subtype), para-fluorohexahydrosiladifendiol (pFHHSiD; similar affinities at human cloned M1-, M3-, and M4-receptors), AF-DX 116 (M2 subtype), and clozapine (antagonist at cloned M1-, M2-, M3-receptors; agonist at cloned M4-receptors). Pirenzepine, pFHHSiD, AF-DX 116, and clozapine (100 nmol/L each) antagonized the inhibitory effect of 100 pmol/L acetylcholine by 83 +/- 20% (n = 6), 83 +/- 9% (n = 8), 50 +/- 14% (n = 6), and 35 +/- 7% (6). In conclusion, a species difference exists in the cholinergic control of histamine release between human and rat airways. In human airways muscarinic receptors most likely of the M1 subtype are involved in the inhibitory control of mast cell function, whereas such an inhibitory pathway does not exist in the rat trachea.

Acetylcholine↗
PubMed1997

Non-neuronal acetylcholine, a signalling molecule synthezised by surface cells of rat and man.

Acetylcholine acts as a prominent transmitter in the central and peripheral nervous system. The aim of the present study was to investigate whether mammalian non-neuronal cells can synthesize and store acetylcholine. A cotton tipped applicator (Q-tip) was used to collect surface cells from airways and alimentary tract. Histological inspection indicated that rubbing of the luminal surface of human bronchi did not penetrate the basal membrane. Acetylcholine was measured by an HPLC-method using substrate-specific enzyme reactor-columns. Non-neuronal acetylcholine was found in cells covering inner and outer surfaces of rat and man. For example, acetylcholine was detected in the surface epithelium of human bronchi (33 pmol/g), mouth (female 0.7 and male 8 pmol/sample), small and large intestine (800 and 16 pmol/g, respectively), gall bladder (12 pmol/g), vagina (6 pmol/sample), skin 1000 (pmol/g) and in pulmonary pleura (5 pmol/sample). Somewhat higher amounts of acetylcholine were found in rat tracheal and intestinal epithelium and in rat skin. The synthesizing enzyme choline acetyltransferase (ChAT) was demonstrated in human surface epithelium by immunohistochemistry and by Western blot analysis. Enzymatic ChAT activity was demonstrated in isolated epithelial cells of human bronchi and small intestine (3.5 and 28 nmol/mg protein/h, respectively). Applied acetylcholine (in nM concentrations) increased, whereas inhibition of ChAT activity by bromoacetylcholine (10 microM) reduced the growth of cultured human bronchial epithelial cells. Inhibition of cell growth occurred also in the presence of atropine (1 microM) together with (+/-)-tubocurarine (30 microM). In conclusion, the present experiments demonstrate a widespread existence of non-neuronal acetylcholine in surface cells of man. Non-neuronal acetylcholine may act as a local signalling molecule.

Acetylcholine↗
PubMed1997

Acetylcholine via muscarinic receptors inhibits histamine release from human isolated bronchi.

Human bronchi were incubated in organ baths to measure histamine release. The calcium ionophore A23187 (10 mumol/L; 1 min) stimulated histamine release by 148 +/- 28% (n = 11) above the prestimulation level but was ineffective in epithelium-denuded bronchi. Neither bradykinin (0.1 mumol/L) nor compound 48/80 (10 micrograms/ml) triggered the release of histamine from epithelium-intact bronchi. Acetylcholine did not affect spontaneous histamine release (about 2 nmol/g x 5 min) but inhibited A23187-evoked histamine release in an atropine-sensitive manner. Already a concentration as low as 0.1 nmol/L acetylcholine was effective, the maximal inhibition (by 89%) occurred at 100 nmol/L, whereas a concentration of 10 mumol/L acetylcholine was ineffective. Oxotremorine (1 nmol/L), a stable agonist at muscarinic receptors, suppressed stimulated histamine release completely. Physostigmine (0.1 mumol/L), an acetylcholinesterase inhibitor, reduced A23187-evoked histamine release by 58%. Antihuman IgE antibody stimulated histamine release by 127 +/- 30% (n = 6) above the prestimulation level. Acetylcholine (100 nmol/L) inhibited also the immunologically evoked histamine release by 70%. In conclusion, the present experiments provide a model to characterize mast cells that are localized in or close to the airway surface epithelium. Acetylcholine via muscarinic receptors strongly inhibits the releasability of these mucosal mast cells being among the first cells to interact with inhaled antigens and environmental agents. The inhibitory action of physostigmine indicates the involvement of endogenous, probably non-neuronal acetylcholine expressed in airway epithelial cells.

Acetylcholine↗
PubMed1995

Release of [3H]acetylcholine in human isolated bronchi. Effect of indomethacin on muscarinic autoinhibition.

Receptor-mediated regulation of acetylcholine release in the airways, particularly in humans, remains unclear. In the present study, the tissue content of acetylcholine and release of [3H]acetylcholine were measured in freshly dissected human bronchi obtained at thoracotomy. Large (main and lobar bronchi) and small (segmental and subsegmental bronchi) airways contained considerable amounts of endogenous acetylcholine (300 +/- 50 pmol/100 mg wet weight), whereas significantly less was found in lung parenchyma (60 +/- 30 pmol/100 mg). Isolated small bronchi incubated in an organ bath with the precursor [3H]choline synthesized significant amounts of [3H]acetylcholine (26,000 +/- 4,000 dpm/100 mg). Subsequent transmural stimulation (four 20 s trains at 15 Hz) of radiolabeled bronchi caused an enhanced tritium outflow that was abolished by removal of extracellular calcium or by tetrodotoxin. HPLC analysis of the medium collected before, during, and after transmural stimulation showed that the electrically stimulated tritium outflow represented exclusively [3H]acetylcholine, whereas the outflow of [3H]choline and [3H]phosphorylcholine was not affected by electrical stimulation. Oxotremorine (0.1 and 1 mumol/L) inhibited evoked [3H]acetylcholine release in a concentration-related manner, whereas atropine (0.03 mumol/L) enhanced evoked [3H]acetylcholine release. Inactivation of cyclooxygenase activity by 3 mumol/L of indomethacin did not impair the inhibitory effect of 0.1 or 1 mumol/L of oxotremorine. In conclusion, the present experiments indicate a considerable cholinergic innervation of human large and small airways.

Acetylcholine↗
PubMed1995

Effect of inhaled steroids on cholinergic transmission in human isolated bronchi.

Steroids have been found to facilitate cholinergic transmission in skeletal muscle, but possible effects in airways smooth muscles have not been studied. Therefore, choline acetyltransferase (CAT) activity, tissue content of stored acetylcholine and release of newly-synthesized [3H]acetylcholine were were measured in freshly-dissected human bronchi. All lung tissue was obtained from patients with lung cancer at thoracotomy. Group I bronchi were obtained from patients who also suffered from chronic obstructive bronchitis and had been treated for at least 6 weeks before surgery with daily doses of four puffs of flusinolid. Group II bronchi were obtained from patients who did not suffer from chronic obstructive airways disease and had not been treated with steroids. Neither CAT activity (3.1 nmol.h-1.mg protein-1) nor acetylcholine tissue content (260 pmol.100 mg-1), or electrically evoked [3H]acetylcholine release (about 2,000 dpm.100 mg-1) differed in the two groups. This cross sectional study indicates that inhaled steroids do not change cholinergic transmission beyond the level observed in the airways obtained from patients with lung cancer who do not suffer from chronic airways disease and have not been treated with inhaled steroids. This suggests that inhaled steroids can be given chronically without the induction of a facilitatory side-effect on cholinergic transmission within the airways.

Acetylcholine↗
PubMed1995

[Does the "Bergetrokar" decrease the rate of intraoperative complications in laparoscopic cholecystectomy?].

Several international surveys have proved the laparoscopic cholecystectomy as a safe surgical technique. In spite of the good results there still exist operation-specific technical problems. The perforation of the gallbladder during dissection or while extracting it from the abdominal cavity can lead to severe complications. We analysed retrospectively 352 extractions of the gallbladder carried out with our 'Bergetrokar'. In 1.4% occurred perforation of the gallbladder and in 0.85% we had trouble with the healing. In 3.5% extraction could not be performed with the 'Bergetrokar'. Regarding these results our rates have been lower as compared in literature. In our opinion the extraction of the gallbladder through the lateral incision using the Bergetrokar represents a further step toward a safe extraction of the stonefilled gallbladder. Further the infection rate at the umbilical incision is reduced.

Cholecystectomy, Laparoscopic↗
PubMed1978

[Insufficient treatment of fractures of the hand (author's transl)].

The treatment of fractures of the hand cannot be standardized, the procedure to be used has to be determined from case to case. Besides age and profession the patients intelligence and his readiness to cooperate are of importance. Sometimes osteosynthesis is not successful because these factors are disregarded. In some cases immediate amputation will not only shorten the time of treatment considerably but also prevent an inept psychic attitude (pension neurosis). Correct assessment of the injury during the first treatment may be decisive for failure or success, because a second operation will not yield a good result.

Amputation, Surgical↗
PubMed1977

[Hemobilia, a rare and dangerous postoperative complication].

3 cases of severe postoperative hemobilia are reported, one patient with an echinococcus cysticus of the liver, two others after surgical procedures on biliary tract. Diagnostic means as cholangiography, coeliacography, scanning of the liver and endoscopic retrograde cholangiography were not possible because of the massive bleeding. In those cases, if no other sources of bleeding are found, only esophago-gastro-duodenoscopy can leed to the correct diagnosis. In gastrointestinal bleeding after surgical manipulation on the biliary tract, the duodenum and the pancreas, hemobilia is a possible cause.

Adult↗
PubMed1976

[Studies on pharmacokinetics and biotransformation of ipratropiumbromide in man (author's transl)].

Studies into the human pharmacokinetics of (8r)-3alpha-hydroxy-8-isopropyl-1 alphaH, 5 alphaH-tropanium-bromide- (+/-)-tropate (ipratropium bromide, Sch 1000, Atrovent) following inhalation and oral and i.v. administration are described. The substance was labelled with 14C. The plasma level (total radioactivity) recorded following oral administration was characterised by a low but broad plateau persisting for several hours. After i.v. injection rapid elimination from the plasma was observed in the first phase. The plasma level following inhalation was characterised by an initially rapid absorption and the curve subsequently resembled that following oral administration. An equi-bronchodilatory dose following inhalation produced a blood level 1000 times lower than those following oral dosing. The half-life of elimination lay between 3.2 and 3.8 h for all routes of administration. The maxima were recorded at 3 h. Cumulative renal excretion was 9.3% following oral administration, 72.1% following i.v. route and 3.2% after inhalation. 88.5% were excreted via the faeces following oral dosing, 6.3% following i.v. application and 69.4% after inhalation. Ipratropiumbromide is partly metabolised. After 4 h, the percentage of unchanged substance in relation to total activity in the urine was 24% (oral), 46% (i.v.) and 13% (inhalation). One of eight metabolites-- six in very small amounts-- was identified as N-isopropyl-methyl-nortropiumbromide.

Administration, Oral↗