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Biomedical subjects

E Ott

Publications and source records attributed to E Ott.

158 records · Page 9Linked to original sources

[Influence of a central cholinergic mode of action on the regulation of the intact and disturbed cerebral blood flow (author's transl)].

Cerebral chemical vasomotor reactivity and autoregulation were tested in normal baboons before and after intravertebral, intravenous and (or) intracarotid infusion of atropine and neostigmine. Furthermore, disordered cholinergic neurotransmission and dysautoregulation after acute experimental cerebral infarction have also been investigated. Intravertebral injection of atropine suppressed the increase of CBF by inhalation of 5% CO2 and enhanced the decrease of CBF induced by hyperventilation, but did not appreciably affect autoregulatory response. On the other hand, cerebral autoregulatory vasoconstriction during increases of CPP was significantly reduced following both intravertebral and intracarotid neostigmine infusion. Cerebral vasodilatory reactivity to CO2 inhalation was significantly enhanced only following intravertebral neostigmine and cerebral vasoconstrictive response to hyperventilation was not influenced by neostigmine. Following experimental cerebral infarction regional dysautoregulation was found in infarcted gray matter and correlated significantly with increased AChE levels in the same zones of cortex and basal ganglia. Intravenous infusion of scopolamine restored autoregulation to the ischemic zones. The results thus obtained support the view that central cholinergic cerebrovascular influences exist and are vasodilatory in nature. Furthermore, in acute experimental cerebral infarction disordered cholinergic neurotransmission seems to play a role in vasoconstrictive dysautoregulation.

Animals↗

[Clinical significance of changes in blood viscosity in cerebrovascular insufficiency (author's transl)].

In 50 patients with encephalomalacia and 50 patients with a transient cerebral ischemic attack (TIA) the risk factors and viscosity of the whole blood as well as the hematocrit were determined before the start of treatment. Compared to a control group, the blood viscosity in patients with encephalomalacia was significantly increased (p less than 0.001) in all ranges of shearing velocity tested, in patients with TIA only at that shearing velocity which may be assumed for the area of microcirculation. This increase was related to the presence of arterial hypertension, hyperlipemia, heart failure, diabetes mellitus, hyperfibrinogenemia and increased tendency of thrombocytes and erythrocytes to aggregate. From the results obtained it was concluded that increased blood viscosity in the cerebral area of microcirculation with insufficient cerebral collateral circulation may decisively favor the development of encephalomalacia.

Acute Disease↗

Detection of polycyclic aromatic hydrocarbon exposure damage using different methods in laboratory animals.

Benzo[a]pyrene, benzo[b]fluoroanthene and dibenzo[a,h]anthracene dissolved in a 1:2 mixture of dimethylsulphoxide (DMSO) and water were administered to two groups of female mice, each group containing 15 mice. The doses were administered orally (via gavage) at the respective rates of 1 and 100 micrograms kg-1 body weight five times per week for a period of 9 weeks. The influence of the polycyclic aromatic hydrocarbons (PAHs) was determined using the following methods: determination of DNA-PAH adducts, of chromosome injuries (micronucleus test), of induction of repair using the unscheduled DNA synthesis (UDS) test, and by examination of the DNA structure after nucleoid sedimentation. All the methods investigated provided evidence of a significant effect resulting from exposure to PAHs on the parameters examined. Following chronic exposure to PAHs, the formation of DNA-PAH adducts and injury to the genetic material, as well as the appearance of micronuclei (micronucleus test), the induction of unscheduled DNA synthesis (UDS test) and mutation of the DNA structure (nucleoid sedimentation), were demonstrated. The described methods therefore provide a means for the detection of genetic damage caused by PAH exposure in humans.

Administration, Oral↗