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Biomedical subjects

E Betz

Publications and source records attributed to E Betz.

At least 91 records · Page 5Linked to original sources
PubMed1975

[Energy state of the cerebral cortex of the cat during hyperventilation (author's transl)].

Average Po2 and Pco2, local blood flow and pH values in the cerebral cortex of the cat were measured during passive hyperventilation (arterial Pco2 below 19 mm Hg). At defined intervals tissue samples were taken for metabolite analysis. The object of the study was to correlate the data obtained on the brain surface with metabolic responses. Immediately after the start of hyperventilation blood flow decreased, average cortical tissue pressures of O2 and CO2 fell, and there was a simultaneous rise in cortical pH. At a later stage in the experiment the local blood supply reverted to its resting level. Despite a fivefold rise in tissue lactate level during hyperventilation and a decrease in local O2 pressure on the brain surface to 5-10 mm Hg the degree of phosphorylation of energy rich phosphates was not less than under normal conditions of oxygenation. Our investigations showed no evidence of energy lack in cerebral cortex cells during hyperventilation. Cellular hypoxia and its characteristics are defined. The possible causes of raised tissue lactate levels during hyperventilation despite the lack of evidence of cellular hypoxia are discussed.

Adenosine Diphosphate↗
PubMed1975

[The effects of elevated calcium concentrations in artificial cerebrospinal fluid on pial arteries during perivascular microperfusion and the Ca++-antagonistic effect of bencyclane (author's transl)].

The influence of artificial cerebrospinal fluid (CSF) containing 6, 9 and 18 mEq/l Ca++, respectively, on 145 pial arteries of nine anesthetized cats was investigated by the perivascular microperfusion technique. The higher the concentration of Ca++ in the perivascular space and the longer these high Ca++ concentrations acted on the vascular wall, the more pronounced were the constrictions of the arteries. If N-[3-(1-benzyl-cycloheptyloxy)-propyl]-N,N-dimethyl-amine (bencyclane-hydrogenfumarate, Fludilat) (10 mg/100 ml) was added to the CSF, dilatations occurred, even if the concentrations of Ca++ were higher than in normal CSF (3 meq/l). The degree of dilatation, however, was dependent on the Ca++ concentration in the CSF. With high Ca++ in the CSF the dilatatory action of bencyclane was inhibited when K+ and H+ in the CSF were kept constant. The reaction can be described as Ca++ antagonism, the possible mechanisms of which are discussed.

Animals↗
PubMed1975

[Blood circulation, oxygen pressure and pH of the cerebral cortex under the influence of bencyclane].

The effect of N-[3-(1-benzyl-cycloheptyl-oxy)-propyl]-N,N-dimethyl-amine (bencyclan-hydrogenfumarate, Fludilat¿ on the cerebral vascular system was studied by means of the following methods: 1. In pigs regional cerebral cortical blood flow was continuously recorded with a heat conduction device, cortical pH with a glass electode in which the flat measuring surface and the reference were close together. Cortical pO2 was recorded with a multiwire platinum electrode. Systemic arterial blood pressure was monitored by means of a Statham transducer. 2. In a second series in cats the perivascular space of small pial arteries or arterioles was perfused with cerebro-spinal fluid (CSF) to which bencyclan had been added. The perfusion was performed by means of micropipettes. Local cortical blood flow increased slightly for some minutes after slow infusion of 1--3 mg/kg bencyclan. Rapid injection caused initially a significant decrease in arterial blood pressure, which was accompanied by a transient decrease in CBF and in cortical pH. After the return of the arterial blood pressure to its initial value, CBF increased. Cortical pO2 and cortical pH returned to initial values. After slow infusion of the substance the pH variation was usually very slight or it was missed completely. Perivascular microperfusion wtih CSF containing bencyclan caused dilatation of those pial sections which were in contact with the drug. High concentration of the drug caused stronger dilatations than did low concentrations. It is concluded that the substance causes dilatations of the cerebral vessels and that this dilatation occurs also during constant perivascular pH.

Animals↗