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Biomedical subjects

H Acker

Publications and source records attributed to H Acker.

At least 127 records · Page 7Linked to original sources
PubMedDate not supplied

Tissue-PO2 (PGO2) in the carotid body of the cat and tidal volume (V) during normovolaemic haemodilution.

During normovolaemic haemodilution with Macrodex (R), the basic respiratory activity is unchanged, while the ventilatory responses to hypoxia and hypercapnia generally decrease. The PGO2 in the cat carotid body remains constant down to an Hk of 10% to 15% and then decreases. This confirms the suggestion of Acker and Lübbers (1976) that increased plasma flow through the carotid body does not influence the oxygen supply to this organ, despite variations of both oxygen transport capacity and haemoglobin concentration. The fine structure of the carotid body is partly destroyed by haemodilution with Macrodex (R) and this could account for the impaired chemoreception.

Animals↗
PubMedDate not supplied

Disturbances of extracellular pK, pNa and pH during no-flow anoxia.

The initial period of no-flow anoxia can be divided in at least two parts. During the first period lasting approximately 1 min., the O2 available in tissue gives rise to CO2 which increases hydrogen ion activity and may lead to Na+ influx2 (presumably due to increased membrane permeability to Na+). In the second period, starting after the first minute, the increase in lactate content leads to further decrease in pH and is accompanied by extensive sodium influx and a distinct potassium efflux. However, it is striking that the isolated perfused rat liver is able to tolerate 1 hour of norm-flow anoxia without severe cellular damage, whereas two minutes of no-flow anoxia lead to a decrease in cellular ATP content by 28%.

Adenosine Triphosphate↗
PubMedDate not supplied

Oxygen tensions in two human tumor cell lines grown and irradiated as multicellular spheroids.

Cells from two human cell lines were irradiated both as multicellular tumor spheroids (MTS) and in monolayer culture. Radiation response of MTS was quantified in terms of specific growth delay and proportion cured, and as clonogenic cell survival for monolayer cells. Radiation was applied either as a single or as a split dose with time intervals of 1, 2, and 4 h to determine the rate of sublethal damage repair. Using as endpoint the fraction of MTS cured at an iso-effect level, in MTS of NB-100 neuroblastoma cells repair of sublethal damage was complete within 1 h, whereas in MTS of HN-1 squamous cell carcinoma cells there was still some unrepaired damage left. At a larger dose for NB-100 MTS the repair curve showed a similar shape as for HN-1 spheroids. Using as endpoint specific growth delay, no difference in repair between the various time intervals was observed. In monolayer cells from both cell lines sublethal damage was not fully repaired in the time intervals used. Polarographic microelectrode measurements of oxygen tension inside MTS showed a marked difference in steepness of oxygen tension profiles between MTS from both cell lines. In HN-1 squamous cell carcinoma MTS with diameters up to 500 microns the central pO2 amounted to about 100 Torr, whereas in NB-100 neuroblastoma MTS with the same diameters central pO2-values lower than 30 Torr were observed. NB-100 MTS were irradiated with doses of 5 and 10 Gy gamma rays and subsequently the oxygen tension was measured 1 and 5 h after irradiation. A reoxygenation effect could not be observed, either after single dose or after split dose irradiation. If spheroids may be regarded as a suitable model for tumor responses in vivo, the results from these experiments indicate that reoxygenation is a process eluding polarographic measurements, or that no dramatic changes in oxygen tension are to be expected shortly after high single doses or early in a fractionation scheme.

Carcinoma, Squamous Cell↗