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Biomedical subjects

J Höper

Publications and source records attributed to J Höper.

At least 37 records · Page 2Linked to original sources
PubMed1993

Effect of epinephrine on local partial pressure of oxygen in the ciliary processes.

Local pO2 was measured close to the ciliary process of the rabbit eye using polarographic microelectrodes under microendoscopic observation. The experiments were performed in 5 anaesthetized New Zealand rabbits. Changes in local pO2, intraocular pressure (IOP) and blood flow velocity (BFV) were investigated after intra-arterial and topical application of epinephrine. After intra-arterial epinephrine, a simultaneous decrease in BFV, IOP and local pO2 was found. pO2 decrease was more pronounced in the anterior part of the ciliary processes than in the posterior part. Topical epinephrine lead to similar changes of all parameters mentioned above, the time constants being 10-20 times longer. In these topical experiments, no recovery of local pO2 was found over a period of at least 30 min despite an increase in BFV. Our results indicate that in the hyperemic phase after epinephrine the activity of the ciliary epithelium (and probably the total aqueous formation) is higher than normal. Thus, the decrease in IOP in this phase must be due to an increased outflow facility.

Administration, Topical↗
PubMed1992

Use of an oxygen multiwire surface electrode for the direct measurement of the distribution of alveolar PO2 at different inspired oxygen concentrations.

Experiments were performed in six anaesthetised, mechanically ventilated rabbits. After thoracotomy, a multiwire surface PO2 electrode was placed at the pleural surface by means of a special holder. The local distribution of PO2 was investigated at different values of inspired oxygen concentration (FIO2). The data were analysed in order to establish (a) whether the PO2 values measured at the lung surface reflect intra-alveolar PO2 and (b) that the distribution of these values represent real physiological differences between alveoli. The mean PO2 values were related to the calculated mean alveolar PO2 (PAO2) values (r = 0.97) indicating that it is possible to study PAO2 by local measurements. It can therefore be concluded that the technique used allows the study of the influence of different FIO2 values on the distribution of PAO2. Each local PAO2 value is the result of the corresponding local ventilation/perfusion ratio (VA/Q) therefore the distribution of PAO2 values represents the distribution of VA/Q. An increasing FIO2 causes an increasing heterogeneity of PAO2 and thus VA/Q leading to a concomitant increase in the alveolo-arterial oxygen difference. At the moment it is not possible to decide if this heterogeneity is primarily caused by heterogeneities in perfusion or ventilation. The results could throw fresh light on the effect of different ventilation procedures.

Animals↗
PubMed1992

Attenuation of hypoxic response in cerebral microcirculation following deprenyl.

Cerebral blood flow (CBF), cerebrocortical microflow (CMF) and local pO2 were measured in the rat brain cortex during normoxia and hypoxic hypoxia before and after administration of the monoamine oxidase-B (MAO-B) inhibitor deprenyl (0.1 mg/100 g b.wt. i.v.). CBF was measured using intraarterial 133-Xenon injection technique. Both, CMF and pO2 were measured using polarographic multiwire surface electrodes. In the control group without deprenyl CBF increased during hypoxaemia (PaO2 = 44.7 +/- 9.3 mm Hg) by 215% while CVR decreased to 27% of the normoxic control value. Hypoxaemia (PaO2 = 34.4 +/- 3.9 mm Hg) also led to a mean increase of CMF by 38% of the normoxic control (p less than 0.02) while the local cerebrocortical pO2 fell from 20.1 +/- 5.1 mm Hg to 5.2 +/- 1.9 mm Hg (p less than 0.02). The administration of deprenyl during normoxia did not cause any significant changes of CBF and CMF although both increased by 29% and 28%, respectively. The increase of CBF during hypoxaemia (PaO2 = 34.9 +/- 6.3 mm Hg) following deprenyl administration, although diminished, was still present (101%, p less than 0.01). CMF decreased under these conditions by 30% on average (p less than 0.05). These results suggest that MAO-B may be involved in the local regulation of cerebrocortical capillary blood flow during hypoxia.

Animals↗
PubMed1988

Constant-pressure perfusion on the isolated rat liver: local oxygen supply and metabolic function.

Isolated rat livers were perfused with a haemoglobin-free Krebs-Ringer solution containing 35 g albumin/1. During a 3 hour perfusion total flow, O2-uptake rate and local O2-supply remained constant. During the same period of time the ATP-content increased from a value of 0.59 +/- 0.17 mumol/g to 1.81 +/- 0.42 mumol/g. The low initial value was due to the ischaemic period during preparation of the organ. The glycogen content increased by 13.4 mg/g, indicating that the organ did not lose the ability for glyconeogenesis. In addition to an increase in glycogen, there was a continuous increase in the glucose concentration of the perfusate, while lactate was taken up by the organ. The results indicate that the isolated organ can be perfused for at least 3 hours without development of disturbances in local O2-supply.

Adenosine Triphosphate↗
PubMed1987

Cerebrocortical microcirculation in different stages of hypoxic hypoxia.

This study investigated the relation between local cerebrocortical oxygen tension (PO2) and cerebrocortical microflow (CMF) during normoxia (FiO2 = 0.3) and hypoxic hypoxemia (FiO2 = 0.16 and 0.1). Measurements were performed on mechanically ventilated rats and rabbits anesthetized with 0.8% Ethrane and maintained within normocapnic limits. Polarographic techniques based on the use of multiwire surface electrodes were applied for measurements of local PO2 and CMF. In both species the mean tissue PO2 values were similar under normoxia (26.0 and 31.5 mm Hg for rats and rabbits, respectively). CMF histograms showed pronounced heterogeneity. The highest CMF values exceeded the lowest ones by a factor of 36 in the rat and by a factor of 26 in the rabbit. Mean CMF values were 6.67 +/- 0.72 and 4.09 +/- 0.14 relative units (for definition see text) in rats and rabbits, respectively. During hypoxemia, if the mean tissue PO2 was greater than 5 mm Hg, mean CMF did not change but a change in the pattern of microflow distribution was observed with increases in some CMF values (up to 670% of control) and decreases in others (down to 12% of control). When mean tissue PO2 values of less than 5 mm Hg were observed during hypoxemia, mean CMF increased in both species by approximately 50% on average. The increase in CMF could be seen in each individual CMF recording. We conclude that in the brain cortex local regulatory mechanisms are responsible for the change in the pattern of distribution of microcirculation during moderate tissue hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗