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Biomedical subjects

J Grote

Publications and source records attributed to J Grote.

At least 55 records · Page 3Linked to original sources
PubMed1989

The interaction between oxygen and vascular wall.

In vascular strips of canine carotid arteries stepwise lowering of oxygen tension from hyperoxic levels of 550 mmHg to 20 mmHg caused in preparations with endothelium a dose-dependent hyperpolarization and relaxation of smooth muscle cells when oxygen tensions between approximately 150 mmHg and 35 mmHg were attained. Pronounced hypoxia with oxygen tensions below 30 mmHg induced a depolarisation and an increase in force generation. During comparable investigations on vessel preparations without endothelium only a slight hyperpolarization and relaxation of the smooth muscle were observed when decreasing the oxygen tension from 550 mmHg to approx. 35 mmHg. In the presence of indomethacin (10(-5) M) a small but significant reduction in the hypoxia-induced hyperpolarization and decrease in smooth muscle tone was found in intact vascular strips with endothelium. Depolarisation and contraction occurred at oxygen tensions below approx. 50-60 mmHg.

Animals↗
PubMed1989

Prostacyclin, endothelium-derived relaxing factor and vasodilatation.

In arterial smooth muscle with normal tone or predepolarized and precontracted by noradrenaline, prostacyclin (10(-9) to 10(-6) M) effects a dose-dependent hyperpolarization and relaxation. The hyperpolarization is due to K+ channel opening. In hypoxic vasodilatation, which is likewise induced by membrane hyperpolarization, a share of 20% falls to prostacyclin and 80% to an endothelium derived hyperpolarizing factor.

Animals↗
PubMed1989

The significance of the endothelium for hypoxic vasodilatation.

In isolated segments of the A. carotis communis of the dog, the membrane potential and isometric tension were recorded in dependence on the oxygen partial pressure. In the range between 535 and 35 mmHg PO2, lowering of oxygen tension leads to a dose-dependent hyperpolarization of maximally 9.8 mV with a simultaneous decrease in tone of 0.746 g. Further reduction of PO2 below 35 mmHg causes depolarization and contraction. These effects can be abolished almost completely by alpha-receptor blockade. Application of 6-hydroxydopamine (1.8 mM) augments the hypoxic hyperpolarization and relaxation in the entire PO2 range between 535 and 0 mmHg, i.e., below 35 mmHg depolarization and contraction fail to appear. The increasing release of noradrenaline from terminal sympathetic nerve endings thus limits the hyperpolarization and relaxation occurring with reduction of PO2 and is mainly responsible for the depolarization and contraction below 35 mmHg. Application of indomethacin (10(-5) M) or BW 755 C (3.8 x 10(-5) M) reduces the hypoxic hyperpolarization and dilatation by circa 20-30%. Their maximum is shifted towards a higher PO2 of 65 mmHg. Only complete removal of the endothelium effects a 70-80% restriction of dilatory vascular reactivity. Identical quantitative statements hold also for control conditions, i.e. in carbogen Krebs solution. This means that the basal release of prostacyclin from endothelial and smooth muscle cells has a share of 20-30%, the basal release of the endothelial dilator EDHF of 70-80% in the membrane polarization and reduction in muscle tone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

The influence of oxygen tension on membrane potential and tone of canine carotid artery smooth muscle.

In vascular smooth muscle of canine carotid artery segments the decrease in oxygen tension from approximately 550 mmHg to approximately 30 mmHg leads to a dose-dependent hyperpolarization and relaxation of the vessel strip. At PO2 values below approximately 15-20 mmHg depolarization and subsequent contraction were found. All changes of the parameters investigated were reversible. Indomethacin (10(-5) M) had no significant effect on the hypoxia-dependent potential and tension changes. The hyperpolarized part of the activation curve was obtained by plotting tension versus membrane potential values.

Animals↗
PubMed1981

Effects of severe arterial hypocapnia on regional blood flow regulation, tissue PO2 and metabolism in the brain cortex of cats.

The effect of a stepwise decrease in PaCO2 from 3.9-1.6 kPa on rCBF, rCMRO2, tissue PO2 and concentrations of glucose, lactate, pyruvate, ATP, ADP, AMP and phosphocreatine in the brain cortex was studied in cats lightly anaesthetized with sodium pentobarbital. 1. Moderate lowering of PaCO2 to 2.5 kPa induced in all animals a homogeneous decrease of rCBF in corresponding areas of the right and left hemisphere. Mean rCBF fell from 129.2 to 103.1 ml X 100 g-1 X min-1, while rCMRO2 remained unchanged (12.7-12.9 ml X 100 g-1 X min-1). The tissue PO2 frequency histograms showed a shift to lower values without indicating the presence of brain tissue hypoxia. 2. Severe arterial hypocapnia (PaCO2 = 1.6 kPa) caused an inhomogeneous blood flow reaction. Both further decreased as well as increased rCBF values were measured simultaneously in the brain cortex of individual animals (mean rCBF = 97.6 ml X 100 g-1 X min-1). At the same time tissue PO2 measurements and metabolite assays indicated the presence of pronounced brain tissue hypoxia. The tissue concentrations of lactate and pyruvate and the lactate/pyruvate ratio were significantly increased, while the phosphocreatine concentration was significantly reduced. In addition, rCMRO2 decreased to 11.3 ml X 100 g-1 X min-1. The results provide conclusive evidence that severe arterial hypocapnia leads to an insufficient O2 supply of the brain cortex, which in turn seems to counteract the influence of hypocapnia on cortical blood flow regulation.

Adenine Nucleotides↗
PubMed1977

Oxygen diffusivity in tumor tissue (DS-carcinosarcoma) under temperature conditions within the range of 20--40 degrees C.

The O2 diffusion constants D and K of tumor tissue (DS-Carcinosarcoma in the rat kidney) were determined at temperatures of 20, 30, 37, and 40 degrees C. The following mean values were obtained for the conditions of 37 degrees C: D = 1.75-10(-5) cm2/s and K = 1.9-10(-5) mlO2/cm-min-atm. Within the range of 20-40 degrees C, temperature variations in tumor tissue cause changes in the O2 diffusion coefficient D of 2.0-2.5%/C and in the Krogh O2 diffusion constant K of 0.5-1.5%/C. The measured O2 diffusion constants for tumor tissue correspond to values of normal tissue with similar water content. This indicates that the insufficient O2 supply in DS-Carcinosarcoma is due not to unfavorable O2 diffusivity of the tumor tissue but rather to a decreased convective O2 transport and to insufficient capillarization. An analysis of O2 diffusion in DS-Carcinosarcoma tissue using the determined O2 diffusion constants lead to the result that, under the conditions of arterial normoxia and normocapnia, critical O2 supply conditions are to be expected when the intercapillary distance exceeds approximately 120 micrometer.

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