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Biomedical subjects

H Neuhof

Publications and source records attributed to H Neuhof.

At least 73 records · Page 4Linked to original sources
PubMed1983

Comparative influence of the Ca-ionophore A 23187, bradykinin, kallidin and eledoisin on the rabbit pulmonary vasculature with special reference to arachidonate metabolism.

In a model of isolated rabbit lungs, perfused with isoionic and isooncotic fluid in a recirculating system, the Ca-ionophore A 23187, bradykinin, (kallidin), and eledoisin all evoke a reversible and reproducible increase in pulmonary vascular resistance, partly with biphasic characteristics. Inhibition of thromboxane-synthetase (imidazole), cyclooxygenase (indomethacin) phospholipase activity (mepacrine), and interference with the Ca-calmodulin-complex (trifluoperazine) each suppresses the increase in resistance due to A 23187 or eledoisin completely and the increase due to bradykinin or kallidin to a great extent. Thus thromboxane A2 appears to be the mainly responsible mediator for the increase in vascular resistance after all three stimuli. Moreover, A 23187 and bradykinin cause an increase in vascular permeability that is augmented by indomethacin and diminished by additional lipoxygenase inhibition with BW 352C and which thus can, at least partly, be ascribed to lipoxygenase products of released arachidonic acid. In spite of the described similarities there are marked differences in the relative potencies of A 23187, bradykinin and eledoisin concerning the increase in vascular resistance and the increase in vascular permeability. Therefore, different stimulus transmission-pathways are suggested, having Ca-calmodulin-complex, phospholipase activity and arachidonic acid transformation via cyclooxygenase/thromboxane synthetase respectively via lipoxygenases as common characteristics.

Animals↗
PubMed1982

Increased pulmonary vascular resistance and permeability due to arachidonate metabolism in isolated rabbit lungs.

Liberation and metabolism of arachidonic acid may be the common final pathway of different stimuli on the pulmonary vascular bed. In a model of isolated, ventilated rabbit lungs, perfused with Krebs Henseleit albumin buffer in a recirculating system, changes of pulmonary vascular resistance and of vascular permeability are monitored continuously. The addition of free arachidonic acid or of the Ca-ionophore A 23187 to the perfusion fluid consistently evokes a biphasic increase in vascular resistance as well as an initially reversible increase in vascular permeability, followed by pulmonary edema. Both phases of increased vascular resistance are completely suppressed by inhibition of the cyclooxygenase, decreased to a large degree by inhibitors of thromboxane synthetase, and markedly augmented by short preincubation of arachidonic acid with ram seminal vesicular microsomes and by sulfhydryl reagents. The increased pulmonary vascular permeability is augmented by inhibition of cyclooxygenase and reduced by simultaneous lipoxygenase inhibition. Antagonists of histamine, serotonin and sympathic or parasympathic activity do not have any influence. PG F2alpha., TxB2, PG E2 and PG I2 alter the pulmonary vascular resistance, but do not increase vascular permeability. In conclusion, increased availability of free arachidonic acid evokes a rise in pulmonary vascular resistance, which can be ascribed to cyclooxygenase products, especially to thromboxane, and causes a rise in vascular permeability which can be ascribed to lipoxygenase products. The findings may be related to acute pulmonary lesions with increase in vascular resistance and with vascular leakage.

Animals↗
PubMed1982

Influence of tocopherol, its chromane compound, phytyl chains and superoxide dismutase on increased vascular resistance and permeability due to arachidonate metabolism in isolated rabbit lung.

In the model of isolated, ventilated rabbit lungs, perfused with isoionic and isooncotic fluid, the addition of arachidonic acid to the perfusion fluid or the liberation of arachidonic acid by the Ca-ionophore A 23187 result in an increase in pulmonary vascular resistance and permeability. The former can be ascribed to cyclooxygenase products, the latter to lipoxygenase products of arachidonic acid. The effect of alpha-tocopherol, its chromane compound, alpha-tocopherolquinone, phytol, 2-methyl-1,4-naphthoquinone, 2-methyl-3-phytyl-1,4-naphthoquinone and of superoxide dismutase (SOD) on the increase in pulmonary vascular resistance and permeability was investigated. A membrane effect of the phytyl side chain and an antioxidative effect of the chromane compound can be distinguished: phytol increase the arachidonate-induced rise of pulmonary vascular resistance and permeability, whereas the chromane compound decreases both to a large degree. Methyl-phytyl-naphthoquinone and methyl-naphthoquinone gave equivalent results. SOD decreases the enhanced vascular resistance and the vascular leakage. The possibility of antioxidative therapy in acute pulmonary lesions with vascular leakage and increased vascular resistance is discussed.

Animals↗
PubMed1981

[Increase of pulmonary vascular resistance and permeability due to the metabolism of free arachidonic acid (author's transl)].

Release and metabolism of arachidonic acid are supposed to form the common final pathway of different stimuli on the pulmonary vascular endothelium. In a model of isolated, ventilated and perfused rabbit lungs we investigated the influence of increased availability of free arachidonic acid on pulmonary vascular resistance and permeability. Addition of arachidonic acid to the perfusion fluid or release of arachidonic acid by Ca-ionophore A 23187 regularly produces a characteristic biphasic increase of the pulmonary vascular resistance as well as a continuous increase in permeability, followed by pulmonary edema. Inhibition of cyclooxygenase by indomethacin prevents the augmentation of vascular resistance, the increase of vascular permeability however is enhanced. thus the raise in pulmonary vascular resistance can be ascribed to cyclooxygenase products, the increased pulmonary vascular permeability to lipoxygenase products of arachidonic acid.

Animals↗
PubMed1981

[The antioxidative chromane structure of alpha-tocopherol protects against the consequences of arachidonic acid release in the pulmonary vascular bed (author's transl)].

In the model of isolated, ventilated and perfused rabbit lungs release of arachidonic acid results in an increase of pulmonary vascular resistance and permeability. The former can be ascribed to cyclooxygenase products, the latter to lipoxygenase products of arachidonic acid. The effect of alpha-tocopherol on the increase of pulmonary vascular resistance and permeability either after the addition of arachidonic acid to the perfusion fluid or after stimulation of arachidonic acid liberation by Ca-ionophore A 23187 was investigated. It is possible to distinguish a membrane effect of the phytol side chain of alpha-tocopherol and an antioxidative effect of its chromane structure: Phytol augments the increase of pulmonary vascular resistance and permeability, whereas the chromane-structure decreases both to a large degree. The possibility of antioxidative therapy in disturbances of pulmonary vascular permeability is discussed.

Animals↗
PubMed1980

[The effects of "relaxing music" on patients, doctors and nursing staff of a medical intensive care unit (author's transl)].

With the intention of reducing the psychological stress and anxiety of patients during their admission to the medical intensive care unit, specially selected and prepared instrumental music was played over a loud speaker to the patient cubicles. The patients' opinions on the programme and their subjective state of health were determined by a questionnaire. 78% of the patients felt that their well-being was improved by the music. With the exception of 7%, who were disturbed by the music, all other patients found it reassuring, diverting, hypnotic or entertaining. In addition to the patients 11 doctors and 16 nurses from the intensive care unit as well as 38 doctors and 80 nurses from 39 medical intensive care units in German university clinics and large hospitals were asked for their opinions on the use of music for intensive care patients.

Acute Disease↗
PubMed1977

The activation of intravascular coagulation by bromocarbamide.

In the rabbit the application of a non-lethal, sleep-inducing dose of bromisovalerianyl carbamide (0.5 g/kg body weight) causes an activation of the coagulation system. This activation is manifested by shortened thrombin and partial thromboplastin times and a decrease of fibrinogen concentration and Factor V activity. In contrast, pentobarbital sodium at a dose (62.5 mg/kg) which causes the same changes in arterial partial oxygen pressure and arterial pH does not influence the coagulation system. The bromocarbamide-induced changes in the coagulation system are not to be considered as a result of hypoxia and acidosis but seem to be caused by early endothelial and tissue lesions which result in the release of procoagulatory substances. In healthy test persons a single dose of 1.5 g bromisovalerianyl carbamide has no demonstrable influence on the system of hemostasis.

Adult↗
PubMed1976

Cardiovascular reactions induced by leucocidin from Pseudomonas aeruginosa.

Leucocidin from Pseudomonas aeruginosa causes cardiovascular failure in rats and mice. The time between i.v. injection and death depends on the dose. After injection of high doses (500 mug/kg) the arterial blood pressure decreases rapidly and cardiac irregularities and AV block occur within about 5 min. In contrast to endotoxin shock no pulmonary hypertension was observed, whereas portal hypertension was seen in our experiments. Injection of lower doses (less than 200 mug/kg) caused peripheral vascular damage with lung oedema, vascular disturbances in various tissues, exudation and bleeding. Finally cardiac insufficiency predominated. Dexamethasone delayed the symptoms but did not prevent death in either rats or mice. Heparin was ineffective in this type of shock.

Animals↗
PubMed1975

Alteration of hemodynamics, blood gases and lung morphology in bromocarbamide intoxication (animal experiments).

The reaction to animals in bromocarbamide intoxication with respect to blood pressure, resistance in the systemic and pulmonary circulation, cardiac output and arterial blood gas values is presented and discussed in reference to morphological changes in the lung. The animals die due to peripheral circulatory failure if paralysis of respiration is prevented by means of artificial ventilation. The observed morphological lung changes are not the cause of death.

Animals↗