Biomedical subjects

J F Zander

Publications and source records attributed to J F Zander.

5 recordsLinked to original sources

PubMed1999

Subarachnoid haemorrhage.

A high percentage of the population has aneurysms of the cerebral vessels, which are detected only by chance or after spontaneous rupture. Subarachnoid haemorrhage is still a problem because of high morbidity and mortality. Many patients do not fully recover neurologically and suffer from physical and psychosocial symptoms. The aims of treatment are to prevent the patient from rebleeding and to prevent secondary neurological damage. Whereas in former times, clipping of the aneurysm was often delayed for days or weeks, early operative intervention is the rule today, if the patient is not moribund and if there is no significant cerebral oedema. The anaesthetist can support the neurosurgeon with a spectrum of different methods of anaesthesia and monitoring, individually tailored to the needs of the patient. Most important, however, is a stable haemodynamic status, stable and normal intracranial pressure and a sufficient cerebral perfusion pressure. Vasospasm is still the main problem, as is early rebleeding. To treat this, nimodipine is the drug of choice combined with volume therapy, a slightly elevated cardiac output and a modestly elevated blood pressure.

Journal Article↗

PubMed1996

Postoperative alpha 2-adrenergic stimulation attenuates protein catabolism.

The metabolic effects of continuous intravenous (IV) application of the alpha 2 agonist clonidine were evaluated by assessment of nitrogen economy and postaggression endocrine patterns. Twenty-four patients undergoing abdominothoracic esophageal cancer resection were studied. Thirteen of these patients with alcohol abuse were treated postoperatively with IV clonidine for prevention of alcohol withdrawal syndrome. Eleven patients who were not treated with clonidine served as controls. All patients were treated in a standardized manner in regard to surgical technique, balanced anesthesia, and postoperative intensive care treatment, including thoracic epidural analgesia with bupivacaine and fentanyl. Isonitrogenous and isocaloric nutrition was comparable in all patients. A significantly improved cumulated 6-day nitrogen balance was found in clonidine-treated patients (-1.5 +/- 4.9 g nitrogen) compared to the control group (-17.6 +/- 4.2 g nitrogen) (P < 0.05). The main reason for improved nitrogen economy may be clonidine-induced growth hormone (GH) release. The pattern of insulin-like growth factor I (IGF-I) and insulin-like growth factor binding protein 3 (IGFBP-3) concentrations could support this hypothesis.

Adrenergic alpha-Agonists↗

PubMed1995

Dexamethasone-induced sodium influx in human lymphocytes.

We evaluated the direct effects of glucocorticoids on intracellular sodium content and cellular transport systems. Cytosolic free sodium concentration ([Na+]i) was measured in intact human lymphocytes using the sodium-sensitive fluorescent dye sodium-binding benzofuran-isophthalate. Administration of dexamethasone for 60 min increased lymphocytic [Na+]i from 17.6 +/- 2.0 mmol/L to 24.3 +/- 3.9 nmol/L (n = 12; P < 0.01). The dexamethasone-induced [Na+]i increase was abolished in the absence of extracellular sodium, by mifepristone and by actinomycin D. The dexamethasone-induced [Na+]i increase was also seen after inhibition of Na+,K(+)-ATPase by 1 mmol/L ouabain. The present results indicate that dexamethasone produces a trans-plasma membrane sodium influx probably by early occurring genomic effects.

Biological Transport↗

PubMed1988

Beta-2 adrenergic responses to tulobuterol in airway smooth muscle, vascular smooth muscle and adrenergic nerves.

Experiments were designed to determine the mechanism of action of the bronchodilator drug tulobuterol. Tissues were suspended in organ chambers for isometric tension recording. Tulobuterol caused concentration-dependent relaxations of guinea pig tracheae, canine saphenous veins and canine bronchi; the compound relaxed canine coronary arteries only at high concentrations and did not affect spontaneously beating guinea pig atria. A metabolite of tulobuterol, 4-hydroxytulobuterol, was more potent in relaxing guinea pig tracheae than tulobuterol, salbutamol and isoproterenol. Other metabolites (3-hydroxy-, 5-hydroxy- and 4,5-dihydroxytulobuterol) were less efficacious than 4-hydroxytulobuterol. Both tulobuterol and 4-hydroxytulobuterol acted as partial agonists. The effects of tulobuterol in the saphenous vein (but not in the coronary artery) were antagonized by the selective beta-2 adrenergic blocker ICI 118,551 but were not affected by the selective beta-1 adrenergic inhibitor metoprolol. In bronchi, removal of the epithelium reduced the relaxations caused by tulobuterol. The drug did not inhibit responses of canine bronchi to electrical stimulation of the cholinergic nerves more than those to exogenous acetylcholine. Tulobuterol caused a moderate augmentation of the evoked release of [3H]norepinephrine in canine saphenous veins previously incubated with the labeled transmitter. Thus, tulobuterol is a selective beta-2 adrenergic agonist with minimal nonselective inhibitory effect on airway and vascular smooth muscle. It also facilitates adrenergic neurotransmission, which may help to explain its bronchodilator effect in the intact organism. Tulobuterol does not activate beta-1 adrenoceptors and has no direct positive chronotropic effect. A metabolite of tulobuterol, 4-hydroxytulobuterol, is more active than the parent compound.

Adrenergic Fibers↗

PubMed1986

Effects of naftidrofuryl on adrenergic nerves, endothelium and smooth muscle in isolated canine blood vessels.

Experiments were designed to determine the effects of the vasoactive drug naftidrofuryl on vascular smooth muscle, endothelial cells and adrenergic nerves in isolated canine blood vessels. Naftidrofuryl inhibited contractions of basilar arteries (in a decreasing order of potency), evoked by 5-hydroxytryptamine greater than KCl = anoxia (in rings with endothelium) greater than prostaglandin F2 alpha = uridine-5'-triphosphate. Naftidrofuryl antagonized competitively the contractions evoked by 5-hydroxytryptamine in the femoral artery and the saphenous vein. Naftidrofuryl caused the release of an endothelium-derived relaxing factor(s) from the endothelium of femoral arteries. The compound depressed contractions of saphenous veins evoked by electrical stimulation of the adrenergic nerve endings, but not those caused by the indirect sympathomimetic amine tyramine or exogenous norepinephrine. In saphenous veins incubated previously with [3H]norepinephrine, the drug inhibited the contractions and the release of transmitter evoked by electrical stimulation. Thus, naftidrofuryl acts at different levels in the blood vessel wall to cause: release of endothelium-derived relaxing factor(s); inhibition of S2-serotonergic receptors on vascular smooth muscle; prejunctional inhibition of adrenergic neurotransmission; and nonselective inhibition of the contractile process in vascular smooth muscle, which is particularly pronounced in cerebral arteries.

Adrenergic Fibers↗