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Antibodies formed against fibrin glue components and their circulatory relevance.

To elucidate the safety of fibrin glue application, antibody formation against fibrinogen and thrombin was studied in rabbits. The pathophysiology of developed antibodies was tested by an intravenous challenge with both components and by related blood pressure measurements. All fibrin glue-treated animals developed antibodies against both components. The quantity of antibodies against thrombin (20.4 mg/mL) was higher than the quantity against fibrinogen (0.38 mg/mL). The intravenous challenge with both components resulted in a significant and long-lasting blood pressure decrease to about 50% of the control values, indicating that these antibodies can induce circulatory disorders by antigen-antibody reaction, activation of the complement cascade, and liberation of histamine. Since rabbits promptly produce antibodies against antigenic material and humans do not, the results of this investigation suggest that fibrin glue should be used with caution in humans.

Animals↗
PubMed1976

[Immunobiological means of identifying hypersensitivity to anesthetics and adjuvants].

The diagnosis of hypersensitivity to anesthetics and adjuvants is based chiefly on immunobiological tests which involve:-sensitized lymphocytes; -IgE or IgG antibodies; -sensitized target cells; -determination of chemical mediators. Comparison between these different methods is only possible for techniques involving the sensitized lymphocyte, such as the LTT and EA rosettes for examples, or T.D.B.H. and liberation of histamine. Comparison between the LTT and RAST is difficult, since the first technique investigates the sensitized lymphocyte while the second involves radio-immune antibody assay. An attempt to establish a correlation between these two types of methods is difficult but they can, however, complement each other.

Adjuvants, Pharmaceutic↗
PubMed2000

Nitric oxide mechanisms in migraine.

The molecular mechanisms of migraine pain have not yet been clarified. Neurogenic inflammation and a subsequent plasma extravasation in the dura mater have been suggested as causative factors. However, monoamine and peptide neurotransmitters involved in neurogenic inflammation do not cause significant head pain. Based on our previous studies of headache induced by i.v. infusions of glyceryl trinitrate (exogenous nitric oxide [NO] donor) and histamine (which liberates NO from the vascular endothelium), it is suggested that NO is a more likely candidate molecule. The present review examines the biology of this small messenger molecule, and the scientific evidence suggesting that it may play a key role in migraine headache. It is hypothesized that the release of NO from blood vessels, perivascular nerve endings or from brain tissue is a molecular mechanism which triggers spontaneous migraine pain. Furthermore, it has been shown that this hypothesis is supported by the recent findings that i.v. infusion of the NO synthase (NOS) inhibitor is effective in the acute treatment of migraine attacks. These novel observations indicate possible new approaches to the pharmacological treatment of migraine.

Animals↗
PubMed1976

[Profile of pharmacological actions of NAB 365 (clenbuterol), a novel broncholytic agent with selective activity on adrenergic beta2-receptors (author's transl)].

Effects of 4-amino-alpha-[(tert.-butylamino)methyl]-3,5-dichlorobenzyl alcohol hydrochloride (clenbuterol, NAB 365) on the adrenergic beta-receptors were investigated and compared with those of isoproterenol and salbutamol. The beta2-mimetic activity of clenbuterol on the smooth muscle of bronchi, uterus and vessels after i.v. injection corresponds to that of salbutamol in all laboratory animals. When given subcutaneously or as an aerosol clenbuterol is even somewhat more effective than isoproterenol. Clenbuterol differs from the known beta-mimetic drugs in its much longer duration of action. Therefore the integral of activity of single doses of clenbuterol, which are equally effective in the period of their maximal action, is remarkably greater than that of the other beta-mimetic substances. Clenbuterol differs from known beta-mimetic drugs used as bronchodilators in its efficacy after oral administration and in its mode of action on the heart. In the isolated auricle of the rabbit it has proved to be a weak partial agonist. In conscious rabbits, anesthetised guinea-pigs, dogs and cats the maximum of tachycardia obtainable by clenbuterol is lower than that of salbutamol. The higher degree of tachycardia in conscious dogs provoked by clenbuterol is a result of a reflex reaction to the vasodilation analogous to that of salbutamol. In higher doses clenbuterol shows beta1-blocking properties. Like other beta-blocking agents it owns qualities of a local-anesthetic and prolongs refractory period of the heart of guinea-pigs. In contrast to other beta-mimetic substances, clenbuterol causes only slight mobilization of heart muscle glycogen by doses higher than those which have broncholytic effects. The lipolytic and lactacidemia inducing activity of clenbuterol in rabbits corresponds to that of isoproterenol. The blood sugar is only slightly increased by clenbuterol as well as by other beta-mimetic agents. Degree and duration of action of clenbuterol and the other sympathomimetic amines on skeletal muscle of the cat shows parallelism with that of the broncholytic effect. In the rat clenbuterol inhibits the gastric secretion more than does isoproterenol. In contrast to other broncholytic substances, a very small dosage of clenbuterol is sufficient to protect rats against the liberation of histamine and serotonin caused by the anaphylactic reaction.

Adrenergic beta-Agonists↗