Intravenous injection of 30 micrograms/kg of B-HT 920 (6-allyl-2-amino-5,6,7,8-tetrahydro-4H-thiazolo-[4,5-d]-azepine dihydrochloride) into cats lead initially to an increase in blood pressure and then to a long-lasting decrease in blood pressure and heart rate. The central site of the hypotensive and bradycardiac action was demonstrated by the significantly greater effect after intracisternal (i.ci.) than after intravenous injection of B-HT 920, 3 micrograms/kg. The drug decreased the rate of spontaneous discharges in preganglionic splanchnic nerve fibers of normal and noradrenaline-depleted cats (3 micrograms/kg, i.ci.). Vagally mediated reflex bradycardia elicited by angiotensin injection in beta-adrenoceptor-blocked dogs was facilitated by intracisternal injection of 10 micrograms/kg B-HT 920. Both sympathoinhibition and vagal reflex facilitation were antagonized by the alpha-adrenoceptor-blocking agent piperoxan (50 micrograms/kg, i.ci). Therefore, B-HT 920 can be classified as an agent of the clonidine type, despite its different chemical structure. Quantitative differences between B-HT 920 and clonidine are discussed with respect to the greater alpha 2/alpha 1 adrenoceptor activity ratio of the former drug, as reported previously.

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[On the pathogenesis of feline picornavirus infection].

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In vivo effect of alpha 1-acid glycoprotein on experimentally enhanced capillary permeability in guinea-pig skin.

Anesthetized guinea-pigs were intravenously injected with Evans blue. After intracutaneous injection of agonists (lys-plasminogen, histamine, platelet-activating factor, thrombin, bradykinin), the resulting wheals appeared blue in a dose-dependent manner, due to an enhanced capillary permeability, alpha 1-Acid glycoprotein, given i.v. in different doses (3.125-50 mg/kg) and at different times (30-180 min) before Evans blue administration, antagonized the effects of all agonists listed above. This was shown by a parallel shift of the agonist dose-response curves to the right. The effect was time-dependent (tmax: mainly 120 min) and dose-dependent. alpha 1-Acid glycoprotein antagonized the agonists in the following order: lys-plasminogen > histamine = platelet-activating factor > thrombin > bradykinin. As all agonist mentioned are suggested to play a major role in the shock-related increase in vascular permeability, a putatively beneficial role of alpha1-acid glycoprotein in shock is discussed.

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