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Biomedical subjects

M Virno

Publications and source records attributed to M Virno.

At least 37 records · Page 2Linked to original sources
PubMed1977

[Vascular effects of adrenergic drugs and their action on intraocular pressure (author's transl)].

By means of the continuous contemporary recording of arterial blood pressure and intraocular pressure, the relationship between the two parameters was analyzed following the intravenous administration of adrenergic drugs. The aim was that of determining if during a change in systemic blood pressure the behaviour of intraocular pressure may indicate an active or passive participation to such a change. In the present studies the most important representatives of the different adrenergic groups (adrenalin, dibenamin, ergotamin, propranolol and isoproterenol) were taken in consideration. The results in normal eyes and in eyes with experimental hypertension showed that the adrenergic drugs affect the intraocular presure through a primary vasomotorial effect. An active vasodilatation of the intraocular vessels could not be demonstrated, whereas an active (adrenalin, ergotamin) as well as a passive (propranolol, isoproterenol) vasoconstriction was evidenced. The present studies allow an interpretation of the ocular hypotonizing mechanism of action of adrenergic drugs.

Animals↗
PubMed1977

[Experimental triethyltin ocular hypertension. Pharmacological and histopathological studies (author's transl)].

The experiments were prompted by the need felt in pharmacology of eyes with hypertension of easy availability, rather long duration and fairly constant levels, to allow observation of the effects of hypotensive agents and to study their mechanism of action. Single doses of 1 mg Triethyltin, a substance producing a hydrodynamic compromission of the brain, were injected into the anterior chamber of rabbit eyes. A rise in ocular tension, beginning within 24 hours and lasting seven to ten days is obtained in about 70% of eyes. The pressure increase ranged from 12 to 30 mm Hg. Biomicroscopic and histologic examinations evidenced an uveitis-like reaction in the first week after treatment. Neoprene casts evidenced an impaired vascularization in the ciliary processes and choroid. Topical and parenteral administration of the most commonly used antiglaucomatous drugs showed how well this hypertension responded to hypotonizing agents. The occurrence of producing an ocular hypertension in the untreated fellow eye following repeated intra-cameral injections of small dosage (1 microgram) of Triethyltin, every two days for more than one month, in the other eye is described. Hypertension resulted in 40% of eyes.

Animals↗
PubMed1976

Possibility of isoproterenol therapy with soft contact lenses: ocular hypotension without systemic effects.

An experimental investigation performed in the rabbit pointed out the possibility of administering isoproterenol at low concentrations with the aid of soft contact lenses presoaked in 0.2% isoproterenol for 60 to 120 minutes. A reduction in intraocular pressure ranging from 23% to 32% was observed in 21 out of 24 glaucomatous patients. Duration of hypotension in 50% of eyes treated was more than 8 hours. Thus, a therapeutic effect was obtained with a concentration (0.2%) approximately 50 times lower than that previously employed clinically (2.4%). No systemic side effects, such as arterial hypotension and increase in heart rate, were noted.

Animals↗
PubMed1975

Acetazolamide, metabolic acidosis, and intraocular pressure.

In order to investigate whether or not there is a causal relationship between the metabolic acidosis and the ocular hypotension induced by acetazolamide, we undertook to correlate over a period of time the blood-acidifying and ocular-hypotonizing effects of administering the lowest intravenous effective dose of acetazolamide; to treat the metabolic acidosis induced by acetazolamide by means of the intravenous introduction of bases, and pulmonary hyperventilation (respiratory alkalosis); to evaluate the effects on the intraocular pressure (IOP) by neutralizing the acetazolamide-induced metabolic acidosis by means of a continuous infusion of sodium bicarbonate; to determine the relationship between the metabolic acidosis induced by blood-acidifying agents, which do not inhibit carbonic anhydrase, and the IOP; and to determine the changes in the acid-base status of the aqueous humor induced by acetazolamide and other blood-acidifying drugs. We found that the hypertonic buffering solution of sodium bicarbonate could reduce the IOP by itself through an osmotic mechanism. On the basis of our results, we believe that a causal relationship exists between the metabolic acidosis induced by acetazolamide, and by other drugs that have a blood-acidifying effect as the result of other mechanisms, and ocular hypotension, bothin the animal and in the glaucomatous patient.

Acetazolamide↗