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Biomedical subjects

J M Rowland

Publications and source records attributed to J M Rowland.

47 records · Page 3Linked to original sources
PubMed1981

Circadian rhythm in intraocular pressure: a rabbit model.

An animal model for study of the circadian rhythm in intraocular pressure (IOP) was developed using carefully maintained environmental lighting conditions. Highly predictable, precipitous increases and decreases in IOP of somewhat more than 10 mm Hg were found to be closely correlated with the onset of darkness and light, respectively. The daily spontaneous variations in IOP, once entrained, were maintained in constant darkness, but were eliminated by constant light, as is similarly seen in many mammalian systems. This model provides a novel means of investigating circadian IOP oscillation, which has been shown to be especially amplified in primary open angle glaucoma (POAG). This new rabbit model may also warrant consideration for use in screening ocular antihypertensive drugs since it could obviate the gross physiological manipulations and concomitant side effects inherent in the popular methods of inducing ocular hypertension in animal models.

Animals↗
PubMed1981

Steric structure activity relationships of various adrenergic agonists: ocular and systemic effects.

Dextrorotatory (d) forms of adrenergic drugs are known to be much less active than the levo (l) forms in effecting classical adrenergically mediated responses (alpha, beta 1, beta 2) in metabolic organs and cardiovascular tissues. Adrenoceptor intrinsic activity and affinity, enzymatic inactivation and neuronal uptake are all known to be relatively selective for the l-forms. It is known, however, that the d-isomers of certain agonists, such as isoproterenol, are as effective or even more effective ocular hypotensive agents than their respective l-forms or the racemates (dl) in rabbits. We tested the d- and l-isomers of epinephrine (alpha, beta 1, beta 2), norepinephrine (alpha, beta 1), phenylephrine (alpha 1), isoproterenol (beta 1, beta 2) and soterenol (alpha, beta 2) for their comparative effects after topical administration on intraocular pressure (IOP), pupil diameter (PD), arterial blood pressure (ABP) (after both topical and i.v. administration), aqueous cAMP, and aqueous and plasma lactate and glucose in the normotensive rabbit model. The results with ABP and concomitant changes in plasma biochemical correlates normally associated with adrenergic mechanisms were consistent with well established theory of stereospecificity. Data from ocular parameters, however, suggest that d-isomers of adrenergic agents evoke ocular responses that are divergent from this theory. The relation of ocular and systemic pressure responses with their respective biochemical correlates suggests that some d-isomers of adrenergic stimulants may be acting as partial agonists.

Adrenergic beta-Agonists↗
PubMed1980

The effects of topical prazosin on normal and elevated intraocular pressure and blood pressure in rabbits.

A 0.1 mg (base) dose of prazosin, a postsynaptic alpha- (alpha 1) adrenoceptor antagonist, in rabbits effected an early decrease in arterial blood pressure, normal intraocular pressure (IOP) and IOP artificially elevated by water loading. The late drug effects suppressed elevated IOP, but not normal IOP. The IOP effects of prazosin seem largely independent of the effect on blood pressure.

Administration, Topical↗
PubMed1980

Acute pretreatment with pyrazole and ethanol: effects on glucose-induced changes in insulin and glucagon.

Ethanol suppressed, in a dose-related manner, glucose-induced insulin (IRI) release and thus delayed the disappearance of glucose from the blood of rats. Pretreatment with pyrazole, an alcohol dehydrogenase inhibitor, exacerbated the effect of ethanol on IRI release, glucose tolerance and glucagon (IRG) release. These results suggest that ethanol produces glucose intolerance by inhibiting glucose-induced IRI release and by augmenting IRG release. Moreover, these findings indicate that ethanol does not have to be metabolized completely in order to produce these effects.

Animals↗
PubMed1979

Effects of adrenergic drugs on aqueous cAMP and cGMP and intraocular pressure.

The following variously selective adrenergic agonists were tested for their effects on the concentration of adenosine 3',5' cyclic monophosphate and guanosine 3',5- cyclic monophosphate in the aqueous humor of treated and fellow eyes of rabbits one hour after topical unilateral application (2 mg, base): Epinephrine (alpha, beta 1.beta 2), phenylephrine alpha), isoproterenol (beta 1, beta 2), tazolol (beta 1) and terbutaline (beta 2). All drugs produced a significant increase in cAMP in the treated eyes and all but terbutaline produced a significant increase in the fellow eye. Terbutaline alone caused an increased in cGMP although a similar dose of pilocarpine, a cholinergic agonist, was ineffective in changing cGMP levels. We conclude that (1) diverse adrenoceptor stimulation can increase cAMP, but (2) not necessarily in direct relation to an agent's hypotension induced by pilocarpine is not accompanied by an increase in aqueous cGMP.

Administration, Topical↗
PubMed1979

Effect of beta-adrenergic drugs on plasma glucose and glucagon in Japanese quail: a preliminary report.

The present study was conducted to determine the effects of beta-adrenergic stimulation on plasma glucose and glucagon (IRG) levels in Japanese quail. Isoproterenol, epinephrine and three relatively selective beta-adrenoceptor agonists (terbutaline, salbutamol and reproterol) produced dose-related hyperglycemia and hypoglucagonemia. This study demonstrates that beta-adrenoceptor agonists produce hyperglycemia in birds as they do in mammals, but that the rise in plasma glucose in birds, unlike mammals, is accompanied by a profound fall in plasma IRG levels.

Adrenergic beta-Agonists↗
PubMed1979

Alterations in arginine-induced pancreatic hormone release: influence of acute and chronic exposure to ethanol.

Acute oral administration of ethanol (150 and 750 mg/100g) to fasted rats produced dose-related inhibition of arginine-induced insulin (IRI) release, an elevation of plasma glucagon (IRG) levels and minor effects on blood glucose. In contrast, chronic consumption of ethanol for 10 weeks augmented arginine-induced hyperglycemia and hperinsulinemia. Thus, acute ethanol administration decreased plasma IRI levels at both doses, presumably by suppressing beta cell function; whereas, function of the alpha cell and plasma IRG levels were increased, but only by the high dose of ethanol. In these experiments the effects exerted by ethanol on the pancreatic endocrine responses to arginine infusion varied according to: dose of ethanol administered; duration of exposure to ethanol; and state of nourishment of the subjects.

Animals↗
PubMedDate not supplied

Ocular hypertensive response to beta-adrenoceptor agonists.

Acute administration of non-selective and relatively selective beta-adrenoceptor agonists elicit a monophasic fall in IOP. The present study indicates that unilateral application of certain beta-agonists on consecutive days can result in marked ocular hypertension. 1-Epinephrine, reproterol and 1-isoproterenol evoked an elevation of IOP on the second and third day after topical administration of a 2% solution in normal rabbits and in rabbits with surgically transected extraocular muscles. In contrast, the same concentration of d-isoproterenol produced hypotensive responses only when administered once daily for three consecutive days. Since d-isoproterenol did not cause a rise in IOP during chronic administration, the mechanism involved in the hypertensive response appears to be more sensitive to the levorotatory form. Administration of timolol inhibited the ocular hypertensive effect of epinephrine and reproterol. Since timolol lowers IOP by depressing formation of aqueous, it is suggested that the rise in IOP following chronic administration of beta-agonists possibly involves an increase in aqueous humor production.

Adrenergic beta-Agonists↗