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At least 415 records · Page 23Linked to original sources

PubMed1998

Phenylephrine and the prevention of postoperative tympanostomy tube obstruction.

OBJECTIVE: To determine the efficacy of phenylephrine hydrochloride, a topical vasoconstrictor, in preventing tympanostomy tube obstruction. DESIGN: Prospective, randomized, double-blind, controlled trial of patients undergoing myringotomy with tympanostomy tube insertion. SETTING: Academic, tertiary referral medical center. PATIENTS: Two hundred eight patients were enrolled in the study; 157 patients (310 ears) returned for postoperative evaluation. INTERVENTIONS: Myringotomy with tympanostomy tube insertion was performed in all ears: 139 control ears received ototopical antibiotics and 171 treatment ears received ototopical antibiotics plus topical phenylephrine. MAIN OUTCOME MEASURE: Postoperative tympanostomy tube obstruction. RESULTS: The overall incidence of tympanostomy tube obstruction was 5.2%: 8.6% in the control group and 2.3% in the treatment group. The treatment group demonstrated an odds ratio of 0.25 (95% confidence interval, 0.08-0.78; P= .02). CONCLUSION: The use of phenylephrine following tympanostomy tube insertion greatly reduces the incidence of tube obstruction.

Adolescent↗

PubMed1989

Alteration of hepatic tissue spaces by platelet-activating factor and phenylephrine.

Mean transit times for the movement of extracellular and intracellular reference compounds through isolated perfused rat livers were determined during exposure of livers to platelet-activating factor (AGEPC; 1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine) and the alpha-adrenergic agonist phenylephrine, using the multiple indicator dilution technique. From the outflow profiles of rapid bolus injections of 3H-sucrose and 14C-urea given to the liver, the estimated intracellular volume of distribution of small freely permeant substances, Vi, and the ratio of intracellular to extracellular space, were computed. Exposure of the liver to AGEPC decreased Vi and by 32 and 34%, respectively, from control values, whereas infusion of phenylephrine increased Vi by 16% and by 33%. The results indicate that the hemodynamic effects of AGEPC in perfused rat liver cause the apparent loss of tissue space accessible to small permeant compounds. Phenylephrine, although increasing hepatic vascular resistance, measured at the portal vein, by the same magnitude as AGEPC, led to an increase in the apparent tissue space accessible to this same species.

Animals↗

PubMed1976

Synthesis and activity of (R)-(-)-m-trimethylacetoxy-alpha-[(methylamino)methyl]benzyl alcohol hydrochloride: a prodrug form of (R)-(-)-phenylephrine.

Optically pure (R)-(-)-m-trimethylacetoxy-alpha-[(methylamino)methyl]benzyl alcohol hydrochloride was synthesized by the following sequence: (R)-(-)-phenylephrine was condensed with acetone in the presence of calcium carbide to give an oxazolidine derivative and then treated with thallous ethoxide in ether followed by trimethylacetyl chloride to yield the phenolic ester. Finally, the oxazolidine ring was cleaved by one equivalent of hydrogen chloride in ethanol. Condensation of phenylephrine with benzaldehyde, with or without solvents, gave either 1,1,2-trimethyl-4,6-dihydroxy-1,2,3,4-tetrahydroisoquinoline or a mixture of side-chain oxazolidine and the tetrahydroisoquinoline. Condensation of epinephrine with opianic acid in pyridine also gave a tetrahydroisoquinoline only. When applied on rabbit eyes, the prodrug (R)-(-)-m-trimethylacetoxy-alpha[(methylamino)methyl]benzyl alcohol hydrochloride exhibited an unexpected, three times higher mydriatic activity than the corresponding racemic prodrug and was 15 times more active than the parent, (R)-(-)-phenylephrine.

Animals↗

PubMed1985

Simultaneous liquid chromatographic determination of glutaric acid, phenylephrine, and benzyl alcohol in a prototype nasal spray with application to di- and tricarboxylic acids.

A rapid reversed-phase high-performance liquid chromatographic method for the simultaneous determination of glutaric acid, phenylephrine, and benzyl alcohol in nasal spray has been developed. UV detection was utilized at 210 nm for the assay of glutaric acid and phenylephrine with an adjustment to 254 nm for the measurement of benzyl alcohol. Linearity and recovery data were obtained for each component in spiked placebo studies. An investigation of the retention mechanisms of the three components showed that phenylephrine was retained by ion-pairing with octanesulfonate anion while glutaric acid and benzyl alcohol partitioned as a suppressed ion and a neutral molecule, respectively. The method has been further extended to the reversed-phase separation of di- and tricarboxylic acids using a totally aqueous 0.0074 M phosphoric acid mobile phase. The retention of these acids was related to their octanol-water partition coefficients and structural variation.

Aerosols↗

PubMed1985

Fluorometric determination of phenylephrine hydrochloride by liquid chromatography in human plasma.

A sensitive method is described for the rapid determination of phenylephrine hydrochloride in human plasma. Phenylephrine was analyzed using high-performance liquid chromatography (HPLC) with fluorecence detection at excitation and emission wavelengths of 270 and 305 nm, respectively. A retention time of approximately 4.25 min was observed on chromatograms. Drug was separated from interfering plasma components by the use of disposable solid-phase extraction columns. Linear standard curves were constructed from drug concentrations of 0.5-5.0 and 2.5-80 ng/mL, for which an average recovery of 76-78% was obtained. Phenylephrine could be quantitatively measured at levels as low as 0.5 ng/mL. An assay precision (CV) of 23.6 and 15.9% was obtained at the lower sensitivities of 0.5 and 1.0 ng/mL, respectively. An example of the method was given for analysis of human plasma levels of drug following topical application of two drops of 2.5% aqueous or 10% viscous opthalmic solution to the eyes of two subjects.

Chromatography, High Pressure Liquid↗

PubMed1996

Stimulation of the Na+/Ca2+ exchanger by phenylephrine, angiotensin II and endothelin 1.

The Na+/Ca2+ exchanger plays an important role in the maintenance of calcium homeostasis in the heart. Therefore, factors which regulate the exchanger have a significant impact on cardiac function. Previously, we showed that the non-hydrolysable GTP analog, 5'guanylyl imidodiphosphate [Gpp(NH)p], stimulates Na+/Ca2+ exchange activity, implying the involvement of a G protein in exchanger regulation. In this study, we examined the effect of G protein agonists on Na+/Ca2+ exchanger activity. Isoproterenol, a Gs agonist, had no effect on exchanger activity. Likewise, the Gi agonist, carbachol, did not influence Na+/Ca2+ exchanger activity. Since these G proteins couple to the adenylate cyclase system, it would appear that cAMP-linked events do not regulate the Na+/Ca2+ exchanger. We next examined the influence of Gq-linked agonists on exchanger activity. Phenylephrine, an alpha 1-adrenergic agonist, increased Na+/Ca2+ exchanger activity up to 111% with an EC50 of 21 microM. Moreover, the Na+/Ca2+ exchanger activity was enhanced by angiotensin II and endothelin 1, which caused maximal stimulation of exchanger activity up to 125% and 211%, respectively. The selective protein kinase C inhibitor chelerythrine significantly attenuated the ability of phenylephrine and angiotensin II to stimulate the Na+/Ca2+ exchanger. In addition, the protein kinase C activator, phorbol 12-myristate 13-acetate, stimulated exchanger activity by 32%, raising the possibility that all three Gq agonists mediate their actions in part through the promotion of phospholipase C activity and the subsequent activation of protein kinase C. The contribution of Na+/Ca2+ exchange to the actions of phenylephrine, angiotensin II, and endothelin 1 is discussed.

Alkaloids↗

PubMed1998

Different aspects of the effects of thapsigargin on automatism, contractility and responsiveness to phenylephrine in cardiac preparations from rats and guinea pigs.

Sarcoplasmic reticulum (SR) Ca(2+)-ATPase play a very important role in excitation-contraction coupling in the heart. The effects of thapsigargin (TG), a selective inhibitor of SR Ca(2+)-ATPase in the heart muscle, on automatism and contractility of the rat and guinea pig heart were examined. Experiments were performed on isolated right auricula and right ventricle papillary muscle. The following parameters were registered: force of contraction (Fc); rate of rise of force (+dF/dt); rate of fall of force (-dF/dt); time to peak contraction (ttp); duration of relaxation phase of contraction at the level of 10% of total amplitude (tt10); and automatism (b.p.m.). Additionally, the influence of thapsigargin on the effects of phenylephrine on the above mentioned parameters were studied. It was found that TG (1 microM) decreased only the automatism in rat heart, but increased automatism and ttp duration and decreased Fc in guinea pig heart. The positive force-frequency relation in the guinea pig heart was attenuated. The effects of phenylephrine in the rat heart were not significantly different before and after pretreatment with TG. Alternatively, pretreatment with TG exerted a profound influence on the effects of phenylephrine in the guinea pig heart. The results indicate that TG has different effects on the guinea pig and rat hearts. The reason for this could be due to species differences, i.e. the weaker crossing of TG through the membrane of rat myocytes or a different mechanism of Ca2+ homeostasis in rat and guinea pig hearts.

Adrenergic alpha-Agonists↗

PubMed1998

The effects of potassium channel modulators on the simulated ischaemia-induced changes in contractility and responsiveness to phenylephrine of rat-isolated papillary muscle.

The aim of the present study was to compare the influence of terikalant, a blocker of inwardly rectifying K+ channels, galanin, a neuropeptide of 29 aminoacids with a complex mechanism of action including an activation of inwardly rectifying K+ channels and glibenclamide, a blocker of ATP-sensitive K+ channels, on simulated ischaemia-induced changes in contractility and response to phenylephrine of rat-isolated heart muscle. Experiments were performed on isolated rat heart papillary muscles. The following parameters were measured: force of contraction (Fc), velocity of contraction (+dF/dt) and velocity of relaxation (-dF/dt), time to peak contraction (ttp) and relaxation time at 10% of total amplitude of contraction (tt10). In the presence of 1 microM of galanin, as well as terikalant, simulated ischaemia caused a decrease in Fc, +dF/dt and -dF/dt, however, it significantly increased a drop in Fc and -dF/dt. After 60 min of reperfusion, all the measured parameters recovered completely except Fc in the galanin group. Terikalant, but not galanin, prevents the negative inotropic action of phenylephrine observed in the control group. On the other hand, addition of 1 microm of glibenclamide to the no-substrate solution prevented the simulated ischaemia-induced decrease in Fc, +dF/dt and -dF/dt. In this group phenylephrine did not cause the negative inotropic action. The above mentioned data reveal that pretreatment with the inhibitors of ATP-sensitive and inwardly rectifying K+ channels protect rat-isolated papillary muscle against ischaemia-induced disturbances in contractility.

Animals↗

PubMed1982

Pharmacokinetics of 3H-phenylephrine in man.

7-3H-phenylephrine was given to 15 volunteers by a short-infusion n = 4) or p.o. (10 volunteers, 1 patient with porto-caval anastomosis). Analysis of serum for free 3H-phenylephrine and fractionation of urinary radioactivity was performed by ion-exchange and thin-layer chromatography. As almost the same 3H-activity was excreted in urine after i.v. and p.o. administration, 86% and 80% of the dose respectively, complete enteral absorption can be assumed. A considerable difference was seen in the fraction of free phenylephrine, i.v. 16% of the dose versus p.o. 2.6%, which suggested reduced bioavailability. This was confirmed by comparison of the areas under the serum curve, which showed a bioavailability factor of 0.38. The result for the patient with porto-caval anastomosis was comparable to that in the normal volunteers. The biological half-life of 2 to 3h was comparable to that of structurally related amines, as were the total clearance of 2 l/h, and the volume of distribution of 340 l. Metabolism to phenolic conjugates mainly after oral ingestion, and to m-hydroxymandelic acid after i.v. injection, again demonstrated that m-hydroxylated amines are predominantly conjugated during the "first-pass" metabolism.

Administration, Oral↗

PubMed1981

The effect of dopamine, atropine, phenylephrine and cardiac pacing on oxygen consumption during fentanyl-nitrous oxide anaesthesia in the dog.

In animals deeply anaesthetized with fentanyl and nitrous oxide the arterial blood pressure and heart rate were increased using dopamine, atropine, electrical pacing and phenylephrine in order to study the accompanying change in whole body oxygen consumption. Seven dogs (16-24 kg) were anaesthetized with fentanyl 1 microgram . kg-1 . min-1. After completing instrumentation a dopamine infusion was started at a rate of 39 micrograms . kg-1 .min-1. After the mean blood pressure reached 18.6 kPa the infusion was reduced to 10 micrograms . kg-1 . min-1 and maintained for 10 minutes. After waiting 45 minutes an infusion of atropine 20 micrograms . kg-1 . min-1 was started and when the heart rate reached 120 b/min the infusion was slowed to 1.25 micrograms . kg-1. min-1 and maintained for 10 minutes. Twenty-five minutes later the heart rate was increased to 150 beats/min and maintained at that level for 10 minutes using electrical pacing. The pacing was removed and an infusion of phenylephrine 5 micrograms . kg-1 . min-1 was started. When the blood pressure reached 21.3 kPa the infusion was reduced to 2.5 micrograms . kg-1 . min-1 and maintained for 10 minutes. The results show increases in oxygen consumption of 14 per cent with dopamine, 19 per cent with atropine, 16 per cent, and 14 per cent with phenylephrine. All changes were significantly different from the control values. The magnitude of change in whole body oxygen consumption was best predicted by either the cardiac output X blood pressure product or by the cardiac output alone.

Anesthesia↗

PubMed1997

Pharmacological differentiation of synergistic contribution of L-type Ca2+ channels and Na+/H+ exchange to the positive inotropic effect of phenylephrine, endothelin-3 and angiotensin II in rabbit ventricular myocardium.

The present study was designed to delineate pharmacologically the role of sarcolemmal L-type Ca2+ channels and Na+/H+ exchange in the positive inotropic effect (PIE) of phenylephrine mediated by alpha-1 adrenoceptors, endothelin (ET) and angiotensin II (Ang II) that stimulate phosphoinositide (PI) hydrolysis in the rabbit ventricular muscle. The PIE of these receptor agonists was compared with the PIE of isoprenaline that accumulates cyclic AMP. For this purpose, we investigated the influence of a Ca2+ antagonist, verapamil, and of an inhibitor of Na+/H+ exchange, 5-(N-ethyl-N-isopropyl) amiloride (EIPA), alone or in combination, on the cumulative concentration-response curve (CRC) for phenylephrine (with 0.3 microM bupranolol). ET-3 and Ang II in isolated right ventricular papillary muscles of the rabbit, which were electrically stimulated at 1 Hz in Krebs-Henseleit solution at 37 degrees C. Verapamil at 0.3 and 1 microM decreased the basal force of contraction to 37.0 +/- 4.0% and 13.2 +/- 1.1% of the control, respectively, while EIPA event at 10 microM affected the basal force to much less extent and decreased it to 87.0 +/- 1.4%. Verapamil (0.3 and 1 microM) and EIPA (1 and 10 microM), when used alone, each significantly attenuated but did not abolish the PIEs induced by phenylephrine, ET-3 and Ang II, while the simultaneous administration of verapamil (1 microM) and EIPA (10 microM) consistently and almost completely inhibited the PIE induced by these receptor agonists. By contrast, the PIE of isoprenaline was retained even in the presence of verapamil and EIPA. These results indicate that both the influx of Ca2+ ions through L-type Ca2+ channels and activation of Na+/ H+ exchange contribute synergistically to the PIE that is mediated by alpha-1 adrenergic, ET and Ang II receptor agonists, while these mechanisms are not essential for the beta-adrenoceptor-mediated PIE.

Amiloride↗

PubMed1980

Mydriasis from topically administered phenylephrine HCl powder.

Microgram amounts of finely powdered phenylephrine HCl were administered to the conjunctiva of volunteers. A dose-response curve for white subjects showed a threshold mydriasis of less than 5 micrograms and a clinically useful mydriasis was obtained with one application of 50 micrograms. The time-response curve for the one time use of 50 micrograms of the powder was equivalent to giving three applications of 10% phenylephrine HCl drops. Twenty-five micrograms of pilocarpine HCl powder produced marked miosis. We investigated methods to deliver nonirritating microgram amounts of powdered phenylephrine HCl, pilocarpine HCl, and fluorescein.

Adult↗

PubMed1988

Thymoxamine reverses phenylephrine-induced mydriasis.

We performed a randomized double-masked evaluation of the alpha-adrenergic blocking agent thymoxamine (0.1%) as compared to placebo for the reversal of phenylephrine-induced mydriasis. Topically applied thymoxamine reversed the mydriasis from a single drop of 2.5% phenylephrine in 36 of 40 eyes (90%) within one hour. The mydriasis was completely reversed in 25 of 40 eyes (63%). Eyes with blue irides responded more quickly and more completely than did those with brown irides. The 40 contralateral eyes, which had also been dilated with phenylephrine, remained dilated or dilated further after receiving a placebo eyedrop. Twenty subjects (50%) reported mild transient ocular irritation upon instillation of thymoxamine. Thymoxamine was useful in individuals with narrow anterior chamber angles who were at risk of acute closed-angle glaucoma following dilation with an adrenergic agent.

Adult↗

PubMed1986

Comparison of the changes in cytoplasmic free calcium concentration induced by phenylephrine, vasopressin and angiotensin II in hepatocytes.

Effects of phenylephrine, vasopressin and angiotensin II on cytoplasmic free calcium concentration, [Ca2+]c, were examined by monitoring aequorin bioluminescence in isolated hepatocytes preloaded with aequorin. In the presence of 0.5 mM calcium in the medium, the pattern of changes in aequorin bioluminescence induced by phenylephrine was different from that induced by vasopressin or angiotensin II. When extracellular calcium concentration was reduced to 1 microM, however, these three agents induced identical changes in aequorin bioluminescence. These results suggest that the mode of action of phenylephrine on cytoplasmic free calcium concentration differs from that of either vasopressin or angiotensin II and that the difference in ability to increase calcium influx may account for the distinct patterns induced by these agents.

Aequorin↗

PubMed1990

Clonidine and phenylephrine injected into the lateral hypothalamus inhibits water intake in rats.

It has been demonstrated that peripheral or intracerebroventricular (i.c.v.) administration of the alpha 2-adrenoceptor agonist, clonidine, blocks the water intake induced by several dipsogenic stimuli in rats. In the present investigation we studied the effect of the injection of clonidine, phenylephrine, prazosin or yohimbine into the lateral hypothalamic area (LHA) on the water intake induced by water deprivation or central angiotensin II (AII) in rats. Rats with chronic cannulas implanted into the lateral ventricle and LHA were used. Injection of clonidine or phenylephrine into the LHA reduced the water intake produced by both water deprivation and i.c.v. injection of AII. Previous injection of the alpha 1- or alpha 2-adrenoceptor antagonists, prazosin or yohimbine, into the LHA reduced the antidipsogenic effect of clonidine or phenylephrine injected into the same area. These results suggest that the alpha 1- and alpha 2-adrenergic receptors of the hypothalamus are part of the central inhibitory system for the thirst produced by dehydration or central AII.

Angiotensin II↗

PubMed1977

Failure of alpha-adrenergic stimulation by phenylephrine to enhance renin secretion in the isolated rat kidney.

The intrarenal effect of the alpha-receptor agonist phenylephrine on renin secretion was examined in the isolated rat kidney. Infusion of phenylephrine in non-vasoconstrictor doses resulted in secretion rates which were not significantly different from control values. Similarly no change in renin secretion was found when phenylephrine was infused at a dose that clearly caused renal vasoconstriction and increased vascular resistance. These results do not support the hypothesis of a role for the alpha-receptor in the stimulation of renin secretion by adrenergic activity.

Animals↗

PubMed1977

Responsiveness of the guinea-pig vas deferens to phenylephrine and norepinephrine in vivo.

A method is described for the study of guinea-pig vas deferens in vivo response to phenylephrine and norepinephrine. Tissue sensitivity to both agonists did not differ in vivo but the maximum response to phenylephrine was smaller. Responsiveness to norepinephrine was depressed in vitro after in vivo experiments. No such effect was observed for phenylephrine. This method allowed the comparison of the responsiveness of the guinea-pig vas deferens to adrenoceptor agonists in vivo and in vitro.

Animals↗

PubMed1977

Vascular beta-adrenoceptor stimulating properties of phenylephrine.

In pithed rats pretreated with propranolol changes occurred in the slopes of dose--pressor response curves to i.v. phenylephrine and noradrenaline but not to LD 3098, a pure alpha-adrenoceptor stimulant. In dogs, cats, and spontaneously hypertensive rats pretreated with an alpha-adrenoceptor blocker, i.v. phenylephrine induced vasodilatory responses which were antagonised by propranolol. These results indicate that phenylephrine, in addition to its known beta1-agonistic properties, stimulates the vascular beta2-adrenoceptors.

Adrenergic beta-Agonists↗