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PubMed1999

Thimerosal enhances agonist-specific differences between [Ca2+]i oscillations induced by phenylephrine and ATP in single rat hepatocytes.

Single rat hepatocytes, microinjected with the Ca(2+)-sensitive photoprotein aequorin, respond to agonists acting through the phosphoinositide signalling pathway by the generation of oscillations in cytosolic free Ca2+ concentration ([Ca2+]i). The duration of [Ca2+]i transients generated is characteristic of the stimulating agonist; the differences lie in the rate of fall of [Ca2+]i from its peak. We considered that differential sensitivity of the InsP3 receptor may underlie agonist specificity. The thiol reagent, thimerosal, is known to increase the sensitivity of the Ca2+ stores to InsP3 by increasing the affinity of the InsP3 receptor for InsP3 in rat hepatocytes. We show here that a low dose of thimerosal (1 microM), insufficient alone to elevate [Ca2+]i, potentiates [Ca2+]i oscillations induced by phenylephrine or ATP in single, aequorin-injected, rat hepatocytes. Moreover, thimerosal enhances both the frequency and amplitude of phenylephrine-induced oscillations, whereas, in contrast, ATP-induced oscillations undergo an increase in the duration of the falling phase of individual [Ca2+]i transients. Thimerosal, therefore, enhances, rather than eliminates, agonist-specific differences in the hepatocyte [Ca2+]i oscillator.

Adenosine Triphosphate↗

PubMed1988

Effect of fructose on phenylephrine-induced glucose output in perfused rat liver.

Glucose output induced by phenylephrine in perfused livers of fed rats was decreased by 34% during an infusion of fructose, but was increased by 30% (compared to controls) following cessation of fructose infusion. Corresponding changes in hepatic inorganic phosphate (Pi) were also observed with a 40% decrease and a 48% increase in Pi concentration being measured during and following fructose infusion, respectively. The data suggest that the glycogenolytic response to phenylephrine is dependent on the hepatic Pi concentration. It is also suggested that enhanced hepatic Pi concentrations and glycogenolytic responses observed following fructose infusion may antagonize insulin-induced suppression of hepatic glucose output and thus play a role in the glucose intolerance and insulin resistance associated with sucrose or fructose feeding.

Animals↗

PubMed1992

[The cycloplegic effect of atropine in comparison with the cyclopentolate-tropicamide-phenylephrine combination].

Atropine is thought to produce the most effective cycloplegia in early childhood. Cyclopentolate and Tropicamide are the best known short acting cycloplegic agents. Phenylephrine is an adrenergic agent and has also a cycloplegic effect. In this study we compared a combination of Cyclopentolate, Tropicamide and Phenylephrine with Atropine and observed no difference between them.

Accommodation, Ocular↗

PubMed2000

Neuropeptide Y (NPY) potentiates phenylephrine-induced mitogen-activated protein kinase activation in primary cardiomyocytes via NPY Y5 receptors.

Neuropeptide Y (NPY) has been shown to participate in the cardiovascular response mediated by the sympathetic system. In this report, we investigate the growth factor properties of NPY on cardiac myocytes. Mitogen-activated protein kinases (MAPK) are key signaling molecules in the transduction of trophic signals. Therefore, the role of NPY in inducing MAPK activation was studied in mouse neonatal cardiomyocytes. Exposure of neonatal cardiomyocytes to either NPY, phenylephrine, or angiotensin II induces a rapid phosphorylation of the extracellular responsive kinase, the c-jun N-terminal kinase, and the p38 kinase as well as an activation of protein kinase C (PKC). Moreover, NPY potentiates phenylephrine-induced MAPK and PKC stimulation. In contrast, NPY has no synergistic effect on angiotensin II-stimulated MAPK phosphorylation or PKC activity. NPY effects are pertussis toxin-sensitive and calcium-independent and are mediated by NPY Y5 receptors. Taken together, these results suggest that NPY, via G(i) protein-coupled NPY Y5 receptors, could participate in the development of cardiac hypertrophy during chronic sympathetic stimulation by potentiating alpha-adrenergic signals.

Angiotensin II↗

PubMed1998

Stimulation of the p38 mitogen-activated protein kinase pathway in neonatal rat ventricular myocytes by the G protein-coupled receptor agonists, endothelin-1 and phenylephrine: a role in cardiac myocyte hypertrophy?

We examined the activation of the p38 mitogen-activated protein kinase (p38-MAPK) pathway by the G protein-coupled receptor agonists, endothelin-1 and phenylephrine in primary cultures of cardiac myocytes from neonatal rat hearts. Both agonists increased the phosphorylation (activation) of p38-MAPK by approximately 12-fold. A p38-MAPK substrate, MAPK-activated protein kinase 2 (MAPKAPK2), was activated approximately fourfold and 10 microM SB203580, a p38-MAPK inhibitor, abolished this activation. Phosphorylation of the MAPKAPK2 substrate, heat shock protein 25/27, was also increased. Using selective inhibitors, activation of the p38-MAPK pathway by endothelin-1 was shown to involve protein kinase C but not Gi/Go nor the extracellularly responsive kinase (ERK) pathway. SB203580 failed to inhibit the morphological changes associated with cardiac myocyte hypertrophy induced by endothelin-1 or phenylephrine between 4 and 24 h. However, it decreased the myofibrillar organization and cell profile at 48 h. In contrast, inhibition of the ERK cascade with PD98059 prevented the increase in myofibrillar organization but not cell profile. These data are not consistent with a role for the p38-MAPK pathway in the immediate induction of the morphological changes of hypertrophy but suggest that it may be necessary over a longer period to maintain the response.

Animals↗

PubMed1988

Allergic blepharoconjunctivitis due to phenylephrine.

Acute allergic blepharoconjunctivitis with mucopurulent discharge due to phenylephrine eye drops is reported. The reaction begins 3-4 hours after drug application, persists for 12 hours and regresses gradually within 72 hours. This clinical picture occurs with a phenylephrine concentration as low as 0.1%. Conjunctival biopsy of the inflamed eyes reveals marked infiltration by lymphocytes, plasma cells and eosinophiles, without predominance of any of these cells.

Acute Disease↗

PubMed1989

Ophthalmic epinephrine, phenylephrine, and pilocarpine affect the systemic absorption of ocularly applied timolol.

Ocularly applied timolol eyedrops may cause serious systemic side-effects in some patients. In this study we evaluated the effects of pretreatment with epinephrine and pilocarpine eyedrops on systemic absorption of ophthalmic timolol. Epinephrine decreased the systemic absorption of timolol, while pilocarpine increased the peak concentrations of timolol in plasma. When applied in the same solution with timolol, pilocarpine had no effect and phenylephrine decreased the systemic absorption of timolol. The observed effects were due to the conjunctival and nasal vasoconstricting effects of epinephrine and phenylephrine and to the vasodilating effects of pilocarpine. These pharmacokinetic interactions demonstrate the importance of the conjunctival and nasal blood flow in the systemic absorption of timolol.

Absorption↗

PubMed1997

Dose-response study of dapiprazole HCl in the reversal of mydriasis induced by 2.5% phenylephrine.

Dapiprazole HCL is currently available in the United States for reversal of diagnostic mydriasis. The recommended dosage for this indication is 2 drops followed 5 minutes later by 2 drops. We studied the dose-response profile and tolerance of three different treatment regimens: 1 drop alone, 1 drop followed by 1 additional drop 5 minutes later, and 2 drops followed by 2 additional drops 5 minutes later. Sixty normal male and female volunteers between 18 and 40 years of age were recruited for a double-masked, placebo-controlled, crossover study in which each eye of each subject was dilated with 2.5% phenylephrine. After one hour, one eye was treated with 0.5% dapiprazole, and the contralateral eye was treated with placebo. Each subject was treated with each of the three dapiprazole regimens in three different study sessions separated by at least 5 days (drug half-life in the eye is 5 hours). Analysis of AUC demonstrated no significant difference (P = 0.620) between the 1 drop regimen and the 2 + 2 regimen. A single drop of dapiprazole has a clinical effect equivalent to the 2 + 2 drop regimen in eyes dilated with 2.5% phenylephrine, which should improve the cost-effectiveness of this mydriolytic agent.

Accommodation, Ocular↗

PubMed1991

Effect of i.v. low-dose adrenaline and phenylephrine infusions on plasma concentrations of bupivacaine after lumbar extradural anaesthesia in elderly patients.

Thirty patients undergoing primary total hip replacement under lumbar extradural anaesthesia with 0.75% bupivacaine 25 ml were allocated randomly to receive either low-dose adrenaline or phenylephrine infusions i.v. throughout surgery. Haemodynamic measurements and arterial blood samples were obtained before the extradural injection and at 10, 20, 30, 40, 50, 60 and 90 min thereafter. Peak arterial plasma concentrations of bupivacaine were observed 10 min after extradural anaesthesia and were significantly lower in patients receiving adrenaline infusions. Cardiac output was significantly greater in patients receiving adrenaline infusions (P less than 0.01). It is postulated that the smaller circulating concentrations of bupivacaine observed in patients receiving adrenaline were caused by increased cardiac output and a greater volume of distribution than in patients receiving phenylephrine.

Aged↗

PubMed1996

The effects of dobutamine and phenylephrine on atrioventricular conduction during combined use of halothane and thoracic epidural lidocaine.

The purpose of this study was to measure cardiac sympathetic nerve activity (CSNA) and atrioventricular (AV) conduction and to test the effects of dobutamine (DOB) and phenylephrine (PHE) on AV conduction during combined use of halothane and thoracic epidural lidocaine. Cats were anesthetized with 1 % halothane and an epidural catheter was inserted through T-9 laminectomy. His bundle and atrial electrocardiograms were obtained and atrial electric stimulation was performed using quadripolar catheter electrodes. Cats underwent left thoracotomy, and CSNA was recorded directly from the left ventrolateral or ventromedial nerve. In addition to sinus cycle length (SCL) measurement during spontaneous beating, the functional refractory period (FRP) of the atrioventricular node (AV node), effective refractory period (ERP) of the atrium, atrium-His (A-H) intervals were determined just before and 10, 20, and 30 min after epidural administration of 1% lidocaine (0.2 mL/kg) in Group C. DOB 5 micrograms/kg/min (Group DOB) and PHE 0.5-1.0 micrograms/kg/min (Group PHE) were intravenously administered from 12 to 22 min after epidural lidocaine. CSNA and mean arterial pressure (MAP) were markedly decreased and SCL, FRP of AV node, ERP of atrium and A-H interval were significantly prolonged after epidural lidocaine. MAP increased to baseline level during DOB or PHE infusion. Worsening of cardiac electrophysiological variables was improved with DOB infusion, but did not change with PHE infusion. We conclude that thoracic epidural lidocaine during halothane anesthesia almost eliminates CSNA, and thereby attenuates sinus node automaticity and AV node function. DOB restored normal cardiac electrophysiological variables, and therefore is preferable to phenylephrine as a pressor drug.

Adrenergic alpha-Agonists↗

PubMed1997

The effects of bupivacaine, L-nitro-L-arginine-methyl ester, and phenylephrine on cardiovascular adaptations to asphyxia in the preterm fetal lamb.

UNLABELLED: The preterm fetal lamb that is exposed to clinically relevant plasma concentrations of lidocaine loses its cardiovascular adaptations to asphyxia, and its condition deteriorates further. Nitric oxide (NO) is an important regulator of vascular tone, and local anesthetics are known to inhibit endothelium-dependent vasodilation. The purpose of the present study was to determine whether the adverse effects of lidocaine noted in the preterm fetal lamb also occur with bupivacaine and whether the inhibition of NO results in effects similar to those of bupivacaine. Thirty-two chronically prepared pregnant sheep were studied at 117-119 days' gestation. Maternal and fetal blood pressure, heart rate, and acid-base state were evaluated. Fetal organ blood flows were determined using 15-microM diameter dye-labeled microspheres. After a control period, mild to moderate asphyxia (fetal PaO2 15 mm Hg) was induced by partial umbilical cord occlusion and maintained throughout the experiment. Ewes in Group I (n = 13) were given a two-step intravenous infusion of bupivacaine for 180 min. Fetuses in Group II (n = 12) received an intravenous injection of L-nitro-L-arginine-methyl ester (L-NAME) (25 mg/kg), and measurements were taken 10 and 30 min after the injection. A third group (Group III) of fetuses (n = 7) were given an intravenous infusion of phenylephrine to mimic the blood pressure increases noted in L-NAME-treated fetuses. At 90 min of stable asphyxia, there was a significant decrease in fetal PaO2 and pHa and an increase in PaCO2 and mean arterial blood pressure. There was also an increase in blood flow to the adrenals, myocardium, and cerebral cortex, whereas blood flow to the placenta decreased. Administration of bupivacaine during asphyxia did not affect the changes in mean arterial blood pressure and acid-base state but did abolish the increases in blood flows to the myocardium and cerebral cortex. Injection of L-NAME to the asphyxiated fetus resulted in an increase in mean arterial blood pressure above the level noted at 90 min of cord occlusion, and an increase in fetal PaO2 toward control levels. This was accompanied by a reduction in organ blood flows to preasphyxia levels. In asphyxiated Group III fetuses, titration of the phenylephrine infusion to achieve blood pressure increases similar to those noted with L-NAME were also associated with an increase in fetal PaO2. These data indicate that bupivacaine abolishes some of the circulatory adaptations to mild to moderate asphyxia induced by partial cord occlusion in the preterm fetal lamb. It is not clear whether these effects of bupivacaine are due to inhibition of NO. IMPLICATIONS: In the preterm fetal lamb, clinically relevant plasma concentrations of bupivacaine achieved by intravenous infusion to the pregnant ewe (80% gestation) abolished some of the fetal cardiovascular adaptations to asphyxia induced by partial umbilical cord occlusion.

Adaptation, Physiological↗

PubMed1997

Actions of phenylephrine, isoproterenol, and epinephrine with halothane on endocardial conduction and activation in canine left ventricular papillary muscles.

BACKGROUND: Myocardial sensitization by halothane to the arrhythmogenic effects of epinephrine involves synergistic actions mediated by alpha 1- and beta-adrenoceptors. Halothane potentiates a transient a1-adrenoceptor-mediated negative dromotropic effect of epinephrine on Purkinje fibers. This study examines how halothane alters the actions of alpha 1- and beta-agonists and epinephrine on endocardial conduction. METHODS: Superfused canine papillary muscles were mapped to locate a Purkinje-ventricular muscle junction (PVJ), and bipolar electrodes were placed to measure Purkinje and endocardial conduction velocity and PVJ conduction time during stimulation of the Purkinje layer. The effects of exposure to 5 microM phenylephrine, 1 microM isoproterenol, or 5 microM epinephrine on conduction were determined in the absence and presence of 0.4 mM halothane in three groups of 10 preparations. RESULTS: Isoproterenol slightly increased Purkinje conduction velocity and markedly improved conduction at the PVJ and in the endocardium similarly in the presence or absence of halothane. Phenylephrine depressed Purkinje velocity (-12%) only in the presence of halothane and did not slow conduction at the PVJ or in the myocardium. Epinephrine transiently depressed Purkinje velocity, more so with (-22%) than without (-12%) halothane (P < or = 0.01), and simultaneously facilitated conduction at the PVJ and in the myocardium. CONCLUSIONS: The prodysrhythmic actions of epinephrine with halothane may involve disparate effects on conduction, including speeding on conduction at the PVJ and in the myocardium, similar to that produced by isoproterenol, accompanied by simultaneous but transient alpha 1-mediated depression of conduction in the Purkinje system.

Adrenergic alpha-Agonists↗

PubMed1976

Effective degree of mydriasis with phenylephrine and tropicamide.

The mydriatic effects of several concentrations of phenylephrine and of tropicamide were studied in 84 young adults for 90 min following topical instillation. Pupillary diameter was estimated (a) under ambient photopic illumination and (b) when illumination was increased to that associated with direct ophthalmoscopy. Evaluation was made of the "degree of mydriasis," i.e., the difference in pupillary diameter between the eye receiving the mydriatic agent and the contralateral control eye when the pupillary light reflex was stimulated. In subjects with light or hazel irides, phenylephrine caused maximal dilatation in 60 to 75 min, mean values being 5.6 mm with 1 drop of 2%, 6.0 mm with 2 drops of 2.5%, and 7.1 mm with 1 drop of 10%. Maxiumum degrees of mydriasis were 3.0 mm with 2 drops of 2.5% and 3.1 mm with 1 drop of 10%. With 0.5% tropicamide, maximum diameter was 8.0 mm in 30 min in subjects with light, hazel, or brown irides, and the maximum degree of mydriasis was 5.0 mm. It is concluded that when a mydriatic agent is used to facilitate intraocular visualization, neither specification in terms of (a) maximum diameter under ambient illumination nor (b) degree of mydriasis provides optimal characterization. It is suggested that the "clinically effective diameter," i.e., pupillary diameter under illumination corresponding to that to be used during examination, would be the most useful specification.

Adaptation, Ocular↗

PubMed1985

Sector pupil dilation with phenylephrine and tropicamide.

A comparison of sector pupil dilation produced with 2.5% phenylephrine and 1.0% tropicamide was carried out on nine subjects. We found that 2.5% phenylephrine produced a significant increase in the vertical as compared to the horizontal diameter at 10, 20, 30, 40, and 50 min after instillation of the drug with the maximum vertical diameter occurring at 40 min. The pupil diameter in the vertical and horizontal meridians before drug instillation was 3.7 mm +/- 0.2 (mean +/- SE) whereas at 40 min the vertical and horizontal diameters were 6.7 mm +/- 0.4 and 5.2 mm +/- 0.3, respectively. Instillation of 1% tropicamide produced equal dilation of the vertical and horizontal diameters, which was maximum at 40 min. Before drug instillation, the pupils were 3.7 mm +/- 0.2 (mean +/- SE) in both the horizontal and vertical meridians. At 50 min the pupil diameter was 7.0 mm +/- 0.2 in both meridians in the eye that received tropicamide.

Adult↗

PubMed1986

Effect of phenylephrine on accommodation.

We studied the effect of the topical instillation of phenylephrine hydrochloride on accommodation. Factors considered were iris color and the influence of the prior application of a topical anesthetic. There has been controversy concerning the role of the sympathetic nervous system in accommodation. Our results indicate that the sympathetic nervous system does influence accommodation. Prior application of an anesthetic prolongs the effect of phenylephrine on the accommodation and on pupil diameter in eyes with either lightly or more heavily pigmented irides.

Accommodation, Ocular↗

PubMed1993

Disagreement between standard transthoracic impedance cardiography and the automated transthoracic electrical bioimpedance method in estimating the cardiovascular responses to phenylephrine and isoprenaline in healthy man.

1. Impedance cardiography is a well-established noninvasive method to assess within-subject changes of cardiovascular function. We compared the standard approach (ZCG) which requires tedious signal analysis with an automated approach (TEB: NCCOM 3) with its own specific equipment, algorithms and equations in order to assess agreement of the method-specific measurements and calculations. 2. Ten healthy men were studied on two occasions with either ZCG or TEB, at rest and at the end of 5 min i.v.-infusions with 1 microgram min-1 isoprenaline and 100 micrograms min-1 phenylephrine. 3. There was good agreement for the method-independent changes (HR, SBP/DBP), but there were large differences for method-specific measurements: dZ/dtmax [TEB-ZCG] = -0.68, CI: -0.83 to -0.53 ohm s-1, PEP [TEB-ZCG] = -22.1, CI: -35.0 to -9.2 ms and QS2c [TEB-ZCG] = -16.5, CI: -32.4 to -0.6 ms and for the calculated stroke volume SV [TEB-ZCG] = 30.3, CI: 15.5 to 45.2 ml. The responses of dZ/dtmax and SV to isoprenaline and phenylephrine, although qualitatively similar, reached no quantitative agreement either. A substantial disagreement was evident for the STI responses to isoprenaline where TEB failed to detect the expected reduction of VETc and thus grossly underestimated the shortening of QS2c. 4. It is concluded that TEB-measurements and -calculations did not agree with standard ZCG, that the methods, albeit related, cannot be considered as interchangeable and that suspicion is justified that TEB might yield erroneous results under specific circumstances.

Adult↗

PubMed1986

Chemical stabilities of lignocaine hydrochloride and phenylephrine hydrochloride in aqueous solution.

The chemical stabilities of lignocaine hydrochloride (lidocaine hydrochloride) and phenylephrine hydrochloride in a combination aqueous solution have been determined using stability-indicating high-performance liquid chromatographic methods. The drugs did not interact and were stable for at least 66 days at room temperature. The pH value changed from 6.0 to 5.8 after 66 days but was still within the optimum pH range for the stabilities of lignocaine and phenylephrine.

Chromatography, High Pressure Liquid↗

PubMed1998

Effects of verapamil, sodium nitroprusside and calcium deprivation on the phenylephrine-induced contraction of smooth muscle strips from the reticular groove of adult cattle.

The effects of verapamil, sodium nitroprusside and calcium deprivation on the smooth muscle strips from the floor of the reticular groove of adult cattle were studied. The mechanical activity of the muscle strip was recorded isometrically. Contraction was induced with phenylephrine (10(-6) mol/l) in Tyrode solution. Verapamil (10(-6) mol/l) produced a high inhibition of the response, phasic and tonic (P < 0.05). Sodium nitroprusside (10(-6) mol/l) reduced mainly the phasic contraction (P < 0.05). Deprivation of Ca2+ from extracellular medium produced a high inhibition of the tonic phase. This study indicates that the action of verapamil on the reticular groove smooth muscle may be partially related to blockade of calcium entry through voltage-dependent channels, opened during phenylephrine stimulation. However, the nitroprusside action could be attributed to effect on the extrusion of calcium.

Animals↗