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PubMed1990

Comparison of 2.5% and 10% phenylephrine in the elevation of upper eyelids with ptosis.

The Mueller's muscle-conjunctival resection procedure has been effective in treating ptosis in eyelids that elevate upon instillation of topical 10% phenylephrine (Neo-Synephrine). The small risk of an adverse systemic reaction to phenylephrine could be even further decreased by using 2.5% phenylephrine instead of 10% phenylephrine. In order to assess the feasibility of using 2.5% phenylephrine instead of 10% phenylephrine in ptosis evaluation, we compared the amount of upper eyelid elevation produced by the two solutions. Thirty ptotic upper eyelids in 20 patients exposed to 10% phenylephrine rose an average of 0.2 mm higher than the same lids exposed to 2.5% phenylephrine. Although this difference was statistically significant, we suspect that the small magnitude of this difference would have little effect on the decision to perform a Mueller's muscle-conjunctival resection procedure or on the calculation of the amount of tissue to resect.

Blepharoptosis↗

PubMed1988

Effect of calcium entry blockade on the actions of phenylephrine on the taenia of the guinea pig caecum.

The interaction between phenylephrine and calcium entry blockers was studied on the taenia of the guinea-pig caecum using the double sucrose gap method. Sustained hyperpolarization, relaxation and attenuation of evoked electrical and mechanical activity were induced by non-cumulative addition of phenylephrine (0.1 to 250 mumol.1-1) for 2 to 4 min. When the alpha 1-adrenoceptor agonist was applied for a prolonged period (20 to 60 min) the initial inhibitory response gradually disappeared both at room temperature and at 32 degrees C. The renewed action potentials were accompanied by a positive afterpotential. The initial hyperpolarization and its delayed recovery in course of the phenylephrine effect were significantly reduced in calcium-free medium containing EDTA (2 mmol.1-1), after pretreatment with nifedipine (0.1 to 1 mumol.1-1), verapamil (10 to 100 mumol.1-1) or procaine (0.5 to 2 mmol.1-1). In contrast sodium nitroprusside (10 to 100 mumol.1-1) which produced biphasic changes similar to those of phenylephrine, did not affect the initial and delayed phase of phenylephrine action. Ba2+(5 mmol.1-1) could substitute for Ca2+ in the generation of action potentials but could not substitute for Ca2+ in the mechanisms responsible for the initial and delayed recovery phase of phenylephrine effects. In the presence of La3+ and Mn2+ (0.5 to 3 mmol.1-1) the phenylephrine effects were reduced. In contrast, in the presence of extracellular Ca2+, pretreatment with Mg2+ (12 mmol.1-1) or Ba2+ (5 mmol.1-1) did not affect the action of phenylephrine. It is concluded that activation of alpha 1-adrenoceptors results in the release of Ca2+ from an intracellular store, which leads to the opening od TEA-sensitive potassium channels, causing the initial phase of alpha 1-adrenoceptor action. Ca2+ is loaded into this intracellular store by entering the cell through the potential sensitive calcium channels. Although the mechanisms responsible for the delayed phase could not be clarified, its dependence on the presence of the initial phase is apparent.

Action Potentials↗

PubMed1983

Blood pressure response to phenylephrine infusion in halothane-anesthetized dogs given acetylpromazine maleate.

To quantitate acetylpromazine-induced alpha-adrenergic receptor blockade, phenylephrine was infused into dogs. The amount of phenylephrine necessary to increase the mean arterial blood pressure (MAP) 50% above base line, with or without the prior administration of acetylpromazine, served to quantify the degree of acetylpromazine-induced alpha-adrenergic receptor blockade. Seven dogs were anesthetized with thiopental, maintained on halothane in oxygen, and mechanically ventilated. All infusions were made through a catheter in the cephalic vein. Continuous recordings were made of MAP and a lead II ECG. After induction of anesthesia, instrumentation, and stabilization of heart rate, MAP, and ventilation, 6 group I dogs were infused with phenylephrine until a 50% increase in MAP was recorded (phenylephrine control). On subsequent research days, each dog was anesthetized, instrumented as described, and given (IV) 1 of 3 dosages of acetylpromazine in the following order--0.05, 0.125, and 0.25 mg/kg. The dose of phenylephrine necessary to increase MAP 50% in the presence of acetylpromazine was recorded. Five group II dogs were studied as in group I, but each dog was given (IM) atropine (0.04 mg/kg) before anesthetization. Two dosages of acetylpromazine were studied in the following order--0.05 and 0.25 mg/kg. Group I dogs, when compared with their phenylephrine controls, were given significantly more phenylephrine to raise MAP 50% at each dose of acetylpromazine studied. The same trend was observed in group II dogs, but at smaller doses of phenylephrine, probably as a result of the positive chronotropic effect of atropine on the heart.

Acepromazine↗

PubMed1984

Pharmacokinetics and neural blockade after subarachnoid lidocaine in the rhesus monkey. III. Effects of phenylephrine.

Using a rhesus monkey model, lidocaine (30 mg) in 7.5% dextrose was compared with lidocaine (30 mg) in 7.5% dextrose containing 1.5 mg of phenylephrine (Neosynephrine). Phenylephrine increased both duration of maximum motor block and time for complete motor recovery. A significantly higher sensory dermatome level and significantly longer time for complete sensory recovery was found when the lidocaine solution contained phenylephrine. Time for two-segment regression of sensory blockade was unaffected by phenylephrine. The slope of the regression phase for motor block was parallel for both treatments, suggesting differences in neural blockade were caused by a more profound initial block when phenylephrine was added. Pharmacokinetic analysis revealed identical absorption and elimination constants. Maximum plasma concentrations of lidocaine and time to reach maximum plasma concentrations were identical with and without phenylephrine. The systemic absorption (fraction of drug absorbed from the subarachnoid space) was complete with and without phenylephrine. No lag times for systemic absorption were found for either treatment. Our data demonstrate that there are no clinically significant differences between phenylephrine and epinephrine when added to lidocaine solutions for spinal anesthesia.

Anesthesia, Spinal↗

PubMed1992

Intracellular calcium-mediated activation of hepatic Na+/H+ exchange by arginine vasopressin and phenylephrine.

The effect of Ca++ mobilizing agonists arginine vasopressin and phenylephrine on Na+/H+ exchange was studied in freshly isolated hepatocytes and isolated perfused rat livers. The activity of Na+/H+ exchange was determined from the rate of H+ efflux, 22Na uptake and pHi recovery. Arginine vasopressin and phenylephrine stimulated H+ efflux and 22Na uptake in isolated rat hepatocytes and increased the rate of pHi recovery from acid-loaded hepatocytes. These effects were inhibited by amiloride. Arginine vasopressin- and phenylephrine-induced increases in H+ efflux were also dependent on extracellular Na+. Arginine vasopressin- and phenylephrine-induced increases in intracellular Ca++ concentration, H+ efflux, 22Na uptake and intracellular pH recovery were decreased in hepatocytes preloaded with the Ca(++)-buffering agent [bis-(2-amino-5-methylphenoxy)-ethane-N,N,N',N'-tetraacetic acid] (MAPTA). Na+/H+ exchange-dependent intracellular pH recovery from cytosolic acidification was stimulated by thapsigargin, which increases intracellular calcium concentration by inhibiting endoplasmic reticulum Ca++ ATPase. Arginine vasopressin- and phenylephrine-induced increases in intracellular pH recovery were not dependent on extracellular Ca++ and were inhibited by calmidazolium, a calmodulin inhibitor. Arginine vasopressin and phenylephrine also increased H+ efflux in the absence but not in the presence of amiloride in perfused rat livers without affecting biliary HCO3- excretion. These results indicate that arginine vasopressin and phenylephrine activate Na+/H+ exchange in rat hepatocytes, an effect mediated in part by intracellular Ca++ and calmodulin kinase. Furthermore, sinusoidal Na+/H+ exchange does not appear to be involved in biliary HCO3- excretion.

Animals↗

PubMed1980

The neuronal and extraneuronal uptake and deamination of 3H-(-)-phenylephrine in the perfused rat heart.

The neuronal and extraneuronal uptake and deamination of 3H-(-)-phenylephrine was studied in perfused rat hearts obtained from reserpine-pretreated animals. 1. Under the conditions of steady-state perfusion with 5 mumol/l 3H-(-)-phenylephrine slightly more than 50% of total deamination took place in adrenergic nerve endings, slightly less than 50% in the extraneuronal tissue. 2. 3H-(-)-phenylephrine is preferentially deaminated to the glycol metabolite. 3. There is pronounced non-saturable, cocaine- and corticosterone-resistant uptake of 3H-(-)-phenylephrine in the perfused rat heart. 4. The apparent rate constants for the efflux of the glycol metabolite is about 20 times higher than that for the efflux of the acid metabolite. 5. For both the glycol and the acid metabolite of 3H-(-)-phenylephrine, apparent rate constants for the efflux declined when the duration of the perfusion with the labelled parent amine was prolonged. This phenomenon was also observed when the deamination of 3H-(-)-phenylephrine was restricted to either the adrenergic nerve endings or the extraneuronal tissue. These results are interpreted as evidence for a distribution of each metabolite into at least two kinetically different compartments. 6. This was confirmed for the acid metabolite by determination of a biphasic efflux curve in wash-out experiments in which MAO was inhibited during wash-out (after an initial loading of the adrenergic nerve endings with 3H-(-)-phenylephrine).

Animals↗

PubMed1986

Analysis of phenylephrine in plasma: initial data about the concentration-effect relationship.

A simple and sensitive assay for phenylephrine in plasma using HPLC with electrochemical detection is presented. Infusion of phenylephrine hydrochloride 0.5, 1.0, 2.0, and 4.0 micrograms X kg-1 X min-1 for 6 min at each dose level to 9 healthy subjects resulted in mean venous plasma concentrations of phenylephrine of 20, 56, 118 and 308 nM, respectively. The systolic and diastolic blood pressures were increased and the heart rate and venous plasma noradrenaline levels fell with increasing phenylephrine concentrations. There was a more than two-fold interindividual variation in the plasma concentration during infusion of the standardized doses of phenylephrine, with overlap of the concentrations achieved at the different dose levels. Estimates of the sensitivity to phenylephrine showed discrepancies within individuals when expressed as the concentration (PC20) or dose (PD20) required to increase systolic blood pressure by 20 mm Hg. Thus, evaluation of concentration-response curves should be more reliable than of dose-response curves when assessing phenylephrine sensitivity during i.v. infusions.

Adult↗

PubMed1988

Differential responses of rat pineal thyroxine type II 5'-deiodinase and N-acetyltransferase activities to either light exposure, isoproterenol, phenylephrine, or propranolol.

1. Compared to pineal N-acetyl transferase (NAT) activity, which exhibited a dramatic drop following acute light exposure at night, nocturnal rat pineal thyroxine type II 5'-deiodinase (5'-D) activity was minimally influenced by the same light exposure. The injection of cycloheximide, a potent inhibitor of protein synthesis, although it did curtail the rise in NAT activity for at least 2 hr, did not elicit decreases in the activities of either 5'-D or NAT enzymes. Propranolol, a beta-adrenergic blocker, either delayed the continued nocturnal rise in 5'-D activity when injected at 0000 hr or slightly enhanced the fall in 5'-D activity when injected at 0200 hr. These results suggest that interruption of the synthesis of proteins is responsible for the slow deterioration of 5'-D activity induced by either light or propranolol. 2. The slight fall in 5'-D activity induced by light at night was prevented by isoproterenol; phenylephrine, however, did not prevent the fall and the effect of isoproterenol + phenylephrine was similar to that obtained with isoproterenol alone. On the other hand, the light-inhibited NAT activity recovered after the injection of isoproterenol; phenylephrine did not elicit any effect, but the injection of both isoproterenol and phenylephrine simultaneously caused a greater NAT response than that induced by isoproterenol alone. 3. When injected during the day, phenylephrine had no effect on either pineal 5'-D or NAT activities; however, the injection of either isoproterenol alone or isoproterenol + phenylephrine elicited 5-fold and 10-fold increases in nocturnal, light-suppressed 5'-D and NAT activities, respectively. During the day, phenylephrine did not potentiate the effects of isoproterenol on NAT activity as it did at night. When the effects of isoproterenol on the 5'-D activity were compared to rats exposed to light during the day and at night, the activity of 5'-D reached a higher level at night than during the day.

Animals↗

PubMed1994

The role of extracellular calcium in pregnancy-induced attenuation of phenylephrine contraction in rat aorta with functional endothelium.

The effect of pregnancy on the supply of calcium ions for the contractile responses of rat aortic rings to phenylephrine was investigated. The contractility of intact aortic rings from pregnant rats, compared with that of similar rings from non-pregnant rats, to phenylephrine and potassium chloride was significantly decreased. Contractions of rings from non-pregnant rats, pretreated with phenylephrine or potassium chloride, in response to calcium chloride were greater than those of similarly treated rings from pregnant rats. When the concentration of calcium chloride in the medium bathing the rings was reduced to 0.8 mmol.l-1, the contractile response to phenylephrine was significantly (P < 0.005) inhibited in rings from both pregnant and non-pregnant rats but to a greater extent in rings from non-pregnant rats. Contractions of aortic rings from pregnant rats in response to phenylephrine in calcium-free medium were similar to those of rings from non-pregnant rats, suggesting equal dependence on calcium from intracellular stores. The results suggest that pregnancy decreased the response to calcium influx into the aortic smooth muscle cells through both receptor- and voltage-operated calcium entry pathways. Since de-endothelialization reversed the pregnancy-induced diminished contraction to phenylephrine, it is likely that pregnancy interfered with contractions induced by activation of receptors with phenylephrine through enhanced production of endothelium-derived relaxing factor(s).

Animals↗

PubMed1995

Enhancement of pressor response to intravenous phenylephrine following oral clonidine medication in awake and anaesthetized patients.

Clonidine, an alpha 2-adrenergic agonist, augments the pressor response to intravenous ephedrine. If this effect is partly due to clonidine-induced potentiation of alpha 1-adrenoceptor-mediated vasoconstriction, it is also assumed that clonidine would enhance the pressor effect of phenylephrine as an alpha 1-adrenergic agonist. The authors studied haemodynamic responses to intravenous phenylephrine in 80 patients who received either preanaesthetic medication with clonidine approximately 5 micrograms.kg-1 po (clonidine group, n = 40), or no medication (control group, n = 40). Each group was further divided into either awake subjects (n = 20) or subjects anaesthetized with enflurane and nitrous oxide in oxygen (n = 20). Haemodynamic measurements were made at one-minute intervals for ten minutes after phenylephrine 2 micrograms.kg-1 iv was injected as a bolus. The magnitudes of maximal mean blood pressure increases in the clonidine group (26 +/- 7% (mean +/- SD) for awake and 32 +/- 15% for anaesthetized subjects) were greater (P < 0.05) than in the control group (13 +/- 7% for awake and 18 +/- 7% for anaesthetized subjects). However, there was no difference in the pressor effect of phenylephrine between awake and anaesthetized patients in both groups. Oral clonidine preanaesthetic medication, 5 micrograms.kg-1, augments the pressor responses to phenylephrine 2 micrograms.kg-1 iv in awake and anaesthetized patients. These results suggest that the enhancement of the pressor responses to phenylephrine following oral clonidine may be due to clonidine-induced potentiation of alpha 1-adrenoceptor-mediated vasoconstriction. This implies that restoration of blood pressure can be achieved effectively by phenylephrine in hypotensive patients with clonidine premedication.

Administration, Oral↗

PubMed2005

C2-ceramide induces vasodilation in phenylephrine-induced pre-contracted rat thoracic aorta: role of RhoA/Rho-kinase and intracellular Ca2+ concentration.

It is known that ceramide may play an important regulatory role in vascular tone although its effect on vascular tone and the mechanisms involved are controversial. The present study was designed to investigate the effects of ceramide and its key initial regulators, TNF-alpha and neutral sphingomyelinase (SMase), on vascular tone of isolated rat thoracic aortic rings and elucidate the mechanisms involved in the changes in vascular tone induced by ceramide. Contractile responses and Fura-2 Ca2+ signals were measured in rat thoracic aortic rings or strips. 10(-5) M C2-ceramide, 0.1 U/ml neutral sphingomyelinase (SMase), and 5x10(-7) g/ml TNF-alpha had no effect on resting tone in rat thoracic aortic rings. However, in phenylephrine-induced pre-contracted rings, treatment with ceramide, SMase, and TNF-alpha evoked a gradual but sustained vasodilation. Vasodilation effect in response to 10(-5) M C2-ceramide was not significantly changed by the absence or presence of endothelium, a cyclooxygenase pathway inhibitor (10(-6) M indomethacin), or PKC inhibitors (10(-5) M H-7 & 5x10(-7) M calphostin-C). Pretreatment with 1 microM Y-27632, a RhoA/Rho-kinase inhibitor, significantly inhibited the phenylephrine-induced contraction itself as well as the C2-ceramide-induced vasodilation. Pre-treatment with 10(-5) M C2-ceramide had no effect on phasic rise in [Ca2+]i and tension evoked by stimulation with 10(-8) M phenylephrine, but post-treatment of C2-ceramide significantly reduced the phenylephrine-induced secondary tonic [Ca2+]i and tension plateau. Our results indicate that C2-ceramide induces vasodilation in phenylephrine-induced pre-contracted rat thoracic aorta. Furthermore, inhibition of phenylephrine-induced activation of RhoA/Rho-kinase pathway as well as phenylephrine-induced elevations in [Ca2+]i are clearly a key factors in C2-ceramide-induced vasodilation.

Animals↗

PubMed1994

Phenylephrine plus propranolol improves the balance between myocardial oxygen supply and demand during experimental cardiopulmonary resuscitation.

Epinephrine increases coronary blood flow but may not improve the balance between myocardial oxygen supply and demand during cardiopulmonary resuscitation (CPR). The objective of this study was to determine whether this balance can be improved by administering a relatively pure alpha-adrenergic vasoconstrictor, alone or in combination with a beta-adrenergic blocker. We measured coronary perfusion pressures during CPR and myocardial adenosine 5'-triphosphate (ATP) and lactate concentrations in biopsies obtained immediately after 10 minutes of CPR in six control dogs and in three groups of six dogs each given large doses of epinephrine, phenylephrine, or phenylephrine plus propranolol during CPR. Coronary perfusion pressure during CPR was higher in the three treated groups than in the control group, although differences were limited to the early portion of CPR in dogs given epinephrine or phenylephrine alone. Postresuscitation myocardial ATP concentration was significantly higher (29.5 +/- 3.0 vs 22.6 +/- 1.8 nmol/mg of protein, p < 0.05) and myocardial lactate concentration tended to be lower (52.8 +/- 13.6 vs 78.5 +/- 15.2 nmol/mg of protein) than in the control group in dogs given both phenylephrine and propranolol. In contrast, myocardial ATP concentration tended to be lower than in the control group in epinephrine-treated dogs, and myocardial lactate concentrations were higher than in the control group in dogs treated with either epinephrine (p < 0.05) or phenylephrine alone (p = 0.052). We conclude that the balance between myocardial oxygen supply and demand during CPR can be improved by administering a combination of phenylephrine and propranolol, but not by administering large doses of epinephrine or phenylephrine alone.

Adenosine Triphosphate↗

PubMed1984

Phenylephrine-induced activity in mice as a model of central alpha 1-adrenoceptor function. Effects of acute and repeated administration of antidepressant drugs and electroconvulsive shock.

Intracerebroventricular injection of the alpha 1-agonists phenylephrine (10-100 micrograms) or methoxamine (10-50 micrograms) produced a dose-dependent increase in locomotor activity and behavioural excitation in mice. The syndrome induced by phenylephrine was inhibited by prazosin but not yohimbine, RX 781094 or propranolol. Methoxamine-induced responses were, however, also reduced by yohimbine. Activity induced by phenylephrine was not affected by metergoline or pirenperone but was reduced by haloperidol and spiroperidol. This latter effect, however, may have been due to inhibition of alpha 1-adrenoceptors and/or dopamine receptors. Pretreatment with alpha-methyl-p-tyrosine or FLA-63 reduced responses to phenylephrine by respectively inhibiting either the locomotor activity or the other behavioural components of the syndrome. This suggests that some residual noradrenergic and possibly also dopaminergic function may be necessary for the behavioural expression of the effects of phenylephrine. The activity was inhibited by mianserin and amitriptyline but not by desmethylimipramine. When these antidepressant drugs were given twice daily for 14 days, mianserin alone affected the activity induced by phenylephrine, tested either 12 or 60 hr after the final injection. This behaviour was also not altered 24 hr after the mice had received an electroconvulsive shock under halothane anaesthesia, once daily for 10 days. In conclusion, the data suggest that the behavioural syndrome induced by phenylephrine probably provides a specific and quantifiable assessment of central alpha 1-adrenoceptor function and that in general this is unaltered following repeated administration of antidepressant drugs or electroconvulsive shock.

Adrenergic alpha-Agonists↗

PubMed2006

Coronary vasomotor response to phenylephrine in heart transplant patients.

BACKGROUND: Coronary vasomotor responses to sympathetic stimulation vary with endothelial-layer integrity or presence of atherosclerosis. Our study objective was to assess the effects of phenylephrine-induced alpha-adrenergic stimulation on coronary vasomotion in heart transplant recipients with and without graft atherosclerosis. METHODS: Intracoronary phenylephrine (alpha(1)-selective agonist) was injected in 6 control subjects, 9 recipients with angiographically normal coronary arteries and 8 recipients with mild or moderate atherosclerosis. Coronary flow velocity was measured using a Doppler guide-wire. The diameters of 3 epicardial segments of the left coronary artery and coronary blood flow and resistance were assessed at baseline, after infusion of increasing acetylcholine doses (10(-7) and 10(-6) mol/liter) and after phenylephrine (150- to 200-microg bolus). Systemic and coronary hemodynamic parameters were measured immediately after acetylcholine and 1, 3, 5, 7, 10 and 15 minutes after phenylephrine. RESULTS: Phenylephrine induced similar significant increases in rate pressure product in the 3 groups. Acetylcholine induced epicardial vasodilation in controls and vasoconstriction in transplant recipients. Phenylephrine induced epicardial vasodilation in controls and in angiographically normal recipients; subsequent vasoconstriction occurred in this last group. In the recipients with angiographic abnormalities, sustained vasoconstriction occurred. At peak phenylephrine effect, coronary blood flow (CBF) increased significantly (p < 0.001 vs baseline) in all 3 groups. Coronary resistance decreased in the 3 groups but the decrease was smaller in the recipients with angiographic abnormalities (p < 0.05 vs controls). CONCLUSIONS: In heart transplant patients, graft atherosclerosis unmasks the direct coronary vasoconstricting effects of pharmacologic alpha-adrenergic stimulation.

Acetylcholine↗

PubMed1987

Improving the therapeutic index of topical phenylephrine by reducing drop volume.

This study examined the effect of reducing eyedrop volume on the efficacy and systemic absorption of a given quantity of phenylephrine hydrochloride. Aqueous phenylephrine hydrochloride (2.5%) given in the commercially available drop volume of 32 microliters was compared with 10% aqueous phenylephrine given in an 8-microliters volume. Both preparations contained the same total amount of phenylephrine per drop. Ten subjects had both eyes dilated with each of the phenylephrine solutions according to a randomized, double-crossover sequence. The mean final pupillary diameter was nearly 1.0 mm larger for the 8-microliters drop (P = 0.0033). Nine of ten subjects achieved a larger pupillary diameter with the 8-microliters drop. Systemic absorption, as measured by plasma phenylephrine level, was similar for the two drop volumes. Thus, the 8-microliters drop achieved a significantly larger pupillary dilation without an increase in systemic absorption. Phenylephrine may have the most favorable risk-benefit ratio when administered as a high concentration in a small volume.

Administration, Topical↗

PubMed1987

The effect of high-dose phenylephrine versus epinephrine on regional cerebral blood flow during CPR.

Prior studies have not found the alpha agonist phenylephrine, in a dose of 0.1 mg/kg, to be as effective as 0.20 mg/kg of epinephrine in improving regional cerebral blood flow (CBF) during CPR in swine. We undertook this study to assess whether higher doses of phenylephrine might improve regional CBF. Fifteen swine were allocated to receive either epinephrine 0.2 mg/kg, phenylephrine 1.0 mg/kg, or phenylephrine 10 mg/kg. Regional CBF measurements were made during normal sinus rhythm, during CPR, and during CPR following drug administration. Epinephrine 0.2 mg/kg was significantly better in improving regional CBF to the left and right cerebral cortices, cerebellum, midbrain, and cervical cord than was phenylephrine 1.0 mg/kg. There was no significant difference in regional CBF between the animals receiving epinephrine 0.2 mg/kg and phenylephrine 10 mg/kg. The study shows that large doses of epinephrine and phenylephrine may be required during CPR to improve regional cerebral blood flow following a prolonged arrest.

Animals↗

PubMed2003

Response of the parotid gland of red kangaroos, Macropus rufus, to phenylephrine stimulation.

Intracarotid infusions of l-phenylephrine at 1.0 or 10 nmol kg(-1) min(-1) were accompanied by increases in salivary amylase activity, protein, potassium, magnesium and chloride relative to cholinergically-stimulated saliva. Intravenous infusions of phenylephrine at the same dose rates had a lesser effect on salivary composition particularly protein. Propranolol administered with phenylephrine via the carotid artery, at an antagonist/agonist ratio of 10:1, was much more effective in blocking the phenylephrine-induced changes in salivary composition than equimolar infusion of phentolamine with phenylephrine. It was concluded that alpha(1)-adrenoreceptors were not present in functionally significant numbers in the gland and that the effect of phenylephrine on the kangaroo parotid was mediated by beta-adrenoreceptors. As the phenylephrine dose rates in the kangaroos were comparable with those used to determine alpha-adrenergic responses of eutherian salivary glands and as phentolamine appeared to have minor beta-sympathomimetic activity, at least one subtype of beta-adrenoreceptors in macropods may not be identical to its eutherian counterpart.

Adrenergic alpha-Agonists↗

PubMed2000

The effect of phenylephrine on pain and flare intensity in eyes with uveitis.

PURPOSE: To investigate the influence of protein concentration in the anterior chamber, measured by laser flare meter, on pain sensation after phenylephrine instillation in patients with iridocyclitis. METHODS: Twenty-five consecutive patients with iridocyclitis were included. Patients with cataract, exfoliation syndrome, diabetes mellitus, glaucoma or any other previous ocular diseases or ocular surgery were excluded. Patients were divided into two groups: Group 1--without fibrinoid reaction (FR) in the anterior chamber (18 patients), and Group 2--with FR (7 patients). Protein concentration in the anterior chamber was measured with laser flare meter (FC 500, Kowa Co., Japan). Pupil size was measured by Alcon Tilo Scale, and pain sensation was estimated by Visual Analogue Scale (VAS, Kabi Pharmacia). All measurements were done before and 1 hour after topical instillation of 10% phenylephrine hydrochloride into the subconjunctival sac of the inflamed eyes. RESULTS: Eyes with iridocyclitis and fibrinoid reaction (FR) have a higher flare intensity compared to those without FR (p<0.05). Pupil size was significantly increased after phenylephrine instillation in both study groups (Wilcoxon test, p<0.05). The VAS pain and flare intensity were significantly decreased in group without FR after phenylephrine instillation (Group 1) compared to values before treatment (Wilcoxon test, p<0.05). In eyes with FR (Group 2), no significant influence of phenylephrine instillation was found on VAS pain and flare intensity. CONCLUSIONS: After phenylephrine instillation, flare intensity and pain were significantly decreased only in eyes with iridocyclitis and without FR. The decreasing level of flare intensity, and paralysis of the pupil after phenylephrine instillation seem to alleviate pain in those eyes.

Adult↗